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![CHOLINERGIC
TRANSMISSIONThe postsynaptic membrane of the receptor dendrite has
specific cholinergic receptors toward which the
neurotransmitter diffuses. Binding of acetylcholine trigger the
opening of ion channels in the postsynaptic membrane initiating
action potential that can pass in the next axon.
Acetylcholine receptors:
Acetylcholine receptors are ion channels receptors made of
many subunits arranged in the form [(α2)(β)(γ)(δ)].
When Acetylcholine is not bounded to the receptors, the bulky
hydrophobic leu side close the central channels preventing the
diffusion of any ions.
Binding of two acetylcholine molecules to the receptors will
rotate the subunits in which the smaller polar residues will line
the ion channel causing the influx of Na+ into the cell and
efflux of K+ resulting in a depolarization of the postsynaptic
neuron and the initiation of new action potential.
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Uploaded byWasiu Adeseji
BIOSYNTHESIS OF ACETYLCHOLINE IN CNS AND CHOLINERGIC TRANSMISSION
Acetylcholine (ACh) is a neurotransmitter synthesized locally within cholinergic neurons from choline and acetyl-CoA. During neurotransmission, an action potential causes calcium influx and vesicle fusion, releasing ACh into the synaptic cleft. ACh then binds post-synaptic nicotinic or muscarinic receptors, opening ion channels and continuing the action potential in the next neuron. In the central nervous system, ACh is involved in processes like learning, memory, and sleep regulation. Deficiencies in central cholinergic systems are implicated in Alzheimer's disease.
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Overview of ACh discovery, its role as a neurotransmitter in CNS, autonomic ganglia, and its functions.
Functions of ACh include pain conduction, REM sleep, and memory formation, with implications for Alzheimer's.
ACh synthesis involves choline and acetyl-CoA, with requirements for enzyme activity and accessibility.
Steps of cholinergic transmission: action potentials causing ACh release and receptor interaction on postsynaptic membrane.
Features, locations, and functions of muscarinic receptors M1, M2, and M3 in various physiological processes.
Effects of ACh on the eyes, heart, blood vessels, lungs, pancreas, urinary bladder, and sweat glands.
Effects of ACh on nicotinic receptors leading to muscle contraction and neurotransmitter release at ganglia.
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BIOSYNTHESIS OF ACETYLCHOLINE IN CNS AND CHOLINERGIC TRANSMISSION
- 1. BIOSYNTHESIS OF ACETYLCHOLINE INCNS AND CHOLINERGIC TRANSMISSION BY ADESEJI, WASIU ADEBAYO (B.Sc Hons) 08/46KA006 ANA 808: ADVANCED NEURONATOMY DEPARTMENT OF ANATOMY, UNIVERSITY OF ILORIN. JULY, 2015. Lecturer: DR O. B. AKINOLA (P.hd)
- 2. OUTLINE INTRODUCTION SYNTHESIS OF ACH CHOLINERGICTRANSMISSION CHOLINERGIC RECEPTORS CONCLUSION REFERENCES 2
- 3. INTRODUCTION Acetylcholine (ACh), thefirst neurotransmitter discovered, was originally described as "vagus stuff" by Otto Loewi because of its ability to mimic the electrical stimulation of the vagus nerve. It is now known to be a neurotransmitter at all autonomic ganglia, at many autonomically innervated organs, at the neuromuscular junction, and at many synapses in the CNS. Ach is a small-molecule excitatory neurotransmitter with a wide variety of known functions Within the central nervous system (CNS), cholinergic cells (neurons that use ACh as a neurotransmitter) are found in several different locations of the brain, including the striatal 3
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- 7. Depending on whicharea of the brain it is found in, ACh may be involved in any one of several different functions. Some of these functions include the conduction of pain, the regulation of neuroendocrine function, the regulation of REM sleep cycles, and the process of learning and memory formation. Within the basal forebrain, it is the cholinergic cells of the septal nuclei that play a large role in learning and memory. These neurons send major projections to the hippocampus, a structure particularly important for the normal formation of declarative memories. Several noteworthy clinical cases have shown that lesions in this area of the brain alone can greatly impair an individual's ability to form new declarative memories. It is this cholinergic system, among others, that has been shown to suffer serious neurodegeneration in Alzheimer's disease, a condition characterized by a significant failure of memory and other cognitive functions. 7
