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pharmacology
Done by.…
Ali Neemah Hussain
University of Baghdad
College of Medicine
Student Selected Component
Acetylcholine
1
1) Introduction _____________________________________ 1
2) Definition of Ach _________________________________ 1
3) history of discovery of Ach _________________________ 2
4) synthesis and release of Ach _______________________ 3
5) mechanism of action of Ach _______________________ 4
6) sites and function of Ach _________________________ 6
7) clinical correlates to Ach(myasthenia gravis , Alzhiemer) 10
8) pharmacology __________________________________ 13
9) Boutilinium toxin ________________________________ 16
Acetylcholine
2
Acetylcholine (ACh):- is an organic chemical that functions in the brain
and body of many types of animals, including humans, as a
neurotransmitter—a chemical released by nerve cells to send signals
to other cells.Its name is derived from its chemical structure: it is an
ester of acetic acid and choline. Parts in the body that use or are
affected by acetylcholine are referred to as cholinergic.[1]
Acetylcholine is the neurotransmitter used at the neuromuscular
junction—in other words, it is the chemical that motor neurons of
the nervous system release in order to activate muscles.
.Acetylcholine is also used as a neurotransmitter in the autonomic
nervous system, both as an internal transmitter for the sympathetic
nervous system and as the final product released by the
parasympathetic nervous system.[2]
Acetylcholine (ACh) was first identified in 1915 by Henry Hallett Dale for
its actions on heart tissue[3]. It was confirmed as a neurotransmitter
by Otto Loewi, who initially gave it the name Vagusstoff because it
was released from the vagus nerve. Both received the 1936 Nobel
Prize in Physiology or Medicine for their work. Acetylcholine was also
the first neurotransmitter to be identified.[4]
Acetylcholine
3
Acetylcholine is synthesized in certain neurons by the enzyme choline
acetyltransferase from the compounds choline and acetyl-CoA.
Cholinergic neurons are capable of producing Ach.[5]
At least half of the choline used in ACh synthesis is thought to come
directly from recycling of released ACh, hydrolyzed to choline by
cholinesterase. Presumably, uptake of this metabolically derived
choline occurs rapidly, before the choline diffuses away from the
synaptic cleft. Another source of choline is the breakdown of
phosphatidylcholine, which may be stimulated by locally released ACh.
Choline derived from these two sources becomes available in the
extracellular space and is then subject to high-affinity uptake into the
nerve ending[6].
Fig (1)
Acetylcholine
4
Like many other biologically active substances, acetylcholine exerts its
effects by binding to and activating receptors located on the surface
of cells. There are two main classes of acetylcholine receptor,
nicotinic and muscarinic. They are named for chemicals that can
selectively activate each type of receptor without activating the
other.
1-Nicotinic acetylcholine receptors:- are ligand-gated ion channels
permeable to sodium, potassium, and calcium ions. In other words,
they are ion channels embedded in cell membranes, capable of
switching from a closed to open state when acetylcholine binds to
them; in the open state they allow ions to pass through. Nicotinic
receptors come in two main types, known as muscle-type and
neuronal-type. The muscle-type can be selectively blocked by curare,
the neuronal-type by hexamethonium. The main location of muscle-
type receptors is on muscle cells, as described in more detail below.
Neuronal-type receptors are located in autonomic ganglia (both
sympathetic and parasympathetic), and in the central nervous
system.[7]
2-Muscarinic acetylcholine receptors:- have a more complex
mechanism, and affect target cells over a longer time frame. In
mammals, five subtypes of muscarinic receptors have been
identified, labeled M1 through M5. All of them function as G protein-
coupled receptors, meaning that they exert their effects via a second
Acetylcholine
5
messenger system. The M1, M3, and M5 subtypes are Gq-coupled;
they increase intracellular levels of IP3 and calcium by activating
phospholipase C. Their effect on target cells is usually excitatory. The
M2 and M4 subtypes are Gi/Go-coupled; they decrease intracellular
levels of cAMP by inhibiting adenylate cyclase. Their effect on target
cells is usually inhibitory. Muscarinic acetylcholine receptors are
found in both the central nervous system and the peripheral nervous
system of the heart, lungs, upper gastrointestinal tract, and sweat
glands.[8]
Acetylcholine
6
1-Neuromuscular junction
Muscles contract when they receive signals from motor
neurons. The neuromuscular junction is the site of the
signal exchange. The steps of this process in
vertebrates occur as follows: (1) The action potential
reaches the axon terminal. (2) Calcium ions flow into
the axon terminal. (3) Acetylcholine is released into the
synaptic cleft. (4) Acetylcholine binds to postsynaptic
receptors. (5) This binding causes ion channels to open
and allows sodium ions to flow into the muscle cell. (6)
The flow of sodium ions across the membrane into the
muscle cell generates an action potential which induces
muscle contraction.[9]
Acetylcholine is the substance the nervous system uses to activate
skeletal muscles, a kind of striated muscle. These are the muscles
used for all types of voluntary movement, in contrast to smooth
muscle tissue, which is involved in a range of involuntary activities
such as movement of food through the gastrointestinal tract and
constriction of blood vessels. Skeletal muscles are directly controlled
by motor neurons located in the spinal cord or, in a few cases, the
brainstem. These motor neurons send their axons through motor
nerves, from which they emerge to connect to muscle fibers at a
special type of synapse called the neuromuscular junction.[10].
