Neuromuscular transmission occurs at the neuromuscular junction, where motor neuron axon terminals synapse with skeletal muscle fibers. Acetylcholine is released from motor neuron terminals and binds to nicotinic acetylcholine receptors on the muscle fiber membrane, causing depolarization and muscle fiber excitation. Acetylcholine is rapidly broken down by acetylcholinesterase to terminate the signal. Diseases like myasthenia gravis can disrupt neuromuscular transmission.
This document discusses neuromuscular transmission and neuromuscular blockers. It begins by describing the neuromuscular junction and its role as a model synapse. It then discusses the structure and function of the motor unit and details the sequence of events in neuromuscular transmission from the arrival of an action potential to muscle contraction. It also describes neuromuscular blockers' mechanisms of action and diseases that affect the neuromuscular junction like myasthenia gravis.
The neuromuscular junction consists of the motor neuron axon terminal, synaptic cleft, and motor end plate of muscle fiber. Acetylcholine is synthesized in the neuron, stored in vesicles, and released into the synaptic cleft upon arrival of an action potential. It binds nicotinic receptors on the muscle, opening ion channels and initiating an endplate potential that spreads and causes muscle contraction. Acetylcholine is then broken down by acetylcholinesterase to terminate its effect. Nondepolarizing muscle relaxants block transmission by preventing acetylcholine binding, while depolarizing relaxants directly activate ion channels. Anesthetic drugs can also impact transmission through desensitization or channel blockade effects.
A brief overview of the physiology of the neuromuscular junction.It includes a video towards the end sourced from the internet with the copyright watermarks intact.
This document summarizes the neuromuscular transmission process, including the structure and function of the neuromuscular junction, the role of acetylcholine, and the effects of various drugs. It describes how motor neurons innervate muscle fibers to form motor units. Transmission involves the release of acetylcholine from the motor neuron terminal, which binds nicotinic receptors and opens ion channels on the muscle fiber membrane. Various toxins and conditions like myasthenia gravis and Lambert-Eaton syndrome can disrupt this process.
The document discusses the neuromuscular physiology of the neuromuscular junction (NMJ). It describes:
1) The anatomy of the NMJ including the pre-synaptic membrane, synaptic cleft, and post-synaptic membrane.
2) The normal process of neuromuscular transmission including the release and binding of acetylcholine to receptors and the generation of an end-plate potential.
3) The role of calcium in the release and regulation of acetylcholine from the nerve terminal.
The document discusses the neuromuscular junction (NMJ), which is the synapse between a motor neuron and muscle fiber that converts electrical signals from the neuron into muscle activity. It describes the structure of the NMJ including the motor endplate and synaptic cleft. Events of neuromuscular transmission such as acetylcholine release and destruction are summarized. The document also discusses myasthenia gravis, an autoimmune disease caused by antibodies against acetylcholine receptors, and its symptoms and treatment with cholinesterase inhibitors.
The spinal cord is approximately 45-50 cm long and 2 cm in diameter. It begins at the foramen magnum and terminates around the L1-L2 vertebrae in adults. The spinal cord has ascending tracts that carry sensory information to the brain and descending tracts that carry motor commands from the brain. It is protected by the vertebrae, meninges, cerebrospinal fluid, and contains gray matter in an H-shaped arrangement surrounded by white matter tracts. Injuries and diseases of the spinal cord can result in sensory and motor deficits depending on the level and severity of the lesion.
This document discusses the neuro-muscular junction, including its structure, function, and related disorders. It begins by outlining the objectives of describing the junction's schematic diagram, transmission events, neuromuscular blockers and their mechanisms, and common disorders. It then provides details on the presynaptic and postsynaptic portions, the synaptic cleft, acetylcholine receptors, and the steps of neuromuscular transmission. Examples are given of neuromuscular blockers like curare and their mechanisms of action. Disorders covered include myasthenia gravis and Lambert-Eaton syndrome.
This document discusses neuromuscular transmission and neuromuscular blockers. It begins by describing the neuromuscular junction and its role as a model synapse. It then discusses the structure and function of the motor unit and details the sequence of events in neuromuscular transmission from the arrival of an action potential to muscle contraction. It also describes neuromuscular blockers' mechanisms of action and diseases that affect the neuromuscular junction like myasthenia gravis.
The neuromuscular junction consists of the motor neuron axon terminal, synaptic cleft, and motor end plate of muscle fiber. Acetylcholine is synthesized in the neuron, stored in vesicles, and released into the synaptic cleft upon arrival of an action potential. It binds nicotinic receptors on the muscle, opening ion channels and initiating an endplate potential that spreads and causes muscle contraction. Acetylcholine is then broken down by acetylcholinesterase to terminate its effect. Nondepolarizing muscle relaxants block transmission by preventing acetylcholine binding, while depolarizing relaxants directly activate ion channels. Anesthetic drugs can also impact transmission through desensitization or channel blockade effects.
A brief overview of the physiology of the neuromuscular junction.It includes a video towards the end sourced from the internet with the copyright watermarks intact.
This document summarizes the neuromuscular transmission process, including the structure and function of the neuromuscular junction, the role of acetylcholine, and the effects of various drugs. It describes how motor neurons innervate muscle fibers to form motor units. Transmission involves the release of acetylcholine from the motor neuron terminal, which binds nicotinic receptors and opens ion channels on the muscle fiber membrane. Various toxins and conditions like myasthenia gravis and Lambert-Eaton syndrome can disrupt this process.
The document discusses the neuromuscular physiology of the neuromuscular junction (NMJ). It describes:
1) The anatomy of the NMJ including the pre-synaptic membrane, synaptic cleft, and post-synaptic membrane.
2) The normal process of neuromuscular transmission including the release and binding of acetylcholine to receptors and the generation of an end-plate potential.
3) The role of calcium in the release and regulation of acetylcholine from the nerve terminal.
The document discusses the neuromuscular junction (NMJ), which is the synapse between a motor neuron and muscle fiber that converts electrical signals from the neuron into muscle activity. It describes the structure of the NMJ including the motor endplate and synaptic cleft. Events of neuromuscular transmission such as acetylcholine release and destruction are summarized. The document also discusses myasthenia gravis, an autoimmune disease caused by antibodies against acetylcholine receptors, and its symptoms and treatment with cholinesterase inhibitors.
The spinal cord is approximately 45-50 cm long and 2 cm in diameter. It begins at the foramen magnum and terminates around the L1-L2 vertebrae in adults. The spinal cord has ascending tracts that carry sensory information to the brain and descending tracts that carry motor commands from the brain. It is protected by the vertebrae, meninges, cerebrospinal fluid, and contains gray matter in an H-shaped arrangement surrounded by white matter tracts. Injuries and diseases of the spinal cord can result in sensory and motor deficits depending on the level and severity of the lesion.
