Acetylcholine release cholinergic

Several cholinergic strategies, other than cholinesterase inhibition, have been employed with the intention of ameliora ting the symptoms of AD. These include precursor loading acetylcholine release enhancement, and direct activation of both muscarinic and nicotinic receptors. 

A related organism, CL botulinum, produces a similar toxin which may contaminate food if the organism has grown in it and conditions are favourable for anaerobic growth. Meat pastes and pates are likely sources. This toxin interferes with acetylcholine release at cholinergic syrrapses and also acts at neuromuscular jimctions. Death fiom this toxin eventually results firm respiratory failure. 

Berlanga M., Simpson T., Alcantra A. (2005). Dopamine D5 receptor localization on cholinergic neurons of the rat forebrain and diencephalon a potential neuroanatomical substrate involved in mediating dopaminergic influences on acetylcholine release. J. Comp. Neurol. 492, 34-49. 

Choline is supplied to the neuron either from plasma or by metabolism of choline-containing compounds 193 A slow release of acetylcholine from neurons at rest probably occurs at all cholinergic synapses 194 The relationship between acetylcholine content in a vesicle and the quanta of acetylcholine released can only be estimated 194 Depolarization of the nerve terminal by an action potential increases the number of quanta released per unit time 194 All the acetylcholine contained within the cholinergic neuron does not behave as if in a single compartment 194... 

Gorman L, Pang K, Frink K, Givens B, Olton D. 1994. Acetylcholine release in the hippocampus Effects of cholinergic and GABAergic compounds in the medial septal area. Neuroscience Letters 166(2) 199-202. 

Each neuron usually releases only one type of neurotransmitter. Neurons that release dopamine are referred to as dopaminergic, for example, while those that release acetylcholine are cholinergic, etc. The transmitters that are released diffuse through the synaptic cleft and bind on the other side to receptors on the postsynaptic membrane. These receptors are integral membrane proteins that have binding sites for neurotransmitters on their exterior (see p. 224). 

The available data are consistent with the present thesis that cholinergic inputs to cerebral cortex mediate intradendritic events fundamental to conscious activity as a primary role, and that cholinergic modulation of electrophysiological activity may be secondary, even epiphenomenal. Transduction pathways exist whereby muscarinic receptors (and possibly nicotinic receptors acting presynaptically to inhibit acetylcholine release) may lead to actions on the cytoskeleton directly relevant to consciousness. The thesis presented here describes these pathways and also suggests a possible explanation for the diversity of neuromodulators and metabotropic receptors. Accordingly, qualitative aspects of our consciousness would be finely tuned by a number of neurochemicals, prominent among which is acetylcholine. 

The rapid, low amplitude EEG activity of REM sleep, like that of waking, is sustained by cholinergic processes (Kinai Szerb, 1965 Phillis 8c Ghong, 1965), principally from neurons in the basal forebrain which project over the entire cortex (Divac, 1975 Lehmann et al., 1980 Bigl et al., 1982). Activation of the nucleus basalis of Meynert results in acetylcholine release in the cortex... 

The parasympathetic nervous system, through the vagus nerve, inhibits the spontaneous rate of depolarization of pacemaker cells. The release of acetylcholine from cholinergic vagal fibers increases potassium conductance (gK+) in pacemaker cells, and this enhanced outward movement of K+ results in a more negative po-... 

Maura G, Andrioli SC, Cavazzani P S-hydroxytryptaminej receptor sites on cholinergic axon terminals of human cerebral cortex mediate inhibition of acetylcholine release. J Neurochem 58 2334-2337, 1992 Mavissakalian M, Turner SM, Michelson L, et al Tricyclic antidepressants in obsessive-compulsive disorder antiobsessional or antidepressant agents 11. Am J Psychiatry 142 572-576, 1985... 

Autonomic nerves can regulate coronary arteriolar tone. Acetylcholine released from postganglionic parasympathetic nerves relaxes coronary arteriolar smooth muscle via the NO/cGMP pathway in humans as described above. Damage to the endothelium, as occurs with atherosclerosis, eliminates this action, and acetylcholine is able to contract arterial smooth muscle and produce vasoconstriction. Skeletal muscle receives sympathetic cholinergic vasodilator nerves, but the view that acetylcholine caused vasodilation in this vascular bed has not been verified experimentally. Moreover, NO, rather than acetylcholine, may be released from neurons. However, this vascular bed responds to exogenous choline esters because of the presence of M3 receptors on endothelial and smooth muscle cells. 

The actions of acetylcholine released from autonomic and somatic motor nerves are terminated by enzymatic hydrolysis of the molecule. Hydrolysis is accomplished by the action of acetylcholinesterase, which is present in high concentrations in cholinergic synapses. The indirect-acting cholinomimetics have their primary effect at the active site of this enzyme, although some also have direct actions at nicotinic receptors. The chief differences between members of the group are chemical and pharmacokinetic—their pharmacodynamic properties are almost identical. 

In contrast to thioperamide, phenylbutanoylhistamine, an H3-receptor antagonist with moderate potency [51], failed to antagonize the inhibitory effect of (R)a-methylhistamine on acetylcholine release from slices of rat entorhinal cortex [52], In addition, this compound also failed to antagonize the (R)a-methylhistamine-induced inhibition of non-adrenergic non-cholinergic contractions of the guinea pig ileum [53],... 

This chapter deals with botulinum toxin type A (BOTOX) in the treatment of strabismus, blepharospasm, and related disorders. Botulinum toxin type A (BOTOX) has been used to treat strabismus, blepharospasm, Meige s syndrome, and spasmodic torticollis. By preventing acetylcholine release at me neuromuscular junction, botulinum toxin A usually causes a temporary paralysis of the locally injected muscles. The variability in duration of paralysis may be related to me rate of developing antibodies to me toxin, upregulation of nicotinic cholinergic postsynaptic receptors, and aberrant regeneration of motor nerve fibers at me neuromuscular junction. Complications related to this toxin include double vision (diplopia) and lid droop (ptosis). 

After release from the presynaptic terminal, acetylcholine molecules may bind to and activate an acetylcholine receptor (cholinoceptor). Eventually (and usually very rapidly), all of the acetylcholine released will diffuse within range of an acetylcholinesterase (AChE) molecule. AChE very efficiently splits acetylcholine into choline and acetate, neither of which has significant transmitter effect, and thereby terminates the action of the transmitter (Figure 6-3). Most cholinergic synapses are richly supplied with acetylcholinesterase the half-life of acetylcholine in the synapse is therefore very short. Acetylcholinesterase is also found in other tissues, eg, red blood cells. (Another cholinesterase with a lower specificity for acetylcholine, butyrylcholinesterase [pseudocholinesterase], is found in blood plasma, liver, glia, and many other tissues.)... 

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