The document defines key terms related to action potentials and summarizes their properties. It describes:
1) Phases of an action potential - depolarization, repolarization, and hyperpolarization.
2) Ionic basis - sodium influx causes depolarization, potassium efflux causes repolarization, and leakage of excess potassium causes hyperpolarization.
3) Propagation through myelinated and unmyelinated nerve fibers. In myelinated fibers, saltatory conduction jumps from node to node, while unmyelinated fibers conduct point-to-point.
4) Properties including the all-or-none law, refractory periods which prevent summation, and factors that determine excitation thresholds like the strength-duration curve
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.
Myelin is a fatty tissue that surrounds nerve cell axons and increases the speed of electrical impulses. It is composed of 80% lipid and 20% protein. In the central nervous system, myelin is produced by oligodendrocytes, while in the peripheral nervous system it is produced by Schwann cells. Myelination allows faster signal transmission and helps prevent electrical currents from leaving the axon. New research has found that axons may signal myelination by releasing ATP, which causes astrocytes to release a factor that promotes myelination by oligodendrocytes.
The patch-clamp technique allows the study of single ion channels in cells. It was developed in the late 1970s and early 1980s by Erwin Neher and Bert Sakmann, who received the Nobel Prize for this work. There are different variations of the patch-clamp technique that provide access to the inside or outside of the cell membrane to study channel properties under various conditions. The technique uses a glass pipette pressed against a cell to form a high resistance seal and then precisely measures electric currents flowing through individual or multiple ion channels.
This document summarizes the molecular mechanisms underlying skeletal muscle contraction. It discusses the structures involved like the sarcomere, thick and thin filaments, and T-tubules. The process of muscle contraction involves excitation-contraction coupling where an action potential triggers the release of calcium from the sarcoplasmic reticulum via T-tubules. Calcium binds to troponin allowing the myosin heads on thick filaments to bind to actin on thin filaments. The power stroke of the myosin heads pulls the thin filaments inward, shortening the sarcomere. Relaxation occurs when calcium is reabsorbed by the sarcoplasmic reticulum allowing detachment of the myosin heads.
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.
The document discusses programmed cell death or apoptosis. It begins by defining apoptosis as a regulated process where cells self-degrade to eliminate unwanted or damaged cells. Between 50-70 billion cells die daily in humans through apoptosis. The document then covers the history of apoptosis research and discovery. It discusses the role of caspases as executioners of apoptosis and the intrinsic and extrinsic pathways. Conditions where apoptosis is increased or decreased are examined, along with potential therapeutic targets like caspase inhibitors.
This document discusses various biophysical principles including diffusion, osmosis, and dialysis. It explains that diffusion is the movement of particles from an area of higher concentration to lower concentration down a concentration gradient. Osmosis is the diffusion of water across a semipermeable membrane from a region of lower solute concentration to higher solute concentration. Osmotic pressure is the hydrostatic pressure required to prevent osmosis. These principles are important for biological processes like gas exchange and kidney function, and conditions like edema can be caused by imbalances in osmotic pressure. Dialysis techniques like hemodialysis and peritoneal dialysis are used to filter waste from blood in kidney failure patients.
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.
Myelin is a fatty tissue that surrounds nerve cell axons and increases the speed of electrical impulses. It is composed of 80% lipid and 20% protein. In the central nervous system, myelin is produced by oligodendrocytes, while in the peripheral nervous system it is produced by Schwann cells. Myelination allows faster signal transmission and helps prevent electrical currents from leaving the axon. New research has found that axons may signal myelination by releasing ATP, which causes astrocytes to release a factor that promotes myelination by oligodendrocytes.
The patch-clamp technique allows the study of single ion channels in cells. It was developed in the late 1970s and early 1980s by Erwin Neher and Bert Sakmann, who received the Nobel Prize for this work. There are different variations of the patch-clamp technique that provide access to the inside or outside of the cell membrane to study channel properties under various conditions. The technique uses a glass pipette pressed against a cell to form a high resistance seal and then precisely measures electric currents flowing through individual or multiple ion channels.
This document summarizes the molecular mechanisms underlying skeletal muscle contraction. It discusses the structures involved like the sarcomere, thick and thin filaments, and T-tubules. The process of muscle contraction involves excitation-contraction coupling where an action potential triggers the release of calcium from the sarcoplasmic reticulum via T-tubules. Calcium binds to troponin allowing the myosin heads on thick filaments to bind to actin on thin filaments. The power stroke of the myosin heads pulls the thin filaments inward, shortening the sarcomere. Relaxation occurs when calcium is reabsorbed by the sarcoplasmic reticulum allowing detachment of the myosin heads.
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.
The document discusses programmed cell death or apoptosis. It begins by defining apoptosis as a regulated process where cells self-degrade to eliminate unwanted or damaged cells. Between 50-70 billion cells die daily in humans through apoptosis. The document then covers the history of apoptosis research and discovery. It discusses the role of caspases as executioners of apoptosis and the intrinsic and extrinsic pathways. Conditions where apoptosis is increased or decreased are examined, along with potential therapeutic targets like caspase inhibitors.
This document discusses various biophysical principles including diffusion, osmosis, and dialysis. It explains that diffusion is the movement of particles from an area of higher concentration to lower concentration down a concentration gradient. Osmosis is the diffusion of water across a semipermeable membrane from a region of lower solute concentration to higher solute concentration. Osmotic pressure is the hydrostatic pressure required to prevent osmosis. These principles are important for biological processes like gas exchange and kidney function, and conditions like edema can be caused by imbalances in osmotic pressure. Dialysis techniques like hemodialysis and peritoneal dialysis are used to filter waste from blood in kidney failure patients.