When a motor neuron generates an action potential, it travels rapidly
along the nerve until it reaches the neuromuscular junction, where it
initiates an electrochemical process that causes acetylcholine to be
released into the space between the presynaptic terminal and the
Acetylcholine
7
muscle fiber. The acetylcholine molecules then bind to nicotinic ion-
channel receptors on the muscle cell membrane, causing the ion
channels to open. Calcium ions then flow into the muscle cell,
initiating a sequence of steps that finally produce muscle
contraction.[11]
Fig (2)
Acetylcholine
8
2- Autonomic nervous system
The autonomic nervous system controls a wide range of involuntary
and unconscious body functions. Its main branches are the
sympathetic nervous system and parasympathetic nervous system.
Broadly speaking, the function of the sympathetic nervous system is
to mobilize the body for action: the slogan often used for it is fight-
or-flight. The function of the parasympathetic nervous system is to
put the body in a state conducive to rest, regeneration, digestion,
and reproduction: it is sometimes described using the slogans "rest
and digest" or "feed and breed". Both branches use acetylcholine,
but in different ways[12].
At a schematic level, the sympathetic and parasympathetic nervous
systems are both organized in essentially the same way:
preganglionic neurons in the central nervous system send projections
to neurons located in autonomic ganglia; these neurons then send
output projections to virtually every tissue of the body. In both
branches the internal connections.the projections from the central
nervous system to the autonomic ganglia—use acetylcholine as
neurotransmitter, and the receptors it activates are of the nicotinic
type. In the parasympathetic nervous system the output
connections—the projections from ganglion neurons to tissues that
don't belong to the nervous system—also release acetylcholine,
acting on muscarinic receptors. In the sympathetic nervous system
the output connections mainly release noradrenaline, although
acetylcholine is released at a few points, such as the sudomotor
innervation of the sweat glands.[13]
Acetylcholine
9
3- Direct Vascular Effects
Acetylcholine in the serum exerts a direct effect on vascular tone by
binding to muscarinic receptors present on vascular endothelium.
These cells respond by increasing production of nitric oxide, which
signals the surrounding smooth muscle to relax, leading to
vasodilation.[14]
Acetylcholine has been implicated in learning and memory in several
ways. The anticholinergic drug, scopolamine, impairs acquisition of
new information in humans and animalsIn animals, disruption of the
supply of acetylcholine to the neocortex impairs the learning of
simple discrimination tasks, comparable to the acquisition of factual
information and disruption of the supply of acetylcholine to the
hippocampus and adjacent cortical areas produces forgetting
comparable to anterograde amnesia in humans.[15]
Acetylcholine
10
Myasthenia gravis
Myasthenia gravis is an autoimmune disease that is characterised by
muscle weakness and fatigue, is B-cell mediated, and is associated
with antibodies directed against the acetylcholine receptor, muscle-
specific kinase (MUSK), lipoprotein-related protein 4 (LRP4), or agrin
in the postsynaptic membrane at the neuromuscular junction.
Patients with myasthenia gravis should be classified into subgroups
to help with therapeutic decisions and prognosis. Subgroups based
on serum antibodies and clinical features include early-onset, late-
onset, thymoma, MUSK, LRP4, antibody-negative, and ocular forms
of myasthenia gravis. Agrin-associated myasthenia gravis might
emerge as a new entity. The prognosis is good with optimum
symptomatic, immunosuppressive, and supportive treatment.
Pyridostigmine is the preferred symptomatic treatment, and for
patients who do not adequately respond to symptomatic therapy,
corticosteroids, azathioprine, and thymectomy are first-line
immunosuppressive treatments. Additional immunomodulatory
drugs are emerging, but therapeutic decisions are hampered by the
scarcity of controlled studies. Long-term drug treatment is essential
for most patients and must be tailored to the particular form of
myasthenia gravis.[16]
Acetylcholine
11
Alzheimer's disease
also referred to simply as Alzheimer's, is a chronic
neurodegenerative disease that usually starts slowly and worsens
over time. It is the cause of 60% to 70% of cases of dementia. The
most common early symptom is difficulty in remembering recent
events (short-term memory loss)[17]. As the disease advances,
symptoms can include problems with language, disorientation
(including easily getting lost), mood swings, loss of motivation, not
managing self care, and behavioural issues.As a person's condition
declines, they often withdraw from family and society. Gradually,
bodily functions are lost, ultimately leading to death.Although the
speed of progression can vary, the average life expectancy following
diagnosis is three to nine years.[18]
Fig (3)
Acetylcholine
12
causes
Genetic.
Cholinergic hypothesis:- The oldest, on which most currently available
drug therapies are based, is the cholinergic hypothesis, which
proposes that AD is caused by reduced synthesis of the
neurotransmitter acetylcholine. The cholinergic hypothesis has not
maintained widespread support, largely because medications
intended to treat acetylcholine deficiency have not been very
effective.[19]
Amyloid hypothesis.
Tau hypothesis.
Acetylcholine
13
Blocking, hindering or mimicking the action of acetylcholine has
many uses in medicine. Drugs acting on the acetylcholine system are
either agonists to the receptors, stimulating the system, or
antagonists, inhibiting it. Acetylcholine receptor agonists and
antagonists can either have an effect directly on the receptors or
exert their effects indirectly, e.g., by affecting the enzyme
acetylcholinesterase, which degrades the receptor ligand. Agonists
increase the level of receptor activation, antagonists reduce it.