This document discusses the neuro-muscular junction, including its structure, function, and related disorders. It begins by outlining the objectives of describing the junction's schematic diagram, transmission events, neuromuscular blockers and their mechanisms, and common disorders. It then provides details on the presynaptic and postsynaptic portions, the synaptic cleft, acetylcholine receptors, and the steps of neuromuscular transmission. Examples are given of neuromuscular blockers like curare and their mechanisms of action. Disorders covered include myasthenia gravis and Lambert-Eaton syndrome.
Dr. Nilesh Kate's document provides an overview of smooth muscle physiology. It discusses the functional anatomy and organization of smooth muscle, including that it is non-striated, involuntary muscle that exists in bundles. It describes the two types of smooth muscle - single unit and multi unit - and their characteristics. The document outlines the structure of smooth muscle fibers and covers the processes of excitability, contraction, and relaxation. It explains excitation and inhibition of smooth muscle can occur through nerves, hormones, pacemakers, stretching or temperature changes. In summary, the document provides a comprehensive review of smooth muscle types, organization, function and physiology.
All about Neuromuscular junction...Structure,Steps involved,Drugs acting at neuromuscular junction , Clinical aspects (Myasthenia gravis and lambert eaton syndrome)
The document discusses the neuromuscular junction and muscle contraction physiology. It defines the neuromuscular junction as the connection between motor neurons and muscle fibers that initiates muscle contraction. The structure and function of the neuromuscular junction is described, including the roles of acetylcholine, receptors, and acetylcholinesterase. The sliding filament model of muscle contraction is introduced. Different muscle fiber types, properties of muscle tissue, and the sarcomere as the contractile unit are defined.
The autonomic nervous system regulates involuntary body functions like heart rate, respiration, digestion and more. It has two divisions:
The sympathetic nervous system prepares the body for "fight or flight" through responses like increased heart rate and dilated pupils. It uses norepinephrine as a neurotransmitter.
The parasympathetic nervous system helps the body "rest and digest" with functions like digestion, salivation and pupil constriction. It uses acetylcholine as a neurotransmitter.
Together these two divisions work to maintain homeostasis and control internal organs through a two-neuron pathway, with cell bodies located in the spinal cord or brainstem and ganglia between pre- and postganglionic neurons.
Synapses are junctions between neurons that allow for communication through either electrical or chemical transmission. Anatomically, synapses can be classified based on where the axon of one neuron connects to the other neuron, such as onto the cell body, dendrite, or axon. Functionally, synapses are either electrical, using gap junctions, or chemical, using neurotransmitters. Chemically, synapses can be excitatory or inhibitory based on the neurotransmitters released, with excitatory synapses transmitting impulses and inhibitory synapses inhibiting transmission. Key properties of synapses include one-way conduction, synaptic delay, fatigue due to depletion of neurotransmitters, summation effects from multiple stimulations, and the generation of
The document summarizes the mechanism of skeletal muscle contraction. It describes how an action potential leads to a rise in intracellular calcium levels through excitation-contraction coupling. This triggers the sliding filament theory where actin and myosin filaments slide past each other through cross-bridge cycling powered by ATP hydrolysis. Calcium binds to troponin C, allowing the power stroke to occur as myosin heads pull the actin filaments towards the center of the sarcomere. Relaxation occurs as calcium is re-sequestered in the sarcoplasmic reticulum, breaking the cross-bridges.
The document discusses the structure and function of chemical synapses. It begins by defining a synapse as the junction between two nerve cells. It then describes the key anatomical components of a chemical synapse, including the presynaptic knob, synaptic cleft, and postsynaptic membrane. It explains the process of neurotransmission, including the release of neurotransmitters into the synaptic cleft, their binding to receptors on the postsynaptic membrane, and the resulting postsynaptic potentials. The document also discusses inhibition at synapses, the properties of synaptic transmission, and examples of neurotransmitters.
Receptor by Pandian M, Tutor, Dept of Physiology, DYPMCKOP, MH. This PPT for ...Pandian M
I. This document discusses sensory receptors and their classification.
II. Sensory receptors are specialized nerve endings that convert stimuli into receptor potentials. There are three main types of receptors structurally: bare nerve endings, capsulated nerve endings, and sense organs.
III. Receptors can be classified in several ways, including by the source of the stimulus (exteroceptors, enteroceptors, telereceptors), the type of stimulus (mechanoreceptors, thermoreceptors, chemoreceptors, nociceptors), or their anatomical location (superficial, deep, visceral).
This document discusses the neuromuscular junction and several disorders that can affect it. It begins by describing the basic anatomy and physiology of the motor unit and neuromuscular junction. It then reviews several disorders in more depth, including myasthenia gravis, Lambert-Eaton myasthenic syndrome, and neuromyotonia. For each disorder, it discusses the epidemiology, clinical features, diagnostic tests, and treatment options. The goal is to provide clinicians with an overview of these neuromuscular junction disorders.
This document summarizes neurotransmitters and their mechanisms of action. It defines neurotransmitters as chemical substances that transmit nerve impulses across synapses. There are over 50 known neurotransmitters that are classified biochemically and physiologically as either excitatory or inhibitory. The document describes the general mechanisms of several major neurotransmitters including acetylcholine, catecholamines, serotonin, histamine, amino acids, and neuropeptides. It explains how they are synthesized, stored in vesicles, released, and deactivated in the synaptic cleft.
Nerve fibers can be classified based on their structure and distribution. There are two main types - myelinated and unmyelinated fibers. Nerve fibers also include somatic and autonomic fibers. Somatic fibers innervate skeletal muscles and the neurotransmitter is acetylcholine, leading to muscle excitation or central inhibition. Autonomic fibers innervate smooth, cardiac muscles and glands to maintain homeostasis, causing excitation or inhibition. Important properties of nerve fibers include excitability, conductivity, unfatigability, refractory periods, all-or-none response, summation, and accommodation.
The document provides information about the autonomic nervous system (ANS). It describes that the ANS acts involuntarily to control organs like the heart, lungs, intestines and glands. The ANS has two divisions - the sympathetic and parasympathetic nervous systems which generally work in opposition. The sympathetic system prepares the body for "fight or flight" while the parasympathetic system helps with "rest and digest" functions. Key neurotransmitters that are discussed are norepinephrine for the sympathetic system and acetylcholine for the parasympathetic system. Drugs can mimic or block these neurotransmitters to affect ANS functions.
Comparison of skeletal and smooth muscles (1)Ilyas Raza
This document compares smooth muscle contraction to skeletal muscle contraction. Some key points:
- Smooth muscle requires 1/300 the energy of skeletal muscle to sustain the same tension. It uses one ATP per contraction cycle.
- Smooth muscle contraction is prolonged, lasting 1-3 seconds, while skeletal muscle contracts and relaxes rapidly.