1. Digestion breaks down carbohydrates into monosaccharides like glucose and fructose. Salivary amylase and enzymes in the small intestine like maltase, lactase, and sucrase aid in this process.
2. Monosaccharides are absorbed into the bloodstream via active transport against concentration gradients or facilitated diffusion. Glucose is transported to tissues like the liver and brain, while pentoses are excreted by the kidneys.
3. Lactose intolerance occurs when lactase enzyme is deficient, causing undigested lactose to pass to the colon and cause gas, bloating, and diarrhea.
This document summarizes the action potential in neurons. It describes how an action potential is initiated by voltage-gated sodium channels opening during depolarization. This allows sodium ions to rush into the neuron, further depolarizing the membrane. Then, the sodium channels quickly inactivate while voltage-gated potassium channels open, allowing potassium ions to leave the neuron and repolarize the membrane back to its resting potential. The precise opening and closing of sodium and potassium channels underlies the generation and propagation of action potentials along neuronal membranes.
The resting membrane potential of neurons and muscle cells is maintained around -70 mV due to selective permeability of ions across the cell membrane. The sodium-potassium pump actively transports 3 Na+ ions out and 2 K+ ions into the cell, contributing to the negative interior potential. When the membrane potential reaches the threshold, voltage-gated sodium channels open rapidly, causing a sharp depolarization as sodium ions rush in. Subsequently, voltage-gated potassium channels open more slowly, repolarizing the membrane as potassium ions efflux from the cell. This generates an action potential that propagates by local current flow between adjacent areas of the membrane. The sodium-potassium pump then restores ion gradients in preparation for the next action potential
Apoptosis is a natural and programmed form of cell death that occurs in multicellular organisms. It was first described in 1842 and distinguished from necrosis in 1965. During apoptosis, a series of biochemical events lead to changes in the cell and its death, allowing it to be eliminated in a controlled way that does not cause inflammation. This process is regulated by complex signaling pathways within the cell and involves mitochondria, caspases and other components. Defects in apoptosis can result in cancer if cell death is inhibited or neurodegenerative diseases if cell death is excessive.
Cardiac output is defined as the volume of blood pumped by the heart each minute and is regulated intrinsically by factors affecting preload and afterload as well as extrinsically by the autonomic nervous system and hormones. Venous return is a primary extrinsic regulator of cardiac output, increasing stretch of cardiac muscles and stimulating an increase in heart rate. A combination of preload, contractility, afterload and heart rate determine cardiac output under normal resting conditions and during physical activity.
Transport across the cell membrane is necessary to maintain cellular function. There are three main types of transport: passive transport which includes diffusion, facilitated diffusion, and osmosis and does not require energy; active transport which uses energy and transports molecules against their concentration gradient, including primary active transport using ATP and secondary active transport utilizing ion gradients; and vesicular transport which transports larger molecules through vesicles via endocytosis, exocytosis, and transcytosis. Specialized proteins are involved in each of these transport mechanisms to regulate the passage of substances into and out of cells.
The voltage clamp is an experimental method used by electrophysiologists to measure the ion currents through the membranes of excitable cells, such as neurons while holding the membrane voltage at a set level. A basic voltage-clamp will iteratively measure the membrane potential, and then change the membrane potential (voltage) to the desired value by adding the necessary current. This "clamps" the cell membrane at a desired constant voltage, allowing the voltage clamp to record what currents are delivered. Because the currents applied to the cell must be equal to (and opposite in charge to) the current going across the cell membrane at the set voltage, the recorded currents indicate how the cell reacts to changes in membrane potential. Cell membranes of excitable cells contain many different kinds of ion channels, some of which are voltage-gated. The voltage clamp allows the membrane voltage to be manipulated independently of the ionic currents, allowing the current-voltage relationships of membrane channels to be studied.
The document discusses membrane potentials, including resting membrane potential and graded and action potentials. Resting membrane potential is maintained by ion concentration gradients established by the sodium-potassium pump and differential membrane permeability. It varies between cell types but is around -70 mV for neurons. Graded potentials are caused by neurotransmitters and can summate to reach threshold for an action potential. Action potentials are rapid, regenerative changes in membrane potential triggered by voltage-gated sodium and potassium channels. They propagate along neurons to transmit signals in the nervous system.
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.
Smooth muscle cells are found within organs and blood vessels. There are two main types - multi-unit smooth muscle composed of separate fibers, and unitary (visceral) smooth muscle with fibers joined by gap junctions. Smooth muscle contraction is activated by calcium ions and sustained through a latch mechanism using little ATP. Contraction can be stimulated by nerves releasing acetylcholine or norepinephrine, hormones, stretch of the muscle, or local chemical factors and pacemaker potentials in some muscles. Prolonged contraction is enabled through action potentials with plateaus or slow wave potentials.
Gluconeogenesis is the synthesis of glucose from non-carbohydrate precursors like lactate, glycerol, and some amino acids. It occurs mainly in the liver and kidney and is important for maintaining blood glucose levels. Gluconeogenesis is not the reversal of glycolysis, but instead uses four alternate reactions to bypass irreversible steps in glycolysis. These reactions include the carboxylation of pyruvate to oxaloacetate, the conversion of oxaloacetate to phosphoenolpyruvate, the dephosphorylation of fructose 1,6-bisphosphate to fructose 6-phosphate, and the dephosphorylation of glucose 6-phosphate to free glucose in the
1. Neurons communicate via graded potentials over short distances and action potentials over long distances. Action potentials are generated when voltage-gated sodium channels open, causing rapid depolarization, followed by voltage-gated potassium channels opening to cause repolarization.
2. At chemical synapses, neurotransmitters are released from presynaptic terminals and bind to receptors on the postsynaptic cell, eliciting an excitatory or inhibitory response.