Examples of drugs
agonists
1-Direct acting agonist: acting directly on cholinoceptors.
pilocarpine*
Pilocarpine is a cholinergic drug, that is, a drug that mimics the
effects of the chemical, acetylcholine which is produced by nerve
cells. Pilocarpine eye drops have been used for many years to treat
glaucoma, a condition in which pressure within the fluid of the eye is
abnormally elevated and ultimately damages the eye and impares
vision. In 1994, an oral formulation of pilocarpine was approved by
the FDA for the treatment of dry mouth caused by radiation therapy
for head and neck cancer, a treatment that damages the salivary
glands and reduces their production of saliva. In 1998, the oral
preparation was approved for the management of Sjögren's
syndrome, an autoimmune disease that damages the salivary and
lacrimal glands.
Acetylcholine
14
Dose:-Oral pilocarpine usually is taken three or four times daily. The
recommended dose for radiation induced xerostomia is 5 to 10 mg
three times daily.
Side effects:- dizziness, vomiting, flushing, diarrhea.[20]
2-indirect acting agonist : acting indirectly by inhibiting the activity of
enzymes responsible for degredation of Ach
Neostigmine*
Competitive inhibitor of cholinesterase resulting in decreased
hydrolysis of acetylcholine by cholinesterase; by reducing the
breakdown of acetylcholine, neostigmine increases acetylcholine in
the synaptic cleft which competes for the same binding site as
nondepolarizing neuromuscular blocking agents, and reverses the
neuromuscular blockade , mainly it is used for symptomatic
treatment of myasthenia gravis.[21]
Dose:-orally, doses depending on medical condition and response
to therapy.
Side effects:- vomiting, diarrhea, abdominal cramps, increased
saliva/mucus, decreased pupil size, increased urination, or increased
sweating may occur. Side effects can be reduced by drinking milk..
pyridostigmine*
same action of neostigmine but with longer duration of action
and it is used for chronic management of myasthenia gravis.[22]
Acetylcholine
15
Edrophonium*
Has very short duration of action and used for diagnosis of
myasthenia gravis.[23]
antagonist
*atropine
a class of medications known as anticholinergics or antimuscarinics.
Atropine occurs naturally and is extracted from the belladonna
alkaloid plant. Atropine works by blocking the actions of a chemical
called acetylcholine. Atropine has numerous uses in clinical medicine
and is available in several dosage forms including oral tablet(0,4 mg),
solution for injection, ophthalmic solution, and ophthalmic ointment.
Side effects:- may cause drowsiness, dizziness, or blurred vision.
Use caution when operating machinery or performing other
hazardous activities.
Fig (4)
Acetylcholine
16
is a neurotoxic protein produced by the bacterium Clostridium
botulinum and related species.It prevents the release of the
neurotransmitter acetylcholine from axon endings at the
neuromuscular junction and thus causes flaccid paralysis. Infection
with the bacterium causes the disease botulism. The toxin is also
used commercially in medicine, cosmetics and research.[25]
Fig (5)
Acetylcholine
17
XMEDICAL USES OF BT
1-Focal dystonias - Involuntary, sustained, or spasmodic patterned
muscle activity
 Cervical dystonia (spasmodic torticollis)
 Blepharospasm (eyelid closure)
 Laryngeal dystonia (spasmodic dysphonia)
 Limb dystonia (writer's cramp)
 Oromandibular dystonia
 Orolingual dystonia
 Truncal dystonia[26]
2-Spasticity - Velocity-dependent increase in muscle tone.
 Stroke
 Traumatic brain injury
 Cerebral palsy
 Multiple sclerosis
 Spinal cord injury[27]
3- Nondystonic disorders of involuntary muscle activity
 Hemifacial spasm
 Tremor
 TicsMyokymia and synkinesis
 Tinnitus (due to myoclonus of stapedius muscle & tensor veli
palatini muscle)
 Hereditary muscle cramps
 Nocturnal bruxism
 Trismus
 Anismus [28]
4- Chronic pain and disorders of localized muscle spasms
Acetylcholine
18
 Chronic low back pain
 Myofascial pain syndrome
 Tension headache.
 Chronic migraine headache.
 Medication overuse headache.
 Lateral epicondylitis.
 Knee pain
 Shoulder pain .
 Neuropathic pain[29].
5- Smooth muscle hyperactive disorders
 Neurogenic bladder – Detrusor hyperreflexia .
 Detrusor-sphincter dyssynergia .
 Benign prostatic hypertrophy.
 Achalasia cardia.
 Hirschsprung disease Sphincter of Oddi dysfunctions .
 Hemorrhoids.
 Chronic anal fissures .
 Raynaud's Phenomenon .[30]
6- Cosmetic use
 Hyperkinetic facial lines (glabellar frown lines, crow's feet).[31]
 Hypertrophic platysma muscle bands.
Adverse Events
Adverse events due to therapeutic and cosmetic injection of BoNT
reported to the FDA include respiratory problems, dysphagia, seizure,
flulike syndrome, facial and other muscle weakness, ptosis, and skin
and injection site reactions[32]
Acetylcholine
19
Ach is a neurotransmitter that transmit signals from one neuron to
another or from neuron to muscle to produce action potential .
Ach was the first neurotransmitter to be identified and its old name
was "vagusstoff".
the type of receptors that Ach act on is cholinoceptors (muscarinic,
nicotinic)
Ach is synthesized at axon terminal by Ach transferase and
hydrolyzed by choline esterase and both are present in neuron
terminal.