- Smooth muscle is able to maintain contraction, or "latch", with very little energy through prolonged cross-bridge attachment and reduced myosin phosphorylation rates.
- Calcium regulation of contraction is similar between muscle types but smooth muscle response is much slower.
This document provides an overview of the autonomic nervous system (ANS). It discusses the divisions of the ANS including the sympathetic and parasympathetic nervous systems. Key points covered include the anatomical organization of the ANS from the central nervous system to peripheral ganglia. The roles and effects of the sympathetic and parasympathetic systems on various organs are described. Neurotransmitters, receptors, and reflexes of the ANS are also summarized.
Properties of nerve fiber by Pandian M, Dept Physiology DYPMCKOP, this ppt fo...Pandian M
Describe the types, functions & properties of nerve fibres
3.2.1 Classify nerve fibres
3.2.2 Classify nerve fibres based on the diameter & conduction velocity
3.2.3 Describe the salient features of Erlanger & Gasser
classification of nerve fibres
3.2.4 State the functions of type A, B & C nerve fibres
3.2.5 Compare & contrast the numerical classification with the
Erlanger & Gasser classification in the sensory nerve fibres
Neuromuscular transmission involves the synthesis and release of acetylcholine from motor neurons. Acetylcholine binds to nicotinic receptors on muscle fibers, causing depolarization and muscle contraction. Acetylcholine is quickly broken down by acetylcholinesterase to allow muscle relaxation. Drugs can mimic or block acetylcholine's effects at the neuromuscular junction to cause contraction or relaxation of muscle fibers.
Here are the key types of mechanoreceptors and their properties:
- Cutaneous mechanoreceptors:
- Meissner's corpuscles - detect light touch and pressure on fingertips and lips. Found in dermal papillae.
- Merkel's discs - detect sustained light touch. Found just below the epidermis.
- Pacinian corpuscles - detect deep pressure and vibration. Found in dermis and connective tissue.
- Ruffini endings - detect skin stretch and joint movement. Found in dermis and connective tissue.
- Free nerve endings - detect pain. Found throughout the dermis and epidermis.
- Proprioceptors:
- Muscle spind
The document provides information about the autonomic nervous system (ANS). It describes the ANS as having two main divisions - the sympathetic and parasympathetic nervous systems. The sympathetic system prepares the body for "fight or flight" responses, while the parasympathetic system allows for "rest and digest" functions. Key differences between the two divisions are described, including their origins in the spinal cord/brain and targets in the body. The pathways of preganglionic and postganglionic neurons, as well as autonomic ganglia, are outlined. Neurotransmitters and receptors of each division are also detailed.
7&8- The Neuromuscular Junction & Physiology of Skeletal Muscle Contraction .pptInamUlHaqKhan6
The document discusses the neuromuscular junction and skeletal muscle contraction. It defines the key components of the neuromuscular junction including the motor end plate, synaptic cleft, and acetylcholine receptors. It explains how a nerve impulse causes acetylcholine release, generating an end plate potential that triggers muscle contraction. Contraction occurs via sliding filament mechanism involving actin, myosin, calcium, and ATP hydrolysis. Drugs can affect the neuromuscular junction by blocking or enhancing acetylcholine transmission or by interfering with acetylcholinesterase.
L4+5 -Muscle_Contraction_(Dr_taha) and nmj medical.2020.pptShoaibmalik367917
The document discusses the neuromuscular junction and skeletal muscle contraction. It defines the key components of the neuromuscular junction including the motor end plate, synaptic cleft, and acetylcholine receptors. It explains how a nerve impulse causes acetylcholine release, generating an end plate potential that triggers muscle contraction. Contraction occurs via sliding filament mechanism involving actin, myosin, calcium, and ATP hydrolysis. Drugs can affect the neuromuscular junction by blocking or enhancing acetylcholine transmission or by interfering with acetylcholinesterase.
Dr. Nilesh Kate's document provides an overview of smooth muscle physiology. It discusses the functional anatomy and organization of smooth muscle, including that it is non-striated, involuntary muscle that exists in bundles. It describes the two types of smooth muscle - single unit and multi unit - and their characteristics. The document outlines the structure of smooth muscle fibers and covers the processes of excitability, contraction, and relaxation. It explains excitation and inhibition of smooth muscle can occur through nerves, hormones, pacemakers, stretching or temperature changes. In summary, the document provides a comprehensive review of smooth muscle types, organization, function and physiology.
All about Neuromuscular junction...Structure,Steps involved,Drugs acting at neuromuscular junction , Clinical aspects (Myasthenia gravis and lambert eaton syndrome)
The document discusses the neuromuscular junction and muscle contraction physiology. It defines the neuromuscular junction as the connection between motor neurons and muscle fibers that initiates muscle contraction. The structure and function of the neuromuscular junction is described, including the roles of acetylcholine, receptors, and acetylcholinesterase. The sliding filament model of muscle contraction is introduced. Different muscle fiber types, properties of muscle tissue, and the sarcomere as the contractile unit are defined.
The autonomic nervous system regulates involuntary body functions like heart rate, respiration, digestion and more. It has two divisions:
The sympathetic nervous system prepares the body for "fight or flight" through responses like increased heart rate and dilated pupils. It uses norepinephrine as a neurotransmitter.
The parasympathetic nervous system helps the body "rest and digest" with functions like digestion, salivation and pupil constriction. It uses acetylcholine as a neurotransmitter.
Together these two divisions work to maintain homeostasis and control internal organs through a two-neuron pathway, with cell bodies located in the spinal cord or brainstem and ganglia between pre- and postganglionic neurons.
Synapses are junctions between neurons that allow for communication through either electrical or chemical transmission. Anatomically, synapses can be classified based on where the axon of one neuron connects to the other neuron, such as onto the cell body, dendrite, or axon. Functionally, synapses are either electrical, using gap junctions, or chemical, using neurotransmitters. Chemically, synapses can be excitatory or inhibitory based on the neurotransmitters released, with excitatory synapses transmitting impulses and inhibitory synapses inhibiting transmission. Key properties of synapses include one-way conduction, synaptic delay, fatigue due to depletion of neurotransmitters, summation effects from multiple stimulations, and the generation of
The document summarizes the mechanism of skeletal muscle contraction. It describes how an action potential leads to a rise in intracellular calcium levels through excitation-contraction coupling. This triggers the sliding filament theory where actin and myosin filaments slide past each other through cross-bridge cycling powered by ATP hydrolysis. Calcium binds to troponin C, allowing the power stroke to occur as myosin heads pull the actin filaments towards the center of the sarcomere. Relaxation occurs as calcium is re-sequestered in the sarcoplasmic reticulum, breaking the cross-bridges.