3. Faster conducting myelinated fibers like A fibers transmit touch and position sense while smaller unmyelinated C fibers transmit pain and temperature sensations. Fiber diameter, myelination and temperature influence conduction velocity.
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 fluid mosaic model of membrane structureJaya Kumar
The cell membrane is made up of a fluid mosaic of phospholipids and proteins. Phospholipids form a bilayer with hydrophobic tails pointing inward and hydrophilic heads facing out. This structure acts as a selective barrier. Embedded and integral proteins carry out important functions like transporting molecules and catalyzing reactions. The fluid mosaic model accounts for the membrane's fluidity and ability to allow movement of components while maintaining selective permeability.
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.
Nerve impulse conduction involves the generation and propagation of action potentials along neurons. At rest, neurons maintain a negative resting potential due to an unequal distribution of ions across the cell membrane. When stimulated, the opening of voltage-gated sodium channels causes rapid depolarization and the generation of an action potential. This potential then propagates along the axon as adjacent regions are depolarized, triggering their own action potentials. At synapses, the action potential is converted to a chemical signal via neurotransmitter release, which can then trigger a new action potential in the post-synaptic cell. Myelination and large axon diameters increase conduction velocity.
The document provides an overview of apoptosis, or programmed cell death. It describes the three main pathways that can trigger apoptosis: the extrinsic or death receptor pathway, the intrinsic or mitochondrial pathway, and the perforin/granzyme pathway. The pathways activate initiator caspases that go on to activate executioner caspases, leading to characteristic cell changes like nuclear fragmentation and membrane blebbing. Apoptotic cells are then phagocytosed to prevent inflammation.
The document discusses the structure and function of neurons. It describes how neurons transmit signals through dendrites, the cell body and axon. An action potential is generated when the membrane potential reaches threshold. This involves the opening of voltage-gated sodium and potassium channels. Action potentials propagate along axons through continuous conduction in unmyelinated axons or saltatory conduction in myelinated axons between nodes of Ranvier. Factors like myelination, axon diameter and temperature can influence conduction velocity.
Lecture 5 (membrane potential and action potential)Ayub Abdi
This document discusses membrane potentials and action potentials in excitable cells like neurons and muscles. It covers:
1. The resting membrane potential of -70mV that is maintained by selective permeability of potassium ions and active transport by the sodium-potassium pump.
2. How an action potential is generated when the membrane reaches its threshold voltage due to an influx of sodium ions, causing rapid depolarization. It then repolarizes as potassium ions efflux.
3. The propagation of action potentials along neurons or muscle fibers to transmit electrical signals and cause effects like muscle contraction or neurotransmitter release.
1. An action potential is a brief change in the membrane potential of a muscle or nerve cell triggered by the stimulation of voltage-gated ion channels.
2. During an action potential, sodium channels open allowing sodium ions to enter the cell, causing rapid depolarization. Then, potassium channels open and sodium channels close, repolarizing the membrane back to its resting potential.
3. The stages of an action potential are resting, depolarization, and repolarization. After an action potential occurs, the cell enters an absolute refractory period where it cannot generate another action potential, followed by a relative refractory period.
1. Digestion breaks down carbohydrates into monosaccharides like glucose and fructose. Salivary amylase and enzymes in the small intestine like maltase, lactase, and sucrase aid in this process.
2. Monosaccharides are absorbed into the bloodstream via active transport against concentration gradients or facilitated diffusion. Glucose is transported to tissues like the liver and brain, while pentoses are excreted by the kidneys.
3. Lactose intolerance occurs when lactase enzyme is deficient, causing undigested lactose to pass to the colon and cause gas, bloating, and diarrhea.
This document summarizes the action potential in neurons. It describes how an action potential is initiated by voltage-gated sodium channels opening during depolarization. This allows sodium ions to rush into the neuron, further depolarizing the membrane. Then, the sodium channels quickly inactivate while voltage-gated potassium channels open, allowing potassium ions to leave the neuron and repolarize the membrane back to its resting potential. The precise opening and closing of sodium and potassium channels underlies the generation and propagation of action potentials along neuronal membranes.
The resting membrane potential of neurons and muscle cells is maintained around -70 mV due to selective permeability of ions across the cell membrane. The sodium-potassium pump actively transports 3 Na+ ions out and 2 K+ ions into the cell, contributing to the negative interior potential. When the membrane potential reaches the threshold, voltage-gated sodium channels open rapidly, causing a sharp depolarization as sodium ions rush in. Subsequently, voltage-gated potassium channels open more slowly, repolarizing the membrane as potassium ions efflux from the cell. This generates an action potential that propagates by local current flow between adjacent areas of the membrane. The sodium-potassium pump then restores ion gradients in preparation for the next action potential
Apoptosis is a natural and programmed form of cell death that occurs in multicellular organisms. It was first described in 1842 and distinguished from necrosis in 1965. During apoptosis, a series of biochemical events lead to changes in the cell and its death, allowing it to be eliminated in a controlled way that does not cause inflammation. This process is regulated by complex signaling pathways within the cell and involves mitochondria, caspases and other components. Defects in apoptosis can result in cancer if cell death is inhibited or neurodegenerative diseases if cell death is excessive.
Cardiac output is defined as the volume of blood pumped by the heart each minute and is regulated intrinsically by factors affecting preload and afterload as well as extrinsically by the autonomic nervous system and hormones. Venous return is a primary extrinsic regulator of cardiac output, increasing stretch of cardiac muscles and stimulating an increase in heart rate. A combination of preload, contractility, afterload and heart rate determine cardiac output under normal resting conditions and during physical activity.