Ach is the substance of nervous system that activate skeletal muscle
.
myasthenia gravis is a popular autoimmune disease occur due to
the antibodies directed against Ach receptors and cause muscle
weakness and many other symptoms .
Alzhiemer disease is very popular age related neurodegenerative
disease cause loss of recent memory and disorientation and loss of
motivation , it related also to deficiency in Ach.
blocking or mimicking the action of Ach have many uses in medicine
, drug that acting on Ach receptor either "agonist" or "antagonist".
Blocking the release of Ach at neuromuscular junction by
"botulinum toxin" ( BTX) have a wide range of uses in medicine
especially in plastic surgery and many other uses.
Acetylcholine
20
1-Tiwari, Prashant; Dwivedi, Shubhangi; Singh, Mukesh Pratap; Mishra, Rahul;
Chandy, Anish (2017-05-15). "Basic and modern concepts on cholinergic
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Nathanson N.M., Silva A.J. Selective cognitive dysfunction in acetylcholine M1
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3- Dale H.H. (1914) The action of certain esters and ethers of choline, and their
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10- Njus D, Kelley P, Harnadek G J. Bioenergetics of secretory vesicles. Biochim.
Biophys. Acta. 1987;853:237–265.
11- Davenport H W. Early history of the concept of chemical transmission of the
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12-Baevsky RM, Baranov VM, Funtova II, Diedrich A, Pashenko AV, Chernikova
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Acetylcholine
21
control during prolonged spaceflights aboard the International Space Station. J
Appl Physiol. 2007;103:156–161.
13- Bungo MW, Charles JB, Johnson PC., Jr Cardiovascular deconditioning
during space flight and the use of saline as a countermeasure to orthostatic
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Epub 2014 Feb 13.
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b158.
18-"Dementia Fact sheet N°362". World Health Organization. March 2015.
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20-
https://www.medicinenet.com/pilocarpine/article.htm#is_pilocarpine_safe_to
_take_if_i'm_pregnant_or_breastfeeding.
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Pharmacology 3rd edition, Lippincott's Illustrated Reviews, 2008, p. 51.
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intolerance". Annals of Pharmacotherapy. 41 (2): 314–8.
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new indications. Muscle Nerve Suppl. 1997. 6:S129-45.
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botulinum toxin type A in managing chronic musculoskeletal pain: a systematic
review and meta analysis. Inflammopharmacology. 2011 Feb. 19(1):21-34.
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injections for adults with overactive bladder syndrome. Cochrane Database
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1994 Jul. 94(1):94-9.
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Acetylcholine 2018

  • 1. pharmacology Done by.… Ali Neemah Hussain University of Baghdad College of Medicine Student Selected Component
  • 2. Acetylcholine 1 1) Introduction _____________________________________ 1 2) Definition of Ach _________________________________ 1 3) history of discovery of Ach _________________________ 2 4) synthesis and release of Ach _______________________ 3 5) mechanism of action of Ach _______________________ 4 6) sites and function of Ach _________________________ 6 7) clinical correlates to Ach(myasthenia gravis , Alzhiemer) 10 8) pharmacology __________________________________ 13 9) Boutilinium toxin ________________________________ 16
  • 3. Acetylcholine 2 Acetylcholine (ACh):- is an organic chemical that functions in the brain and body of many types of animals, including humans, as a neurotransmitter—a chemical released by nerve cells to send signals to other cells.Its name is derived from its chemical structure: it is an ester of acetic acid and choline. Parts in the body that use or are affected by acetylcholine are referred to as cholinergic.[1] Acetylcholine is the neurotransmitter used at the neuromuscular junction—in other words, it is the chemical that motor neurons of the nervous system release in order to activate muscles. .Acetylcholine is also used as a neurotransmitter in the autonomic nervous system, both as an internal transmitter for the sympathetic nervous system and as the final product released by the parasympathetic nervous system.[2] Acetylcholine (ACh) was first identified in 1915 by Henry Hallett Dale for its actions on heart tissue[3]. It was confirmed as a neurotransmitter by Otto Loewi, who initially gave it the name Vagusstoff because it was released from the vagus nerve. Both received the 1936 Nobel Prize in Physiology or Medicine for their work. Acetylcholine was also the first neurotransmitter to be identified.[4]
  • 4. Acetylcholine 3 Acetylcholine is synthesized in certain neurons by the enzyme choline acetyltransferase from the compounds choline and acetyl-CoA. Cholinergic neurons are capable of producing Ach.[5] At least half of the choline used in ACh synthesis is thought to come directly from recycling of released ACh, hydrolyzed to choline by cholinesterase. Presumably, uptake of this metabolically derived choline occurs rapidly, before the choline diffuses away from the synaptic cleft. Another source of choline is the breakdown of phosphatidylcholine, which may be stimulated by locally released ACh. Choline derived from these two sources becomes available in the extracellular space and is then subject to high-affinity uptake into the nerve ending[6]. Fig (1)