The document discusses the structure and function of chemical synapses. It begins by defining a synapse as the junction between two nerve cells. It then describes the key anatomical components of a chemical synapse, including the presynaptic knob, synaptic cleft, and postsynaptic membrane. It explains the process of neurotransmission, including the release of neurotransmitters into the synaptic cleft, their binding to receptors on the postsynaptic membrane, and the resulting postsynaptic potentials. The document also discusses inhibition at synapses, the properties of synaptic transmission, and examples of neurotransmitters.
Receptor by Pandian M, Tutor, Dept of Physiology, DYPMCKOP, MH. This PPT for ...Pandian M
I. This document discusses sensory receptors and their classification.
II. Sensory receptors are specialized nerve endings that convert stimuli into receptor potentials. There are three main types of receptors structurally: bare nerve endings, capsulated nerve endings, and sense organs.
III. Receptors can be classified in several ways, including by the source of the stimulus (exteroceptors, enteroceptors, telereceptors), the type of stimulus (mechanoreceptors, thermoreceptors, chemoreceptors, nociceptors), or their anatomical location (superficial, deep, visceral).
This document discusses the neuromuscular junction and several disorders that can affect it. It begins by describing the basic anatomy and physiology of the motor unit and neuromuscular junction. It then reviews several disorders in more depth, including myasthenia gravis, Lambert-Eaton myasthenic syndrome, and neuromyotonia. For each disorder, it discusses the epidemiology, clinical features, diagnostic tests, and treatment options. The goal is to provide clinicians with an overview of these neuromuscular junction disorders.
This document summarizes neurotransmitters and their mechanisms of action. It defines neurotransmitters as chemical substances that transmit nerve impulses across synapses. There are over 50 known neurotransmitters that are classified biochemically and physiologically as either excitatory or inhibitory. The document describes the general mechanisms of several major neurotransmitters including acetylcholine, catecholamines, serotonin, histamine, amino acids, and neuropeptides. It explains how they are synthesized, stored in vesicles, released, and deactivated in the synaptic cleft.
Nerve fibers can be classified based on their structure and distribution. There are two main types - myelinated and unmyelinated fibers. Nerve fibers also include somatic and autonomic fibers. Somatic fibers innervate skeletal muscles and the neurotransmitter is acetylcholine, leading to muscle excitation or central inhibition. Autonomic fibers innervate smooth, cardiac muscles and glands to maintain homeostasis, causing excitation or inhibition. Important properties of nerve fibers include excitability, conductivity, unfatigability, refractory periods, all-or-none response, summation, and accommodation.
The document provides information about the autonomic nervous system (ANS). It describes that the ANS acts involuntarily to control organs like the heart, lungs, intestines and glands. The ANS has two divisions - the sympathetic and parasympathetic nervous systems which generally work in opposition. The sympathetic system prepares the body for "fight or flight" while the parasympathetic system helps with "rest and digest" functions. Key neurotransmitters that are discussed are norepinephrine for the sympathetic system and acetylcholine for the parasympathetic system. Drugs can mimic or block these neurotransmitters to affect ANS functions.
Comparison of skeletal and smooth muscles (1)Ilyas Raza
This document compares smooth muscle contraction to skeletal muscle contraction. Some key points:
- Smooth muscle requires 1/300 the energy of skeletal muscle to sustain the same tension. It uses one ATP per contraction cycle.
- Smooth muscle contraction is prolonged, lasting 1-3 seconds, while skeletal muscle contracts and relaxes rapidly.
- Smooth muscle is able to maintain contraction, or "latch", with very little energy through prolonged cross-bridge attachment and reduced myosin phosphorylation rates.
- Calcium regulation of contraction is similar between muscle types but smooth muscle response is much slower.
This document provides an overview of the autonomic nervous system (ANS). It discusses the divisions of the ANS including the sympathetic and parasympathetic nervous systems. Key points covered include the anatomical organization of the ANS from the central nervous system to peripheral ganglia. The roles and effects of the sympathetic and parasympathetic systems on various organs are described. Neurotransmitters, receptors, and reflexes of the ANS are also summarized.
Properties of nerve fiber by Pandian M, Dept Physiology DYPMCKOP, this ppt fo...Pandian M
Describe the types, functions & properties of nerve fibres
3.2.1 Classify nerve fibres
3.2.2 Classify nerve fibres based on the diameter & conduction velocity
3.2.3 Describe the salient features of Erlanger & Gasser
classification of nerve fibres
3.2.4 State the functions of type A, B & C nerve fibres
3.2.5 Compare & contrast the numerical classification with the
Erlanger & Gasser classification in the sensory nerve fibres
Neuromuscular transmission involves the synthesis and release of acetylcholine from motor neurons. Acetylcholine binds to nicotinic receptors on muscle fibers, causing depolarization and muscle contraction. Acetylcholine is quickly broken down by acetylcholinesterase to allow muscle relaxation. Drugs can mimic or block acetylcholine's effects at the neuromuscular junction to cause contraction or relaxation of muscle fibers.
Here are the key types of mechanoreceptors and their properties:
- Cutaneous mechanoreceptors:
- Meissner's corpuscles - detect light touch and pressure on fingertips and lips. Found in dermal papillae.
- Merkel's discs - detect sustained light touch. Found just below the epidermis.
- Pacinian corpuscles - detect deep pressure and vibration. Found in dermis and connective tissue.
- Ruffini endings - detect skin stretch and joint movement. Found in dermis and connective tissue.
- Free nerve endings - detect pain. Found throughout the dermis and epidermis.
- Proprioceptors:
- Muscle spind
The document provides information about the autonomic nervous system (ANS). It describes the ANS as having two main divisions - the sympathetic and parasympathetic nervous systems. The sympathetic system prepares the body for "fight or flight" responses, while the parasympathetic system allows for "rest and digest" functions. Key differences between the two divisions are described, including their origins in the spinal cord/brain and targets in the body. The pathways of preganglionic and postganglionic neurons, as well as autonomic ganglia, are outlined. Neurotransmitters and receptors of each division are also detailed.
7&8- The Neuromuscular Junction & Physiology of Skeletal Muscle Contraction .pptInamUlHaqKhan6
The document discusses the neuromuscular junction and skeletal muscle contraction. It defines the key components of the neuromuscular junction including the motor end plate, synaptic cleft, and acetylcholine receptors. It explains how a nerve impulse causes acetylcholine release, generating an end plate potential that triggers muscle contraction. Contraction occurs via sliding filament mechanism involving actin, myosin, calcium, and ATP hydrolysis. Drugs can affect the neuromuscular junction by blocking or enhancing acetylcholine transmission or by interfering with acetylcholinesterase.