Transport across the cell membrane is necessary to maintain cellular function. There are three main types of transport: passive transport which includes diffusion, facilitated diffusion, and osmosis and does not require energy; active transport which uses energy and transports molecules against their concentration gradient, including primary active transport using ATP and secondary active transport utilizing ion gradients; and vesicular transport which transports larger molecules through vesicles via endocytosis, exocytosis, and transcytosis. Specialized proteins are involved in each of these transport mechanisms to regulate the passage of substances into and out of cells.
The voltage clamp is an experimental method used by electrophysiologists to measure the ion currents through the membranes of excitable cells, such as neurons while holding the membrane voltage at a set level. A basic voltage-clamp will iteratively measure the membrane potential, and then change the membrane potential (voltage) to the desired value by adding the necessary current. This "clamps" the cell membrane at a desired constant voltage, allowing the voltage clamp to record what currents are delivered. Because the currents applied to the cell must be equal to (and opposite in charge to) the current going across the cell membrane at the set voltage, the recorded currents indicate how the cell reacts to changes in membrane potential. Cell membranes of excitable cells contain many different kinds of ion channels, some of which are voltage-gated. The voltage clamp allows the membrane voltage to be manipulated independently of the ionic currents, allowing the current-voltage relationships of membrane channels to be studied.
The document discusses membrane potentials, including resting membrane potential and graded and action potentials. Resting membrane potential is maintained by ion concentration gradients established by the sodium-potassium pump and differential membrane permeability. It varies between cell types but is around -70 mV for neurons. Graded potentials are caused by neurotransmitters and can summate to reach threshold for an action potential. Action potentials are rapid, regenerative changes in membrane potential triggered by voltage-gated sodium and potassium channels. They propagate along neurons to transmit signals in the nervous system.
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.
Smooth muscle cells are found within organs and blood vessels. There are two main types - multi-unit smooth muscle composed of separate fibers, and unitary (visceral) smooth muscle with fibers joined by gap junctions. Smooth muscle contraction is activated by calcium ions and sustained through a latch mechanism using little ATP. Contraction can be stimulated by nerves releasing acetylcholine or norepinephrine, hormones, stretch of the muscle, or local chemical factors and pacemaker potentials in some muscles. Prolonged contraction is enabled through action potentials with plateaus or slow wave potentials.
Gluconeogenesis is the synthesis of glucose from non-carbohydrate precursors like lactate, glycerol, and some amino acids. It occurs mainly in the liver and kidney and is important for maintaining blood glucose levels. Gluconeogenesis is not the reversal of glycolysis, but instead uses four alternate reactions to bypass irreversible steps in glycolysis. These reactions include the carboxylation of pyruvate to oxaloacetate, the conversion of oxaloacetate to phosphoenolpyruvate, the dephosphorylation of fructose 1,6-bisphosphate to fructose 6-phosphate, and the dephosphorylation of glucose 6-phosphate to free glucose in the
1. Neurons communicate via graded potentials over short distances and action potentials over long distances. Action potentials are generated when voltage-gated sodium channels open, causing rapid depolarization, followed by voltage-gated potassium channels opening to cause repolarization.
2. At chemical synapses, neurotransmitters are released from presynaptic terminals and bind to receptors on the postsynaptic cell, eliciting an excitatory or inhibitory response.
3. Faster conducting myelinated fibers like A fibers transmit touch and position sense while smaller unmyelinated C fibers transmit pain and temperature sensations. Fiber diameter, myelination and temperature influence conduction velocity.
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 fluid mosaic model of membrane structureJaya Kumar
The cell membrane is made up of a fluid mosaic of phospholipids and proteins. Phospholipids form a bilayer with hydrophobic tails pointing inward and hydrophilic heads facing out. This structure acts as a selective barrier. Embedded and integral proteins carry out important functions like transporting molecules and catalyzing reactions. The fluid mosaic model accounts for the membrane's fluidity and ability to allow movement of components while maintaining selective permeability.
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.
Nerve impulse conduction involves the generation and propagation of action potentials along neurons. At rest, neurons maintain a negative resting potential due to an unequal distribution of ions across the cell membrane. When stimulated, the opening of voltage-gated sodium channels causes rapid depolarization and the generation of an action potential. This potential then propagates along the axon as adjacent regions are depolarized, triggering their own action potentials. At synapses, the action potential is converted to a chemical signal via neurotransmitter release, which can then trigger a new action potential in the post-synaptic cell. Myelination and large axon diameters increase conduction velocity.
The document provides an overview of apoptosis, or programmed cell death. It describes the three main pathways that can trigger apoptosis: the extrinsic or death receptor pathway, the intrinsic or mitochondrial pathway, and the perforin/granzyme pathway. The pathways activate initiator caspases that go on to activate executioner caspases, leading to characteristic cell changes like nuclear fragmentation and membrane blebbing. Apoptotic cells are then phagocytosed to prevent inflammation.
The document discusses the structure and function of neurons. It describes how neurons transmit signals through dendrites, the cell body and axon. An action potential is generated when the membrane potential reaches threshold. This involves the opening of voltage-gated sodium and potassium channels. Action potentials propagate along axons through continuous conduction in unmyelinated axons or saltatory conduction in myelinated axons between nodes of Ranvier. Factors like myelination, axon diameter and temperature can influence conduction velocity.
Lecture 5 (membrane potential and action potential)Ayub Abdi
This document discusses membrane potentials and action potentials in excitable cells like neurons and muscles. It covers:
1. The resting membrane potential of -70mV that is maintained by selective permeability of potassium ions and active transport by the sodium-potassium pump.
2. How an action potential is generated when the membrane reaches its threshold voltage due to an influx of sodium ions, causing rapid depolarization. It then repolarizes as potassium ions efflux.