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- 9. SYNTHESIS OF ACHACh ismade up of choline and acetate. These precursors must be readily available to the neuron terminal at all times so that ACh can be synthesized whenever it is needed. Choline is a compound that can be obtained from foods such as egg yolks, kidney, liver, seeds, legumes, and various vegetables. It is also naturally produced by the liver. Free choline circulating in blood plasma readily crosses the blood-brain barrier and is taken up by cholinergic nerve terminals, for the most part, by a high- affinity choline uptake (HACU) system that is temperature-, energy- and sodium-dependent. The rate-limiting steps in ACh synthesis are the availability of choline and acetyl-CoA. During increased neuronal activity the availability of acetyl-CoA from the mitochondria is upregulated as is the uptake of choline into the nerve ending from the synaptic cleft. Ca2+9
- 10. SYNTHESIS OF ACH ACh isan example of an excitatory small-molecule neurotransmitter. Small-molecule neurotransmitters are synthesized locally within the axon terminal. The synthesis of ACh requires the enzyme choline actyltransferase and, like all small-molecule neurotransmitters, takes place within the nerve terminal. 10
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- 12. CHOLINERGIC TRANSMISSION 1)When the nerveimpulse (Action potential) moves down the presynaptic axon to the terminal bulb the change in the membrane action potential causes the opening of voltage gated calcium channels open allowing Ca2+ ions to pass from the synaptic cleft into the axon bulb. 2) Within the bulb the increase in Ca2+ concentration causes the synaptic vesicles that contain acetylcholine to fuse with the axonal membrane and open spilling their contents into the synaptic cleft. 12
- 13. CHOLINERGIC TRANSMISSIONThe postsynaptic membraneof the receptor dendrite has specific cholinergic receptors toward which the neurotransmitter diffuses. Binding of acetylcholine trigger the opening of ion channels in the postsynaptic membrane initiating action potential that can pass in the next axon. Acetylcholine receptors: Acetylcholine receptors are ion channels receptors made of many subunits arranged in the form [(α2)(β)(γ)(δ)]. When Acetylcholine is not bounded to the receptors, the bulky hydrophobic leu side close the central channels preventing the diffusion of any ions. Binding of two acetylcholine molecules to the receptors will rotate the subunits in which the smaller polar residues will line the ion channel causing the influx of Na+ into the cell and efflux of K+ resulting in a depolarization of the postsynaptic neuron and the initiation of new action potential. 13
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- 16. MUSCARINIC RECEPTOR Features M1M2 M3 Location Autonomic and enteric ganglia Paracrine cell gastric gland CNS SA node , AV node , presynaptic terminal Exocrine gland , smooth muscle , vascular endothelium Function Gastric acid Cns excitation Gi motility Dercrase rate of impulse generation Velocity of conduction Bradycardia contractility Increase in exocrine secretion , smooth muscle contraction Mechanism ip3 , DAG , increase in ca 2+ conc. Inhibition of adenyl cyclase , decrease CAMP opening of k+ channel Same as the M1 receptor Agonist Oxotremorine Methacholine Bethacholine Antagonist Pirenzepine Telenzepine Triptramine Tolterodine Darifenacin
- 17. Eyes: contraction ofciliary muscle and smooth muscle of the iris sphincter (miosis) Heart : Bradycardia (possibly preceded by tachycardia), decrease force of conytraction Blood vessel : vasodilation ( EDRF) Lung : bronchoconstriction and increase secretion Pancreas : increased pancreatic juice Urinary bladder : voiding of urine ( detrusor and spincter) Sweat gland : increased sweating ACETYLCHOLINE – MUSCARINIC ACTION
- 18. ACETYCHOLINE : NICOTINIC ACTION Neuro-muscularJunction: nicotinic Nm receptor Stimulation lead to muscle contraction Sympathetic And P. Sympathetic Ganglia: Nn receptor Release of NE and Ach Adrenal Medulla : Nn receptor Release of adrenaline
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- 20. LOCATION OF ACHRECEPTOR Nicotinic receptor 1. Neuromuscular junction 2. All the autonomic ganglia 3. In the brain Muscarinic receptor Parasympathetic neuro-effector junction 1. M1 – sympathetic ganglia , gastric parietal cell , cerebral cortex(+) 2. M2 – myocardium , smooth muscle (-), presynaptic nerve terminal 3. M3- glandular and visceral smooth muscle (+)
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