L4+5 -Muscle_Contraction_(Dr_taha) and nmj medical.2020.pptShoaibmalik367917
The document discusses the neuromuscular junction and skeletal muscle contraction. It defines the key components of the neuromuscular junction including the motor end plate, synaptic cleft, and acetylcholine receptors. It explains how a nerve impulse causes acetylcholine release, generating an end plate potential that triggers muscle contraction. Contraction occurs via sliding filament mechanism involving actin, myosin, calcium, and ATP hydrolysis. Drugs can affect the neuromuscular junction by blocking or enhancing acetylcholine transmission or by interfering with acetylcholinesterase.
Neuromuscular Junction and Muscle Contraction Physiology Asri.pptxDRMOHAMEDASRIBINMOHA1
The document discusses the physiology of skeletal muscle contraction. It describes the anatomy and function of the neuromuscular junction, including the roles of acetylcholine and motor end plates. The molecular mechanisms of muscle contraction and relaxation are explained, including excitation-contraction coupling and the sliding filament theory. Disorders that can affect the neuromuscular transmission such as myasthenia gravis are also reviewed. The objectives are to understand the anatomy and physiology of skeletal muscle and the neuromuscular junction, and the mechanisms of muscle contraction and relaxation.
The neuromuscular junction is where the terminal branch of a nerve fiber meets with a muscle fiber. An action potential is transmitted from the nerve to the muscle through this junction, allowing for muscle contraction. The nerve fiber terminal contains acetylcholine vesicles which release acetylcholine into the synaptic cleft when an action potential arrives. Acetylcholine then binds to nicotinic receptors on the muscle fiber, opening sodium channels and generating an endplate potential that can trigger a muscle action potential if it surpasses a threshold. Acetylcholine is quickly broken down by acetylcholinesterase to allow muscle relaxation.
Talks about Neuromuscular transmission in NMJ. It explains how Acetylcholine at a pre synaptic terminal transmits an impulse to the post synaptic terminal
The document discusses the structure and mechanism of synaptic transmission at the neuromuscular junction. It describes how acetylcholine is released from the presynaptic neuron into the synaptic cleft upon arrival of an action potential. Acetylcholine then binds to nicotinic receptors on the postsynaptic membrane of muscle fibers, causing depolarization and generation of an action potential in the muscle fiber. Acetylcholine is then broken down by acetylcholinesterase in the synaptic cleft, allowing the muscle membrane to repolarize. The effects of various toxins on this process are also summarized.
ANATOMY AND PHYSIOLOGY OF NMJ Prabhat (3).pptxpkumarchoudhuri
- The neuromuscular junction (NMJ) is the synapse between a motor neuron and a muscle fiber, where electrical signals from the nerve cause muscle contraction.
- There are three key components: the presynaptic motor nerve terminal, synaptic cleft, and postsynaptic muscle end plate.
- Acetylcholine is released from the nerve terminal into the synaptic cleft and binds to nicotinic acetylcholine receptors on the muscle membrane, causing depolarization and muscle contraction.
- Depolarization is terminated by acetylcholinesterase which rapidly breaks down acetylcholine in the cleft.
Large motor neurons originates from the anterior horn cells of spinal cord
They are myelinated nerve fibers
They innervates skeletal muscles
Each nerve fiber after entering the muscle belly, branches and stimulates 3- several hundreds of skeletal muscle fibers
Each nerve ending makes a junction – Neuromuscular Junction
NMJ is present at midpoint of the muscle
AP initiated in the muscle fiber by the nerve impulse, travels in both directions towards the muscle fiber ends
This document discusses neuromuscular junctions in skeletal, smooth, and cardiac muscles. It focuses on neuromuscular junctions in skeletal muscles, describing the anatomical structures involved including axon terminals, synaptic clefts, and acetylcholine receptors. It explains how acetylcholine is synthesized and released and how it activates acetylcholine receptors to produce an end plate potential and muscle contraction. Substances that block neuromuscular transmission at different steps are also outlined. Clinical conditions involving the neuromuscular junction like myasthenia gravis and tetany are briefly described.
The document discusses muscle relaxants and the neuromuscular junction. It describes how skeletal muscle relaxants act either peripherally at the neuromuscular junction or centrally in the spinal cord to reduce muscle tone. Neuromuscular blocking agents are used during anesthesia and ventilation to provide muscle relaxation. The document then goes into detail about the motor neuron, acetylcholine synthesis and receptors, and classification of different muscle relaxants.
The neuromuscular junction is where motor neurons in the spinal cord synapse with voluntary muscles. It consists of a motor neuron, synaptic cleft, and postsynaptic muscle fibers. Acetylcholine is released from the presynaptic neuron into the synaptic cleft and binds to nicotinic acetylcholine receptors on the postsynaptic membrane, generating an endplate potential that depolarizes the muscle fiber membrane and triggers muscle contraction. Myasthenia gravis is an autoimmune disorder where antibodies impair signal transmission at the neuromuscular junction by targeting acetylcholine receptors or proteins involved in receptor clustering like MuSK. Current treatments aim to increase acetylcholine levels or reduce autoantibody concentrations to restore neurom
The document discusses muscle relaxants and neuromuscular blocking agents. It covers their classification, mechanisms of action, administration, and side effects. Specifically, it describes how succinylcholine causes initial muscle stimulation followed by paralysis through prolonged depolarization of motor end plates. It also notes that residual paralysis can occur in 42% of patients even after administration of reversal agents, and that a train-of-four ratio above 0.7 correlates with clinical recovery.
The neuromuscular junction is the synapse between a motor neuron and a muscle fiber. It contains a presynaptic membrane, synaptic cleft, and postsynaptic membrane. Acetylcholine is synthesized in the motor neuron and stored in vesicles. When an action potential reaches the motor neuron terminal, calcium enters and causes acetylcholine vesicles to fuse with the presynaptic membrane and release acetylcholine into the synaptic cleft. Acetylcholine then binds and opens channels in the postsynaptic membrane of the muscle fiber, generating an endplate potential that triggers a muscle action potential and contraction. Acetylcholinesterase in the cleft rapidly breaks down acetylcholine to terminate its effects.
Neuromuscular junction and synapses by DR.IRUMSMS_2015
The neuromuscular junction (NMJ) is the connection between a motor neuron and skeletal muscle fiber. At the NMJ, the motor neuron terminal releases acetylcholine into the synaptic cleft, which binds to acetylcholine receptors on the muscle fiber membrane. This opens ion channels and generates an endplate potential in the muscle fiber, causing it to contract. Key aspects of the NMJ include synaptic vesicles containing acetylcholine, voltage-gated calcium channels that trigger vesicle fusion and release, and densely packed acetylcholine receptors in the subneural cleft that respond to the neurotransmitter.
This document summarizes key concepts in neuromuscular physiology including nerve conduction, the neuromuscular junction, and muscle contraction. It discusses the resting membrane potential, action potentials, propagation of action potentials, and factors that influence membrane potential. It also describes the structure and function of the neuromuscular junction, including acetylcholine release and receptor activation. Finally, it discusses neuromuscular blocking agents and disorders like myasthenia gravis.