3. The propagation of action potentials along neurons or muscle fibers to transmit electrical signals and cause effects like muscle contraction or neurotransmitter release.
1. An action potential is a brief change in the membrane potential of a muscle or nerve cell triggered by the stimulation of voltage-gated ion channels.
2. During an action potential, sodium channels open allowing sodium ions to enter the cell, causing rapid depolarization. Then, potassium channels open and sodium channels close, repolarizing the membrane back to its resting potential.
3. The stages of an action potential are resting, depolarization, and repolarization. After an action potential occurs, the cell enters an absolute refractory period where it cannot generate another action potential, followed by a relative refractory period.
1. When an axon is depolarized past its threshold, voltage-gated sodium channels open, allowing sodium ions to enter and further depolarize the membrane in a positive feedback loop.
2. As the membrane depolarizes further, voltage-gated potassium channels open, allowing potassium ions to exit and repolarize the membrane.
3. After an action potential occurs, sodium-potassium pumps actively transport ions to restore the resting membrane potential, before the axon can initiate another action potential.
Action potential is an abrupt change in membrane potential lasting 1-2 milliseconds. It involves a reversal of the membrane potential where the inside becomes positive and outside negative. Key properties include: being all-or-none, self-propagating, and not decreasing in amplitude with distance. It has distinct phases of depolarization, repolarization, and hyperpolarization before returning to resting potential. The mechanism involves voltage-gated sodium and potassium channels, and the sodium-potassium pump, which regulate ion movements and concentrations to generate the pulse.
- An action potential is a brief change in the membrane potential of an excitable cell, such as a neuron, that occurs when the membrane potential rapidly rises and falls.
- The phases of an action potential include the resting stage, depolarization, repolarization, and hyperpolarization. Depolarization is caused by an influx of sodium ions, repolarization by an efflux of potassium ions.
- For an action potential to occur, the membrane potential must reach the threshold potential, around -55 mV. Once initiated, the action potential propagates along the cell membrane via voltage-gated ion channels.
The nervous system is a complex collection of nerves and specialized cells known as neurons that transmit signals between different parts of the body. The presentation provides a simplified overview of the nervous system and its functions
- Nerve and muscle cells are excitable tissues that respond to stimuli through generation of electrical impulses.
- Nerve cells called neurons transmit signals through electrical impulses called action potentials. Action potentials are generated when the membrane potential rapidly changes from resting potential to threshold potential.
- At chemical synapses, an action potential causes release of neurotransmitters which may excite or inhibit the next neuron. Summation of multiple synaptic signals can trigger action potentials in post-synaptic neurons.
1. An action potential occurs when there is a rapid change in the membrane potential of a neuron from a negative resting potential to a positive potential and then back to a negative potential. This is driven by the movement of ions across the cell membrane through voltage-gated ion channels.
2. For an action potential to be initiated, the membrane potential must be depolarized beyond the threshold potential of around -65mV. This opens voltage-gated sodium channels, allowing sodium ions to enter the cell.
3. The influx of sodium ions causes further depolarization, followed by the opening of voltage-gated potassium channels which causes repolarization back to the resting potential and then hyperpolarization below the resting potential.
TOPIC 6 : HUMAN HEALTH AND PHYSIOLOGY ALIAH RUBAEE
The document discusses the resting potential, graded potential, and action potential in neurons. It provides details on:
1) The resting potential of neurons is normally between -60 to -80 mV due to concentrations of potassium and sodium ions inside and outside the cell. The sodium-potassium pump helps maintain this gradient.
2) A graded potential is an intermediate voltage change before an action potential. It involves the opening of voltage-gated potassium and sodium ion channels, making the intracellular voltage more negative or less negative.
3) An action potential is a brief, all-or-nothing increase in voltage caused by the rapid influx of sodium ions through opened voltage-gated channels, followed by the efflux
This document summarizes the generation and propagation of action potentials in neurons. It discusses:
- The resting membrane potential is maintained by selective permeability to potassium ions.
- Action potentials are initiated by the opening of voltage-gated sodium channels, causing rapid depolarization. If the threshold is reached, an action potential fires.
- After firing, potassium channels open to repolarize the membrane back to the resting potential. Some axons are myelinated to promote faster signal conduction via saltatory propagation between nodes of Ranvier.
This presentation contains the basic information about nerve cells and action potential. This work is done for academic purpose only so if you are using give proper reference.
At rest, the activation gate of sodium channels is closed, preventing sodium entry, while the membrane potential is polarized at -90mV. When adequately stimulated, the activation gates open rapidly, allowing sodium to enter and depolarize the membrane towards its equilibrium potential. As the membrane reaches +35mV, the inactivation gates close, causing repolarization back to -90mV. Some potassium channels remain open, causing temporary hyperpolarization before returning to resting potential.
Neural signals are transmitted through both electrical and chemical means. An electrical signal travels down a neuron's dendrites to its cell body. If the signal reaches the axon hillock's threshold, the axon is activated and fires, transmitting an electrical signal down the axon. At the axon terminals, neurotransmitters are released across the synaptic cleft to the next cell. The membrane potential, maintained by ion concentration gradients and sodium-potassium pumps, underlies the neuron's resting potential. When neurotransmitters bind to receptors on the post-synaptic cell, they generate graded excitatory or inhibitory post-synaptic potentials that are integrated and can trigger an all-or-none action potential for signal transmission along the ax
This explains in detail about the different nerve potentials like Resting Membrane Potential and Action Potential.
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The document summarizes the structure and function of the human nervous system. It describes the three main types of neurons - sensory, motor, and interneurons - and how they transmit nerve impulses via electrical and chemical signals. It also explains the process of synaptic transmission between neurons and how homeostasis is maintained through negative feedback mechanisms that monitor and respond to changes in the internal environment.