  • 5. Acetylcholine 4 Like many other biologically active substances, acetylcholine exerts its effects by binding to and activating receptors located on the surface of cells. There are two main classes of acetylcholine receptor, nicotinic and muscarinic. They are named for chemicals that can selectively activate each type of receptor without activating the other. 1-Nicotinic acetylcholine receptors:- are ligand-gated ion channels permeable to sodium, potassium, and calcium ions. In other words, they are ion channels embedded in cell membranes, capable of switching from a closed to open state when acetylcholine binds to them; in the open state they allow ions to pass through. Nicotinic receptors come in two main types, known as muscle-type and neuronal-type. The muscle-type can be selectively blocked by curare, the neuronal-type by hexamethonium. The main location of muscle- type receptors is on muscle cells, as described in more detail below. Neuronal-type receptors are located in autonomic ganglia (both sympathetic and parasympathetic), and in the central nervous system.[7] 2-Muscarinic acetylcholine receptors:- have a more complex mechanism, and affect target cells over a longer time frame. In mammals, five subtypes of muscarinic receptors have been identified, labeled M1 through M5. All of them function as G protein- coupled receptors, meaning that they exert their effects via a second
  • 6. Acetylcholine 5 messenger system. The M1, M3, and M5 subtypes are Gq-coupled; they increase intracellular levels of IP3 and calcium by activating phospholipase C. Their effect on target cells is usually excitatory. The M2 and M4 subtypes are Gi/Go-coupled; they decrease intracellular levels of cAMP by inhibiting adenylate cyclase. Their effect on target cells is usually inhibitory. Muscarinic acetylcholine receptors are found in both the central nervous system and the peripheral nervous system of the heart, lungs, upper gastrointestinal tract, and sweat glands.[8]
  • 7. Acetylcholine 6 1-Neuromuscular junction Muscles contract when they receive signals from motor neurons. The neuromuscular junction is the site of the signal exchange. The steps of this process in vertebrates occur as follows: (1) The action potential reaches the axon terminal. (2) Calcium ions flow into the axon terminal. (3) Acetylcholine is released into the synaptic cleft. (4) Acetylcholine binds to postsynaptic receptors. (5) This binding causes ion channels to open and allows sodium ions to flow into the muscle cell. (6) The flow of sodium ions across the membrane into the muscle cell generates an action potential which induces muscle contraction.[9] Acetylcholine is the substance the nervous system uses to activate skeletal muscles, a kind of striated muscle. These are the muscles used for all types of voluntary movement, in contrast to smooth muscle tissue, which is involved in a range of involuntary activities such as movement of food through the gastrointestinal tract and constriction of blood vessels. Skeletal muscles are directly controlled by motor neurons located in the spinal cord or, in a few cases, the brainstem. These motor neurons send their axons through motor nerves, from which they emerge to connect to muscle fibers at a special type of synapse called the neuromuscular junction.[10]. When a motor neuron generates an action potential, it travels rapidly along the nerve until it reaches the neuromuscular junction, where it initiates an electrochemical process that causes acetylcholine to be released into the space between the presynaptic terminal and the
  • 8. Acetylcholine 7 muscle fiber. The acetylcholine molecules then bind to nicotinic ion- channel receptors on the muscle cell membrane, causing the ion channels to open. Calcium ions then flow into the muscle cell, initiating a sequence of steps that finally produce muscle contraction.[11] Fig (2)
  • 9. Acetylcholine 8 2- Autonomic nervous system The autonomic nervous system controls a wide range of involuntary and unconscious body functions. Its main branches are the sympathetic nervous system and parasympathetic nervous system. Broadly speaking, the function of the sympathetic nervous system is to mobilize the body for action: the slogan often used for it is fight- or-flight. The function of the parasympathetic nervous system is to put the body in a state conducive to rest, regeneration, digestion, and reproduction: it is sometimes described using the slogans "rest and digest" or "feed and breed". Both branches use acetylcholine, but in different ways[12]. At a schematic level, the sympathetic and parasympathetic nervous systems are both organized in essentially the same way: preganglionic neurons in the central nervous system send projections to neurons located in autonomic ganglia; these neurons then send output projections to virtually every tissue of the body. In both branches the internal connections.the projections from the central nervous system to the autonomic ganglia—use acetylcholine as neurotransmitter, and the receptors it activates are of the nicotinic type. In the parasympathetic nervous system the output connections—the projections from ganglion neurons to tissues that don't belong to the nervous system—also release acetylcholine, acting on muscarinic receptors. In the sympathetic nervous system the output connections mainly release noradrenaline, although acetylcholine is released at a few points, such as the sudomotor innervation of the sweat glands.[13]