The neuromuscular junction is where a motor neuron connects to a muscle fiber. When an action potential reaches the axon terminal, calcium enters and causes vesicles containing acetylcholine to fuse with the membrane and release the neurotransmitter into the synaptic cleft. Acetylcholine then binds nicotinic receptors on the muscle fiber, causing sodium entry and developing an endplate potential that can trigger an action potential in the fiber. Acetylcholine is quickly broken down by acetylcholinesterase to allow muscle relaxation. A motor unit consists of a motor neuron and the fibers it innervates, so stimulating the neuron causes contraction of those fibers in a graded manner based on recruitment of additional motor units.
Motor units, synaptic clefts, and muscle end plates are the three essential components of neuromuscular transmission. The number of muscle fibers innervated depends on the precision of movement required. Neurotransmitter is stored in vesicles at the presynaptic end and released into the synaptic cleft through a calcium-dependent process involving SNARE proteins, where it binds to nicotinic acetylcholine receptors on the postsynaptic end to generate an action potential. Acetylcholinesterase in the cleft degrades acetylcholine to terminate the signal.
This document discusses congenital myasthenic syndrome (CMS), which is an inherited disorder of neuromuscular transmission associated with weakness and fatiguability. It compares CMS to myasthenia gravis, which is an autoimmune condition. The document then provides details on the basic anatomy and physiology of the neuromuscular junction, including the roles of acetylcholine, acetylcholinesterase, and ion channels. It discusses various classifications and frequencies of identified mutations in CMS. The rest of the document focuses on different types of presynaptic CMS syndromes, including choline acetyltransferase deficiency, paucity of synaptic vesicles, Lambert-Eaton-like syndrome, and congenital end plate acetylcholin
This document provides information on the neuromuscular junction (NMJ) and neuromuscular blockade. It discusses:
1. The physiology of the NMJ, including the parts (pre-synaptic membrane, synaptic cleft, post-synaptic membrane), acetylcholine receptors, and how an action potential is generated.
2. How neuromuscular blocking drugs work by competitively blocking acetylcholine receptors to prevent muscle contraction.
3. Methods for monitoring neuromuscular blockade including train-of-four stimulation which assesses fade or weakness of subsequent muscle contractions indicating residual blockade.
This document discusses the neuromuscular junction and neurotransmitters. It begins with an introduction to the neuromuscular junction between motor neurons and muscle fibers. It then discusses the neurotransmitters acetylcholine, dopamine, GABA, and glutamate. For each neurotransmitter, it describes their synthesis, function, and role in various neurological disorders. Mechanisms of action are provided for acetylcholine, dopamine, GABA, glutamate, and cholinergic drugs. References are listed at the end.
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This document discusses intellectual property rights (IPR) and patents in India. It defines intellectual property and IPR, and outlines the types of intellectual property including patents, designs, trademarks, geographical indications, and copyright. It then discusses the history and development of patent laws in India, prerequisites for a patent, and differences between the Indian and US patent acts. The document also outlines the patent procedure in India and types of special patents including for textiles, electronics, software, food, pharmaceuticals, and microorganisms.
Rodent Biology provides information about rats including their:
- Taxonomic classification as mammals in the order Rodentia.
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Gene Therapy, Somatic cell gene therapy, germ line gene therapy, classical gene therapy, non-classical gene therapy, targets of gene therapy, barriers of gene therapy, ex vivo gene therapy, in vivo gene therapy, vectors for gene delivery, antisense therapy
Chromatography is a method of separating components of a mixture through their interactions with two phases - a stationary phase and a mobile phase. The components are distributed between the phases based on properties like solubility and affinity. There are several types of chromatography classified by the shape of the stationary phase (e.g. thin layer), the state of the mobile phase (e.g. gas, liquid), or the interaction between solute and stationary phase (e.g. adsorption, partition). Chromatography techniques are used in various applications including pharmaceutical quality control, forensic analysis, and biological research like protein purification.
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Major histocompatility complex (Antigen Presentation to T cells, Autoimmunity...Pradeep Singh Narwat
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The document discusses various types of non-coding DNA sequences, including repetitive sequences, transposons, non-coding RNAs, introns, and pseudogenes. It notes that while genes only make up 2-3% of human DNA, recent projects like ENCODE have found that a much larger portion of non-coding DNA is functionally important, for example through transcriptional and translational regulation of protein-coding sequences. The document outlines different classes of transposons, introns, non-coding RNAs and their various roles in gene expression, epigenetics, and genome evolution.
Fibrinolysis is the process of dissolving blood clots through the activation of plasminogen into plasmin. Plasmin is the main enzyme that degrades fibrin clots. Plasminogen is activated by plasminogen activators such as tissue plasminogen activator (tPA) and urokinase plasminogen activator (uPA). These activators help initiate a cascade of reactions that results in the breakdown of fibrin clots. There are also inhibitors that help regulate fibrinolysis, with alpha-2-antiplasmin being the most important naturally occurring inhibitor of plasmin to prevent excessive clot breakdown.
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This document discusses the purification of proteins. It begins with an introduction to proteins and their structures. It then discusses various techniques used to purify proteins, including salting out, dialysis, gel filtration chromatography, ion-exchange chromatography, gel electrophoresis, isoelectric focusing, and HPLC. The key techniques discussed in detail are salting out, dialysis, gel filtration chromatography, ion-exchange chromatography, gel electrophoresis, and affinity chromatography. The document emphasizes that different techniques are used to purify proteins based on their properties such as solubility, molecular size, ionic charge, and binding specificity.
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
2. Neuromuscular Junction
Synapses are the junctions where the
axon or some other portion of one cell
(the presynaptic cell) terminates on the
dendrites, soma, or axon of another
neuron or in some cases a muscle or
gland cell (the postsynaptic cell)
Synapses between axons of motor
neurons and skeletal muscle fibers are
called NEUROMUSCULAR JUNCTION or
MYONEURAL JUNCTIONS
3. Motor Unit
Motor unit
One neuron
Muscle cells
stimulated by
that neuron
Motor neuron &
all the muscle
fibers it supplies
5. Physiological Anatomy of NMJ
1. PRESYNAPTIC MEMBRANE (TERMINAL
BOUTONS/END FEET) : small, clear vesicles
containing acetylcholine
2. SYNAPTIC CLEFT/SPACE : space between pre
and post-synaptic membrane, 20-40 nm, also
contain enzyme ACETYLCHOLINESTERASE
3. POSTSYNAPTIC MEMBRANE (MOTOR END
PLATE): thickened portion of muscle
membrane at the junction
6.