Neurons transmit electrical signals along their axons via action potentials. At synapses, neurotransmitters carry signals between neurons. When an action potential reaches a presynaptic neuron, calcium ions enter and cause neurotransmitter vesicles to fuse and release their contents. Neurotransmitters diffuse across the synapse and bind to receptors, sometimes triggering an action potential in the postsynaptic neuron. Myelination allows saltatory conduction to increase signal propagation speed along axons.
Action potential (the guyton and hall physiology)Maryam Fida
ACTION POTENTIAL
Action potential is abrupt pulse like change in the membrane potential lasting for a fraction of second
During action potential there is reversal of membrane potential i.e. inside becomes positive and outside becomes Negative.
We can see the action potential on cathode ray oscilloscope
Abrupt or sudden in onset
2. Have limited magnitude or amplitude i.e. Inside, the potential will go to + 35 or + 45 mV and not beyond that.
3. It is of short duration. Duration is in milli seconds. Duration of spike potential Is 1 -2 milli second. Action potential with plateau has longer duration i.e. may be up to 300 m sec
4. It obeys All or None law i.e. if stimulus is sub threshold it is not produced and when the stimulus is threshold or supra threshold it will be produced with maximum amplitude.
5. It is self propagated i.e. once produced in a membrane it is automatically propagated in both directions.
6. It is not decremented with distance i.e. it will travel with same amplitude through all the distance.
7. It has refractory period. The period during which the tissue will not respond to second stimulus after the application of first stimulus. It could be Absolute and Refractory.
Absolute no response of tissue what so ever may be the strength of stimulus example closure of inactivation gate of sodium channels.
Relative response with higher stimulus than threshold stimulus
DEPOLARIZATION: Sudden loss of Negativity inside the membrane is depolarization.
REPOLARIZATION: return of negativity inside the membrane is Repolarization.
HYPERPOLARIZATION: More Negativity inside
Resting Membrane Potential
Understanding of
Channels Involved
Voltage gated Sodium Channels
Voltage gated Potassium Channels
Sodium Potassium ATPase Pump
Movements of ions
Concentrations of Sodium and Potassium in ECF and ICF
Direction of movement
Plateau is known as Sustained depolarization.
In some instances, the excited membrane does not repolarize immediately after depolarization.
Duration of depolarization of cardiac muscle is 300 milli sec.
Plateau phase has got advantages:
1. It prolongs the duration of depolarization, AP and Contraction. It prolongs the refractory period. Cardiac muscle cannot be tetanized because of this.
2. There is influx of calcium into the sarcoplasm from the ECF which is used for muscle contraction.
This document discusses the nervous system and how it coordinates the activities of sensory receptors, decision making in the central nervous system, and effectors like muscles and glands. It describes the three types of neurons - sensory, intermediate, and motor neurons. It explains how motor neurons transmit impulses from the CNS to effectors and discusses their structure. The document also covers myelin sheaths, nodes of Ranvier, reflex arcs, impulse transmission through action potentials, and synaptic transmission between neurons.
Local anesthesia is the reversible loss of sensation in a body area caused by inhibiting nerve conduction. This document discusses the introduction, composition, mechanism of action, and dose calculation of local anesthesia. It covers topics like nerve physiology, electrophysiology of nerve conduction, impulse propagation, and the site and mode of action of local anesthetics. The document provides details on how local anesthetics work by blocking sodium channels and raising the firing threshold of nerves.
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These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
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Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
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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.
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2. DEFINITIONS:
Stimulus:
A stimulus is an external force or event which when applied to
an excitable tissue produces a characteristic response.
Subthreshold stimulus:
A stimulus which is too weak to produce a response is called a
Subthreshold stimulus.
Threshold stimulus:
The minimum strength of stimulus that can produce excitation
is called a Threshold stimulus.
Suprathreshold stimulus:
Stimuli having strengths higher than threshold stimulus are
called Suprathreshold stimuli.
3. REMEMBER:
IMPORTANT:
• Sodium voltage-gated
channels: are fast channels &
have 2 gates:
- An outer Activation
gate(closed in resting state)
- An Inner Inactivation
gate(open in resting state)
• Potassium channels are slow
channels & have only ONE
gate.
• These channels are different
from Sodium & Potassium
leak channels.
• The Sodium-Potassium PUMP
is present separately.
6. Action Potential:
Definition:
An Action Potential is a self-propagating wave of
electro-negativity that passes along the
surface of the axolemma of the nerve fibers.
7. • We know that the inside of the nerve membrane
is negative with respect to the outside
(RMP=—90 mv)
• When an effective stimulus(threshold or
suprathreshold) is applied, the electrical charge
on the membrane is reversed: at the active part
of the nerve fibre the outside becomes negative
as compared to the corresponding region in the
interior. This is called DEPOLARIZATION and forms
the Action Potential.
8.
9. PHASES OF AN ACTION POTENTIAL:
Phase 1: Depolarization
Phase 2: Repolarization
Phase 3: Hyperpolarization
10.
11.
12.
13.
14.
15. IONIC BASIS OF AN ACTION POTENTIAL:
1. DEPOLARIZATION: Sodium (Na) Influx
2. REPOLARIZATION: Potassium (K) Efflux
3. HYPERPOLARIZATION: Leakage of excess
Potassium (K) ions through the slow closing K
channels.
4. RETURN OF THE AP TO THE RMP FROM
HYPERPOLARIZATION: Sodium-Potassium
Pump
16.
17. Why does the depolarization not reach the
Nernst potential of +66mv for sodium?