  • 10. Acetylcholine 9 3- Direct Vascular Effects Acetylcholine in the serum exerts a direct effect on vascular tone by binding to muscarinic receptors present on vascular endothelium. These cells respond by increasing production of nitric oxide, which signals the surrounding smooth muscle to relax, leading to vasodilation.[14] Acetylcholine has been implicated in learning and memory in several ways. The anticholinergic drug, scopolamine, impairs acquisition of new information in humans and animalsIn animals, disruption of the supply of acetylcholine to the neocortex impairs the learning of simple discrimination tasks, comparable to the acquisition of factual information and disruption of the supply of acetylcholine to the hippocampus and adjacent cortical areas produces forgetting comparable to anterograde amnesia in humans.[15]
  • 11. Acetylcholine 10 Myasthenia gravis Myasthenia gravis is an autoimmune disease that is characterised by muscle weakness and fatigue, is B-cell mediated, and is associated with antibodies directed against the acetylcholine receptor, muscle- specific kinase (MUSK), lipoprotein-related protein 4 (LRP4), or agrin in the postsynaptic membrane at the neuromuscular junction. Patients with myasthenia gravis should be classified into subgroups to help with therapeutic decisions and prognosis. Subgroups based on serum antibodies and clinical features include early-onset, late- onset, thymoma, MUSK, LRP4, antibody-negative, and ocular forms of myasthenia gravis. Agrin-associated myasthenia gravis might emerge as a new entity. The prognosis is good with optimum symptomatic, immunosuppressive, and supportive treatment. Pyridostigmine is the preferred symptomatic treatment, and for patients who do not adequately respond to symptomatic therapy, corticosteroids, azathioprine, and thymectomy are first-line immunosuppressive treatments. Additional immunomodulatory drugs are emerging, but therapeutic decisions are hampered by the scarcity of controlled studies. Long-term drug treatment is essential for most patients and must be tailored to the particular form of myasthenia gravis.[16]
  • 12. Acetylcholine 11 Alzheimer's disease also referred to simply as Alzheimer's, is a chronic neurodegenerative disease that usually starts slowly and worsens over time. It is the cause of 60% to 70% of cases of dementia. The most common early symptom is difficulty in remembering recent events (short-term memory loss)[17]. As the disease advances, symptoms can include problems with language, disorientation (including easily getting lost), mood swings, loss of motivation, not managing self care, and behavioural issues.As a person's condition declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death.Although the speed of progression can vary, the average life expectancy following diagnosis is three to nine years.[18] Fig (3)
  • 13. Acetylcholine 12 causes Genetic. Cholinergic hypothesis:- The oldest, on which most currently available drug therapies are based, is the cholinergic hypothesis, which proposes that AD is caused by reduced synthesis of the neurotransmitter acetylcholine. The cholinergic hypothesis has not maintained widespread support, largely because medications intended to treat acetylcholine deficiency have not been very effective.[19] Amyloid hypothesis. Tau hypothesis.
  • 14. Acetylcholine 13 Blocking, hindering or mimicking the action of acetylcholine has many uses in medicine. Drugs acting on the acetylcholine system are either agonists to the receptors, stimulating the system, or antagonists, inhibiting it. Acetylcholine receptor agonists and antagonists can either have an effect directly on the receptors or exert their effects indirectly, e.g., by affecting the enzyme acetylcholinesterase, which degrades the receptor ligand. Agonists increase the level of receptor activation, antagonists reduce it. Examples of drugs agonists 1-Direct acting agonist: acting directly on cholinoceptors. pilocarpine* Pilocarpine is a cholinergic drug, that is, a drug that mimics the effects of the chemical, acetylcholine which is produced by nerve cells. Pilocarpine eye drops have been used for many years to treat glaucoma, a condition in which pressure within the fluid of the eye is abnormally elevated and ultimately damages the eye and impares vision. In 1994, an oral formulation of pilocarpine was approved by the FDA for the treatment of dry mouth caused by radiation therapy for head and neck cancer, a treatment that damages the salivary glands and reduces their production of saliva. In 1998, the oral preparation was approved for the management of Sjögren's syndrome, an autoimmune disease that damages the salivary and lacrimal glands.