7. Physiological Anatomy of NMJ
Axon makes a single point of synaptic
contact with a skeletal muscle fiber,
midway along the length of the fiber
As axon approaches its termination, it
loses its myelin sheath and divides into a
number of terminal buttons, or endfeet
The endfeet contain many small, clear
vesicles that contain acetylcholine (Ach),
the transmitter at these junctions
8. Physiological Anatomy of NMJ
Vesicles – formed in the cell body
and are transported by fast axonal
transport via the microtubules
ACh is synthesized in the nerve
terminal – outside the vesicle –
from choline and acetyl coenzyme
A by the enzyme choline
acetyltransferase
The ACh moves into the synaptic
vesicles via a specific ACh-H+
exchanger
9.
10. Release of Acetylcholine
Nerve impulse reaching axon terminal
increases permeability of pre-synaptic
membrane to Ca2+
Ca2+ enters the nerve terminal through
voltage-gated channels
Ca2+ causes fusion of synaptic vesicles
with the pre-synaptic membrane
Amount of neurotransmitter released is directly
proportional to Ca2+ influx
Mg2+ decreases this process
11. Physiological Anatomy of NMJ
Synaptic vesicles fuse at differentiated
regions of the presynaptic membrane
called Active Zones and releases ACh
Endings fit into junctional folds, which
are depressions in the motor end plate
Synaptic basal lamina contains high
concentration of enzyme AChE
(Acetylcholinesterase) - terminates
transmission by rapidly hydrolyzing free
ACh to choline and acetate
12.
13.
14. Effect of ACh on Postsynaptic
Membrane
ACh binds to ACh Receptors which are
ligand-gated ion channels in postsynaptic
membrane
ACh receptor is a heteropentamer with a
subunit composition of α2βγδ
Subunits are homologous to one another
Each α subunit has 4 membrane spanning
segments
18. Effect of ACh on Postsynaptic
Membrane
Binding of acetylcholine to these receptors
increases the Na+ and K+ conductance
Na+ influx, creates a local positive potential
change inside the muscle fiber membrane called
the END PLATE POTENTIAL (EPP)
ACh released into synaptic cleft is removed
rapidly by enzyme Acetylcholinesterase,
present in synaptic cleft. Removal is rapid to
prevent re-excitation of the receptors after
first action potential
19. Entry of sodium
ions
(Depolarization)
Depolarization causes opening
of voltage gated calcium
channels.
Calcium entry
Opening of potassium
channels
(hyperpolarization)
Closure of calcium channels
Entry of Calcium after the arrival of
impulse (action potential)
Events at the end of the nerve fiber
20. Release of
vesicles
Entry of Calcium
Movement of vesicle
towards membrane
Release of Ach
One impulse = 125 vesicles
released
At rest = 1 – 2 Hz release
Events at the end of the nerve fiber
23. Binding of ACh to receptor increases the Na+ and
K+ conductance of the membrane
Resultant influx of Na+ produces a depolarizing
potential - end plate potential
Current sink created by this local potential
depolarizes the adjacent muscle membrane to its
firing level
Normally not recordable as action potential is
almost always generated
End Plate Potential (EPP)
24. End Plate Potential (EPP)
Average human end plate contains about
15–40 million ACh receptors
Each nerve impulse releases about 60 ACh
vesicles, and each vesicle contains about
10,000 molecules of the neurotransmitter
Can activate 10 times the number of
acetylcholine receptors
Therefore, a propagated response in the
muscle is regularly produced
25. End Plate Potential (EPP)
Only 6 vesicles are reqd for activation
from -90 to -65 mv
Each nerve impulse releases
60 ACh vesicles
Every vesicle has 10,000 molecules of ACh
10-fold safety factor
Action potential always generated
26. Depolarization due to net entry of cations
threshold
Time (ms)
Membranevoltage
(mv)
End plate potential (graded potential)
Action potential
Events on the Muscle Fiber
27. End Plate Potential (EPP)
EPP can be seen if the tenfold safety
factor is overcome
Administration of small doses of curare
(competitive inhibitor of ACh) is used for
studying EPP
The response is then recorded only at the
end plate region and decreases
exponentially away from it
EPP undergoes temporal summation
28. Miniature End Plate Potential (MEPP)
At rest - Random release of small packets /
quanta of ACh - Quantal Release of
Transmitter
Small depolarising spike
Amplitude = 0.5mv
Amount released ∞ Ca2+ concentration
1/∞ Mg++ concentration
When a nerve impulse comes, no. of quanta
released increases resulting in large EPP
that exceeds the firing level of the muscle
fiber producing AP
29. Muscle Nerve
RMP -90mv -70mv
Action
Potential
Duration
2-4msec varies
Velocity 5 m/sec
Varies with
fiber
Absolute
Refractory
period
1-3 msec 2-4 msec
Ionic distribution is similar to that in nerve
30.
31. Transmission of Nerve Impulse to
Muscle
Sodium rushes into the cell generates an
action potential (AP)
The action potential travels along the T-
tubules to the SR to stimulate release of
Calcium ions
The Ca2+ ions travels to the muscle tissue
and bind to the ACTIN regulatory proteins
(Troponin C)
32. Transmission of Nerve Impulse to
Muscle
This UNCOVERS Myosin Head BINDING Sites on
ACTIN so as to allow CROSS BRIDGING ( once
myosin is powered by ATP)
Activation by nerve causes myosin heads
(crossbridges) to attach to binding sites on the
thin filament
Myosin heads then bind to the next site of the
thin filament - Sliding Filament Theory of
Muscle Contraction
34. End of Neuromuscular
Transmission
Acetylcholine, the neurotransmitter is broken
down by the enzyme acetylcholinesterase
SO the stimulus to muscle ceases! – prevents
continued muscle reexcitation
Calcium ions are actively transported back to the
SR by SERCA (calcium ATPase)
The actin and myosin cross bridges break
RELAXES------S T R E T C H of the sarcomere
35. Drugs that Enhance or Block
Transmission at N-M Junction
1. STIMULATE THE MUSCLE FIBER BY
ACh LIKE ACTION:
methacholine, carbachol and nicotine:
o these drugs are not destroyed or are
destroyed very slowly by cholinesterase,
action persists for many minutes to
several hours
o can cause muscle spasm
36. 2.STIMULATE THE NEURO-MUSCULAR
JUNCTION BY INACTIVATING ACETYL-
CHOLINESTERASE
• neostigmine, physostigmine : inactivate
acetylcholinesterase for upto several hours
• diisopropyl flourophosphate : inactivate
acetylcholinesterase for weeks, “nerve” gas
poison
Drugs that Enhance or Block
Transmission at N-M Junction
37. 3. BLOCK TRANSMISSION AT NEURO-
MUSCULAR JUNCTION
Curariform drugs
d-Tubocurarine blocks the action of ACh
on the muscle fiber Acetylcholine
receptors, thus preventing sufficient
increase in permeability of the muscle
membrane channels to initiate an action
potential
Drugs that Enhance or Block
Transmission at N-M Junction
38. Neuromuscular blocking agents:
Used in surgery because they relax muscle
and abolish reflexes
Reduces the dose of anesthetic agent
necessary
Patient who receive neuromuscular
blockers, need artificial respiration,
because respiratory muscles
(S.K.muscles/diaphragm) being paralysed,
may lead to death within minutes
42. Myasthenia Gravis
Afflicts 25-125 of every million people
Can occur at any age but has a bimodal
distribution with peak occurrences in 20s (mainly
women) and 60s (mainly men)
Antibodies against ACh receptors are present in
blood of most patients with this disease
Autoimmune disease
Antibody detected in
50% of pts with pure ocular MG
90-95% of pts with generalized MG
43. Myasthenia Gravis
Antibodies destroy some of the receptors
and bind others to neighboring receptors,
triggering their removal by endocytosis
Normally, number of quanta released
declines with successive repetitive stimuli
Neuromuscular transmission fails at these
low levels of quantal release
Leads to the major clinical feature of the
disease–muscle fatigue with sustained or
repeated activity
45. Myasthenia Gravis
Two major forms of the disease –
Involves weakness of only the extraocular
muscles
Results in generalized weakness of all skeletal
muscles
In severe cases, paralysis of respiratory
muscles can lead to death
46. Clinical Manifestation of MG
Symptoms worsen with exercise, end of day (Fatigue)
Ocular
Droopy eyelids (ptosis)
Double vision (diplopia)
Extremity weakness
Arms > legs
Dysarthria & Dysphagia
Respiratory
Shortness of breath
48. Myasthenia Gravis
Treatment: neostigmine or some other
anticholinesterase drug – alone or
combined with thymectomy or
immunosuppression
Cholinesterase inhibitors prevent metabolism
of ACh compensating for the normal decline in
released neurotransmitters during repeated
stimulation
Removal of Thymoma leads to clinical
improvement in 75% of cases
49. Clinical Problem
A 18-year-old college woman comes to the
student health service complaining of
progressive weakness.