There are 2 main reasons. At +35 mv:
• Sodium Influx stops because Inactivation gates
of Sodium channels close although the
activation gates are open & thus no sodium
can enter
• Potassium Efflux starts because slow
Potassium channel gates open and potassium
moves out.
18.
19. State of SODIUM channel gates:
• Resting state:
- Inactivation gates: OPEN
- Activation gates: CLOSED
• Depolarization:
- Activation gates: OPEN
- Inactivation gates: OPEN
• Peak:
- Inactivation gates: CLOSED
- Activation gates: OPEN
• Repolarization:
- Inactivation gates: OPEN
- Activation gates: CLOSED
20.
21.
22. VIVA QUESTIONS:
• AFTER-DEPOLARIZATION:
The descending limb of the action potential
does not reach the baseline abruptly, but it
shows a delay of several milliseconds. This is
due to decreased rate of K efflux at this time.
The excitability & conductivity of the fibre are
increased during this phase.
• AFTER-HYPERPOLARIZATION:
Same as Hyperpolarization....
23. DEFINITIONS:
LATENT PERIOD:
It is the time period between the application of a stimulus and the
start of the response (Action Potential)
DEPOLARIZATION:
When during the transit changes in the action potential, the Potential
difference between the inside of the membrane (-90mv) and
outside (0mv) decreases it is called depolarization. ( the tracing
will move upwards in the AP diagram)
REPOLARIZATION:
A return to the resting membrane potential from either direction (i.e.
de- or hyper-polarization) is called repolarization.
HYPERPOLARIZATION: When during the transit changes in the action
potential, the Potential difference between the inside of the
membrane (-90mv) and the outside (0mv) increases it is called
Hyperpolarization.
24. PROPAGATION OF AN ACTION
POTENTIAL:
Conduction of an Action
Potential in an Unmyelinated
nerve fibre:
25.
26. Question:
• Why and how does the action potential
spread in the forward direction only?
• Why does NOT the action potential spread in
the reverse direction?
27.
28.
29.
30.
31. Unmyelinated Nerve fiber
• Once an action potential is initiated at the axon hillock, no further
triggering event is necessary to activate the remainder of the nerve
fiber. The impulse is automatically conducted throughout the
neuron.
• For the action potential to spread from the active to the inactive
areas, the inactive areas must somehow be depolarized to
threshold. This depolarization is accomplished by local current flow
between the area already undergoing an action potential and the
adjacent inactive area
• This depolarizing effect quickly brings the involved inactive area to
threshold, at which time the voltage-gated Na channels in this
region of the membrane are all thrown open, leading to an action
potential in this previously inactive area. Meanwhile, the original
active area returns to resting potential as a result of K efflux.
32. VIVA Question:
• Does the action potential become weak (decremental)
as it travels down the nerve fiber?
• NO, the action potential does NOT become weak as it
travels down the nerve fiber. In fact, the AP does NOT
travel down the nerve fiber but triggers a new AP in
every new part of the membrane. It is like a “wave” at
a stadium. Each section of spectators stands up (the
rising phase of an action potential), then sits down (the
falling phase) in sequence one after another as the
wave moves around the stadium. The wave, not
individual spectators, travels around the stadium.
33. Thus, the last action potential at the end of the
axon is identical to the original one, no matter
how long the axon is. In this way, action
potentials can serve as long-distance signals
without becoming weak or distorted or
decremental.
34. VIVA Question:
• Why does NOT the action potential spread in the
reverse direction?
• If AP were to spread in both directions, which is
forward and backward, it would be chaos, with
the numerous AP’s bouncing back & forth along
the axon until the axon eventually fatigued. This
does not happen due to the Refractory period.
During and after the generation of an AP, the
changing status of the voltage-gated Na and K
channels prevents the AP from being generated
in these areas again.
36. Continuous Conduction
• Occurs in unmyelinated axons.
• In this situation, the wave of de- and repolarization simply
travels from one patch of membrane to the next adjacent
patch.
• APs moved in this
fashion along the
sarcolemma of a muscle
fiber as well.
• Analogous to dominoes
falling.
37.
38.
39.
40. In a Myelinated Nerve Fibre an Action Potential
travels by SALTATORY Conduction, which is in
a jumping manner from one Node of Ranvier
to the next Node of Ranvier, While in an
Unmyelinated Nerve Fibre an Action Potential
travels from POINT TO POINT.
At the nodes of ranvier, there are an increased
number of Sodium channels present.
41. • Which do you think has a faster rate
of AP conduction – myelinated or
unmyelinated axons?
42. • The answer is a myelinated axon.
• If you can’t see why, then answer this
question:
Could you move 100ft faster if you walked
heel to toe or if you bounded in a way that
there were 3ft in between your feet with each
step?
43. • Which do you think would conduct
an AP faster – an axon with a large
diameter or an axon with a small
diameter?
44. • The answer is an axon with a large diameter.
• If you can’t see why, then answer this
question:
Could you move faster if you walked through a
hallway that was 6ft wide or if you walked
through a hallway that was 1ft wide?
45. Name the events & ions responsible for:
–Depolarization
–Repolarization
–Hyperpolarization OR Undershoot
–Return of the AP from the Overshoot to
the RMP
47. 1. ALL OR NONE LAW
(also called the All or Nothing Law)
On application of a stimulus, an excitable membrane
either responds with a maximal or full-fledged action
potential that spreads along the nerve fiber, or it does not
respond with an action potential at all. This property is
called the all-or-none law.
(This is in direction proportion to the strength of the stimulus applied.)
e.g: This is similar to firing a gun. Either the trigger is NOT
pulled sufficiently to fire the gun (subthreshold stimulus)
OR it is pulled hard enough to fire the gun (threshold is
reached). Squeezing the trigger harder does not produce
a greater explosion, just as pulling the trigger halfway
does not cause the gun to fire halfway.