  • 15. Acetylcholine 14 Dose:-Oral pilocarpine usually is taken three or four times daily. The recommended dose for radiation induced xerostomia is 5 to 10 mg three times daily. Side effects:- dizziness, vomiting, flushing, diarrhea.[20] 2-indirect acting agonist : acting indirectly by inhibiting the activity of enzymes responsible for degredation of Ach Neostigmine* Competitive inhibitor of cholinesterase resulting in decreased hydrolysis of acetylcholine by cholinesterase; by reducing the breakdown of acetylcholine, neostigmine increases acetylcholine in the synaptic cleft which competes for the same binding site as nondepolarizing neuromuscular blocking agents, and reverses the neuromuscular blockade , mainly it is used for symptomatic treatment of myasthenia gravis.[21] Dose:-orally, doses depending on medical condition and response to therapy. Side effects:- vomiting, diarrhea, abdominal cramps, increased saliva/mucus, decreased pupil size, increased urination, or increased sweating may occur. Side effects can be reduced by drinking milk.. pyridostigmine* same action of neostigmine but with longer duration of action and it is used for chronic management of myasthenia gravis.[22]
  • 16. Acetylcholine 15 Edrophonium* Has very short duration of action and used for diagnosis of myasthenia gravis.[23] antagonist *atropine a class of medications known as anticholinergics or antimuscarinics. Atropine occurs naturally and is extracted from the belladonna alkaloid plant. Atropine works by blocking the actions of a chemical called acetylcholine. Atropine has numerous uses in clinical medicine and is available in several dosage forms including oral tablet(0,4 mg), solution for injection, ophthalmic solution, and ophthalmic ointment. Side effects:- may cause drowsiness, dizziness, or blurred vision. Use caution when operating machinery or performing other hazardous activities. Fig (4)
  • 17. Acetylcholine 16 is a neurotoxic protein produced by the bacterium Clostridium botulinum and related species.It prevents the release of the neurotransmitter acetylcholine from axon endings at the neuromuscular junction and thus causes flaccid paralysis. Infection with the bacterium causes the disease botulism. The toxin is also used commercially in medicine, cosmetics and research.[25] Fig (5)
  • 18. Acetylcholine 17 XMEDICAL USES OF BT 1-Focal dystonias - Involuntary, sustained, or spasmodic patterned muscle activity  Cervical dystonia (spasmodic torticollis)  Blepharospasm (eyelid closure)  Laryngeal dystonia (spasmodic dysphonia)  Limb dystonia (writer's cramp)  Oromandibular dystonia  Orolingual dystonia  Truncal dystonia[26] 2-Spasticity - Velocity-dependent increase in muscle tone.  Stroke  Traumatic brain injury  Cerebral palsy  Multiple sclerosis  Spinal cord injury[27] 3- Nondystonic disorders of involuntary muscle activity  Hemifacial spasm  Tremor  TicsMyokymia and synkinesis  Tinnitus (due to myoclonus of stapedius muscle & tensor veli palatini muscle)  Hereditary muscle cramps  Nocturnal bruxism  Trismus  Anismus [28] 4- Chronic pain and disorders of localized muscle spasms
  • 19. Acetylcholine 18  Chronic low back pain  Myofascial pain syndrome  Tension headache.  Chronic migraine headache.  Medication overuse headache.  Lateral epicondylitis.  Knee pain  Shoulder pain .  Neuropathic pain[29]. 5- Smooth muscle hyperactive disorders  Neurogenic bladder – Detrusor hyperreflexia .  Detrusor-sphincter dyssynergia .  Benign prostatic hypertrophy.  Achalasia cardia.  Hirschsprung disease Sphincter of Oddi dysfunctions .  Hemorrhoids.  Chronic anal fissures .  Raynaud's Phenomenon .[30] 6- Cosmetic use  Hyperkinetic facial lines (glabellar frown lines, crow's feet).[31]  Hypertrophic platysma muscle bands. Adverse Events Adverse events due to therapeutic and cosmetic injection of BoNT reported to the FDA include respiratory problems, dysphagia, seizure, flulike syndrome, facial and other muscle weakness, ptosis, and skin and injection site reactions[32]
  • 20. Acetylcholine 19 Ach is a neurotransmitter that transmit signals from one neuron to another or from neuron to muscle to produce action potential . Ach was the first neurotransmitter to be identified and its old name was "vagusstoff". the type of receptors that Ach act on is cholinoceptors (muscarinic, nicotinic) Ach is synthesized at axon terminal by Ach transferase and hydrolyzed by choline esterase and both are present in neuron terminal. Ach is the substance of nervous system that activate skeletal muscle . myasthenia gravis is a popular autoimmune disease occur due to the antibodies directed against Ach receptors and cause muscle weakness and many other symptoms . Alzhiemer disease is very popular age related neurodegenerative disease cause loss of recent memory and disorientation and loss of motivation , it related also to deficiency in Ach. blocking or mimicking the action of Ach have many uses in medicine , drug that acting on Ach receptor either "agonist" or "antagonist". Blocking the release of Ach at neuromuscular junction by "botulinum toxin" ( BTX) have a wide range of uses in medicine especially in plastic surgery and many other uses.