She reports that occasionally her eyelids
“droop”
she tires easily, even when completing
ordinary daily tasks such as brushing her
hair.
She has fallen several times while climbing
a flight of stairs.
These symptoms improve with rest.
50. Lambert-eaton Myasthenic Syndrome
(LEMS)
Antibodies against Ca2+ channels in the
motor nerve terminals
no. of Ca2+ channels decrease less
calcium enters the nerve terminal and less
neurotransmitter is released
Symptoms - muscular weakness &
diminished stretch reflexes
Muscle strength increases with prolonged
contraction as more Ca becomes available
51. Lambert-eaton Myasthenic Syndrome
(LEMS)
The major clinical finding is progressive weakness
that does not usually involve the respiratory
muscles and the muscles of face
In contrast to MG, symptoms of LEMS tend to be
worse in the morning and improve with exercise
The proximal parts of the legs and arms are
predominantly affected
Many patients have autonomic symptoms like dry
mouth or impotence. Reflexes are usually
reduced or absent
52. Differences between
MG LEMS
Antibodies are formed
against the ACh
Receptors on the Post
synaptic membrane
Primarily attacks the
ocular and bulbar
muscles
Repeated muscle
stimulation leads to
decrease in
contractile strength
Antibodies are formed
against the
presynaptic Calcium
channels
Primarily attacks the
limb muscles
Repeated muscle
stimulation leads to
increasing contractile
strength
54. Autonomic nerve fibers that innervate
smooth muscle branch diffusely on top of
sheet of muscle fibers
These fibers do not make direct contact
with smooth muscle fiber cell membranes
but form diffuse junctions
Vesicles may contain ACh in some & NE in
other autonomic nerve fiber endings
N-M Junction in Smooth & Cardiac
Muscle
55. N-M Junction in Smooth & Cardiac
Muscle
No typical end feet as seen in skeletal muscle,
axons have multiple varicosities distributed along
their axes
Varicosities are about 5 μm apart, with up to
20,000 varicosities per neuron
Transmitter is liberated at each varicosity, ie, at
many locations along each axon
This arrangement permits one neuron to innervate
many effector cells
The type of contact in which a neuron forms a
synapse on the surface of another neuron or a
smooth muscle cell and then passes on to make
similar contacts with other cells is called a
synapse en passant
57. Denervation Hypersensitivity
When the motor nerve to skeletal muscle
is cut and allowed to degenerate
muscle gradually becomes extremely sensitive
to acetylcholine -denervation
hypersensitivity or supersensitivity due to
an upregulation of its receptors
Muscle atrophies
Also seen in smooth muscle
Does not atrophy
hyperresponsive to the chemical mediator that
normally activates it
59. Thank you
References:
Guyton- Textbook of Medical Physiology
Ganong’s- Review of Medical Physiology
Boron-Medical Physiology
Kandel-Principles of Neural Science
Silbernagl-Color atlas of Physiology
Ira Fox- Medical Physiology
Editor's Notes
When channel opens – can transmit 15,000 to 30,000 sodium ions in 1 millisec
Negative ions such as chloride ions do not pass thru because of strong negative charges in the mouth of the channel that repel these negative ions
Each nicotinic cholinergic receptor is made up of five subunits that form a central channel which, when the receptor is activated, permits the passage of Na+ and other cations
Safety factor – margin of security
36
By Huxley and Huxley
39
Curare is also used as an arrow poison. It is a reversible competitive inhibitor of nicotinic Ach receptor at NM Junction. Death from curare is by asphyxia because skeletal muscles (respiratory muscles) become relaxed and paralyzed. Only works in blood, not if orally ingested nor by vapours. Does not affect heart as heart continues to beat even after breathing stops.
Tetanus toxin and botulinum toxins act by preventing release of neurotransmitters in CNs and neuromuscular jn. Botulinum toxins A and E act on SNAP-25 and B acts on synaptobrevin – blocks Ach release – Flaccid paralysis. Clinically, tetanus toxin causes spastic paralysis by blocking presynaptic transmitter release in the CNS, and botulism causes flaccid paralysis by blocking the release of acetylcholine at the neuromuscular junction. On the positive side, however, local injection of small doses of botulinum toxin (botox) has proved effective in the treatment of a wide variety of conditions characterized by muscle hyperactivity. Examples include injection into the lower esophageal sphincter to relieve achalasia and injection into facial muscles to remove wrinkles.
50
genetic predisposition to autoimmune disease. The thymus may play a role in the pathogenesis of the disease by supplying helper T cells sensitized against thymic proteins that cross-react with acetylcholine receptors. In most patients, the thymus is hyperplastic, and 10–15% have thymomas. Thymectomy is indicated if a thymoma is suspected. Even in those without thymoma, thymectomy induces remission in 35% and improves symptoms in another 45% of patients