48. Some Action Potential Questions
• What does it mean when we say an AP is “all
or none?”
– Can you ever have ½ an AP?
• How does the concept of threshold relate to
the “all or none” notion?
• Will one AP ever be bigger than another?
– Why or why not?
51. 2a: ABSOLUTE REFRACTORY PERIOD
Definition:
Once an action potential has been generated , the time period during which even a
suprathreshold stimulus will fail to produce a new action potential is called the
Absolute Refractory period.
During this time the membrane becomes completely refractory (‘stubborn’ or
‘unresponsive’) to any further stimulation.
It corresponds to the entire Depolarization phase & most of the Repolarization phase.
Due to Absolute refractory period, one AP must be over before another can be
initiated at the same site. APs cannot be overlapped or added one on top of
another.
52. • BASIS OF AN ABSOLUTE REFRACTORY PERIOD:
During the depolarization phase of AP, the voltage-
gated Sodium channels have still NOT reset to
their original position. For the Sodium channels
to respond to a stimulus, 2 events are important:
1. Sodium channels be reset to their closed but
capable of opening position. i.e: inactivation
gates open and activation gates closed.
2. The Resting membrane potential must be re-
established.
53. 2b: Relative Refractory Period
Definition:
Following the absolute refractory period is seen a
period of short duration during which a second
action potential can be produced, only if the
triggering event is a suprathreshold stimulus.
This period is called the Relative Refractory
Period.
It corresponds to the last half of the Repolarization
phase.
54. • Basis of a Relative Refractory Period:
An action potential can be produced by a
suprathreshold stimulus because of the following
reasons:
1. By the end of the repolarization phase, some Na
channels have reset while some K channels are
also still open.
2. Thus, a greater than normal triggering event
(suprathreshold stimulus) is required to produce
an AP.
55. Absolute VS Relative Refractory
Period
• Imagine, if you will, a toilet.
• When you pull the handle, water floods the
bowl. This event takes a couple of seconds and you
cannot stop it in the middle. Once the bowl empties,
the flush is complete. Now the upper tank is empty.
If you try pulling the handle at this point, nothing
happens (absolute refractory). Wait for the upper
tank to begin refilling. You can now flush again, but
the intensity of the flushes increases as the upper
tank refills (relative refractory)
57. What is the significance of the REFRACTORY
PERIOD (both absolute & relative):
1. There is no fusion or summation of the action potentials. This intermittent, ie. Not
continuous conduction of nerve impulses is one of the reasons why a nerve fibre
can respond to continuous stimulation for hours without getting tired. Thus, it
decreases fatigue in a nerve fibre.
2. The Action Potentials are produced separate from each other. So, a new AP is
produced in each part of the nerve fibre. This ensures that the AP does not die out
as it is conducted along the membrane.
3. Only a certain number of Action Potentials can be produced in a nerve fibre
because the interval between any 2 action potentials cannot be shorter than the
Absolute Refractory Period. This prevents fatigue of the nerve fibers and sets an
upper limit on the maximum numbers of AP that can be produced in a nerve fibre
in a given period of time.
4. By the time the original site has recovered from its refractory period and is
capable of being restimulated by normal current flow, the action potential has
been propagated in the forward direction only and is so far away that it can no
longer influence the original site. Thus, the refractory period ensures the one-way
propagation of the action potential down the axon away from the initial site of
activation.
59. 3. Compound Action Potential is seen
in a “nerve trunk” & NOT a nerve fibre:
• An action potential having
more than one peak/spike is
called a Compound action
potential.
CAUSE: A nerve trunk contains
many nerve fibres differing
widely in their excitability &
different speeds of conduction
of AP. Multiple peaks are
recorded with the AP from
fastest conducting nerve fibre
first to be recorded followed
by the slower ones....
61. 4. Strength Duration Curve:
Strength duration curve represents 2 (two) factors which
control the final strength of the stimulus. These are:
i. Voltage or current strength of the stimulus applied
ii. Duration of the stimulus
By varying the above 2 factors and plotting the results, a curve
is obtained which is called the STRENGTH-DURATION
CURVE. (See Mushtaq, vol. 1, ed. 5th , page: 118-119)
It is obvious that a stimulus with a low voltage will have to be
applied for a long period of time to reach the threshold
level, while high voltage stimulus will need a much
shorter duration....
62. 4. Strength Duration Curve:
• RHEOBASE:
It is the minimum voltage stimulus which when applied
for an adequately prolonged time will produce an AP.
• UTILIZATION TIME:
The minimum time that a current equal to rheobase must
act to induce an AP is called the Utilization Time.
• CHRONAXIE:
It is the minimum duration for which a stimulus equal to
twice the rheobase value has to be applied in order to
start an AP.
Tissues which are more excitable will have a shorter chronaxie and vice
versa...
63. PROPERTIES OF AN ACTION POTENTIAL:
1. All or none Law
2. Absolute & Relative Refractory period
3. Compound Action Potential
4. Strength-Duration Curve
5. Conduction through
- A myelinated nerve fiber (Saltatory
conduction)
- An unmyelinated nerve fiber (Point to
Point Conduction)
Editor's Notes
Axons vary in length from less than a millimeter in neurons that communicate only with neighboring cells to longer than a meter in neurons that communicate with distant parts of the nervous system or with peripheral organs. For example, the axon of the neuron innervating your big toe must traverse the distance from the origin of its cell body within the spinal cord in the lower region of your back all the way down your leg to your toe.
This is important as it helps the nervous system to discriminate between important and unimportant events. Stimuli that are too weak to bring the membrane to threshold DO NOT fire an AP and therefore do not clutter up the nervous system by transmitting insignificant signals.