  • 21. Acetylcholine 20 1-Tiwari, Prashant; Dwivedi, Shubhangi; Singh, Mukesh Pratap; Mishra, Rahul; Chandy, Anish (2017-05-15). "Basic and modern concepts on cholinergic receptor: A review". Asian Pacific Journal of Tropical Disease. 2-Anagnostaras S.G., Murphy G.G., Hamilton S.E., Mitchell S.L., Rahnama N.P., Nathanson N.M., Silva A.J. Selective cognitive dysfunction in acetylcholine M1 muscarinic receptor mutant mice. Nat. Neurosci. 2003;6:51–58. 3- Dale H.H. (1914) The action of certain esters and ethers of choline, and their relation to muscarine. J. Pharmacol. Exp. Ther. 6, 147–190 4- Dale H. (1935) Pharmacology and nerve-endings. Proc. R. Soc. Med. 28, 319– 332 5- Wu D, Hersh L B. Choline acetyltransferase: Celebrating its fiftieth year. J. Neurochem. 1994;62:1653–1663. 6- Taylor P, Radic Z. The cholinesterases: From genes to proteins. Annu. Rev. Pharmacol. Toxicol. 1994;34:281–320. 7- Lewis J.A. , Wu C.H. , Levine J.H. , Berg H. Levamisole-resistant mutants of the nematode Caenorhabditis elegans appear to lack pharmacological acetylcholine receptors. Neuroscience. (1980a);5:967–989. 8- Culotti J.G. , Klein W.L. Occurrence of muscarinic acetylcholine receptors in wild-type and cholinergic mutants of C. elegans. J. Neurosci. (1983);3:359–368. 9- Davenport H W. Early history of the concept of chemical transmission of the nerve impulse. Physiologist. 1991;34:129–190. 10- Njus D, Kelley P, Harnadek G J. Bioenergetics of secretory vesicles. Biochim. Biophys. Acta. 1987;853:237–265. 11- Davenport H W. Early history of the concept of chemical transmission of the nerve impulse. Physiologist. 1991;34:129–190. 12-Baevsky RM, Baranov VM, Funtova II, Diedrich A, Pashenko AV, Chernikova AG, Drescher J, Jordan J, Tank J. Autonomic cardiovascular and respiratory
  • 22. Acetylcholine 21 control during prolonged spaceflights aboard the International Space Station. J Appl Physiol. 2007;103:156–161. 13- Bungo MW, Charles JB, Johnson PC., Jr Cardiovascular deconditioning during space flight and the use of saline as a countermeasure to orthostatic intolerance. Aviat Space Environ Med. 1985;56:985–990. 14-Kellogg, D.L.; Zhao, J.L.; Coey, U.; Green, J.V. (February 2005). "Acetylcholine-induced vasodilation is mediated by nitric oxide and prostaglandins in human skin". Journal of Applied Physiology. 98 (2): 629–632. 15-Crow, T.J.; Grove-White, I.G. (October 1973). "An analysis of the learning deficit following hyoscine administration in man". British Journal of Pharmacology. 49 (2): 322–327. 16-J Autoimmun. 2014 Feb-Mar;48-49:143-8. doi: 10.1016/j.jaut.2014.01.003. Epub 2014 Feb 13. 17-Burns A, Iliffe S (5 February 2009). "Alzheimer's disease". The BMJ. 338: b158. 18-"Dementia Fact sheet N°362". World Health Organization. March 2015. Archived from the original on 18 March 2015. Retrieved 13 January 2016. 19- The Cholinergic Hypothesis of Alzheimer's Disease: a Review of Progress. Journal of Neurology, Neurosurgery, and Psychiatry. 1999;66(2):137–47. 20- https://www.medicinenet.com/pilocarpine/article.htm#is_pilocarpine_safe_to _take_if_i'm_pregnant_or_breastfeeding. 21- Howland, R.D., Mycek, M.J., Harvey, R.A., Champe, P.C., and Mycek, M.J., Pharmacology 3rd edition, Lippincott's Illustrated Reviews, 2008, p. 51. 22- Gales BJ, Gales MA (2007). "Pyridostigmine in the treatment of orthostatic intolerance". Annals of Pharmacotherapy. 41 (2): 314–8. 23- KD Tripati MD. Essentials of Medical Pharmacology (fifth ed.). Jaypee Brothers Medical Publishers(P) Ltd. p. 84.
  • 23. Acetylcholine 22 24- Bryan E, Bledsoe; Robert S. Porter; Richard A. Cherry (2004). "Ch. 3". Intermediate Emergency Care. Upper Saddle River, NJ: Pearson Prentice Hill. p. 260. 25- Montecucco C, Molgó J (June 2005). "Botulinal neurotoxins: revival of an old killer". Current Opinion in Pharmacology. 5 (3): 274–79. 26- Jankovic J, Brin MF. Botulinum toxin: historical perspective and potential new indications. Muscle Nerve Suppl. 1997. 6:S129-45. 27- Shaw LC, Price CI, van Wijck FM, Shackley P, Steen N, Barnes MP. Botulinum Toxin for the Upper Limb after Stroke (BoTULS) Trial: effect on impairment, activity limitation, and pain. Stroke. 2011 May. 42(5):1371-9. 28- Costa J, Espírito-Santo C, Borges A, Ferreira JJ, Coelho M, Moore P, et al. Botulinum toxin type A therapy for hemifacial spasm. Cochrane Database Syst Rev. 2005 Jan 25. 29- Zhang T, Adatia A, Zarin W, Moitri M, Vijenthira A, Chu R. The efficacy of botulinum toxin type A in managing chronic musculoskeletal pain: a systematic review and meta analysis. Inflammopharmacology. 2011 Feb. 19(1):21-34. 30- Duthie JB, Vincent M, Herbison GP, Wilson DI, Wilson D. Botulinum toxin injections for adults with overactive bladder syndrome. Cochrane Database Syst Rev. 2011. (12):CD005493. 31- Keen M, Blitzer A, Aviv J, et al. Botulinum toxin A for hyperkinetic facial lines: results of a double-blind, placebo-controlled study. Plast Reconstr Surg. 1994 Jul. 94(1):94-9. 32- Coté TR, Mohan AK, Polder JA, Walton MK, Braun MM. Botulinum toxin type A injections: adverse events reported to the US Food and Drug Administration in therapeutic and cosmetic cases. J Am Acad Dermatol. 2005 Sep. 53(3):407-15.
  • 24. Acetylcholine 23 1- https://encrypted- tbn0.gstatic.com/images?q=tbn:ANd9GcTQswQEZgBjkqWG6lmi5kHkXDfjbpduQtpOQMG91K aolxo1e2oB 2- https://encrypted-tbn0.gstatic.com/images?q=tbn:ANd9GcTATR-QyQL0N- QX0T4vrTY26VWST92EQElO9M2sTLIk-EsfjlW_ 3- https://www.google.com/imgres?imgurl=http%3A%2F%2Fwww.getmedurgentcare.com%2F wp- content%2Fuploads%2F2016%2F11%2Falzehimer.jpg&imgrefurl=http%3A%2F%2Fwww.get medurgentcare.com%2Fwhat-you-should-know-about-alzheimers-disease-and- awareness%2F&docid=SdsYc- 6C8VNPeM&tbnid=Tw05SdVIHXe_eM%3A&vet=10ahUKEwixit7S3sHZAhUMWywKHZhSA7o QMwgxKAEwAQ..i&w=2868&h=1888&client=firefox- b&bih=659&biw=1366&q=alzhiemer&ved=0ahUKEwixit7S3sHZAhUMWywKHZhSA7oQMwgx KAEwAQ&iact=mrc&uact=8 4- https://encrypted- tbn0.gstatic.com/images?q=tbn:ANd9GcTFeaK1ZmuchqdeapfXTKEshqcLuQCGZvgpdJsHrL88E HrU5jOM