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Nerve fibers cholinergic

Cholinergic blocking dragp inhibit die activity of acetylcholine in parasympadietic nerve fibers (see Chap. 24 for a description of die role of acetylcholine in the transmission of nerve impulses across parasympadietic nerve fibers). When die activity of acetylcholine is inhibited, nerve impulses traveling along parasympadietic nerve fibers cannot pass from die nerve fiber to die effector organ or structure ... [Pg.229]

The two most common neurotransmitters released by neurons of the ANS are acetylcholine (Ach) and norepinephrine (NE). Several distinguishing features of these neurotransmitters are summarized in Table 9.3. Nerve fibers that release acetylcholine are referred to as cholinergic fibers and include all preganglionic fibers of the ANS — sympathetic and parasympathetic systems all postganglionic fibers of the parasympathetic system and sympathetic postganglionic... [Pg.97]

Cholesterogenesis. Synthesis of cholesterol. Cholinergic. Relating to nerve fibers that cause effects similar to those induced by acetylcholine. [Pg.565]

It has been known for many years that autonomic effector tissues (eg, gut, airways, bladder) contain nerve fibers that do not show the histochemical characteristics of either cholinergic or adrenergic fibers. Both motor and sensory NANC fibers are present. Although peptides are the most common transmitter substances found in these nerve endings, other substances, eg, nitric oxide synthase and purines, are also present in many nerve terminals (Table 6-1). Capsaicin, a neurotoxin derived from chili peppers, can cause the release of transmitter (especially substance P) from such neurons and, if given in high doses, destruction of the neuron. [Pg.119]

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). [Pg.213]

As noted previously, the airways are richly supplied with afferent and efferent vagal nerves. The cholinergic motor fibers are clearly responsible in some patients for a portion of the bronchoconstriction characteristic of acute asthma. Such fibers innervate M3 receptors on the smooth muscle and contain modulatory M2 receptors on the nerve terminals. Selective inhibition of M2 receptors can increase bronchoconstrictor responses to a variety of stimuli, while M3 inhibitors can produce dilation of constricted airways. [Pg.469]

Cholinergic stimulation Stimulation of the nerve fibers utilizing acetylcholine as the neurotransmitter. [Pg.379]

The primary action is to bind irreversibly to the presyn-aptic nerve terminals of peripheral cholinergic nerve fibers. Because the drug does not penetrate the blood-brain barrier, it has no effect on the central nervous system. The binding of botulinum to the nerve terminals blocks the release of acetylcholine at the neuromuscular junction, resulting in a temporary paralysis of the muscle. [Pg.668]

Interruption of the septal hippocampal tract and elimination thereby of cholinergic afferencs to the hippocampus reduced by about 70Z the activity of choline acetyltransferase In homogenates of the hippocampus, but did not alter the binding of [3h]BZ by particles of such homogenates (8). The investigators proposed that presynaptlc muscarinic sites that are innervated by Che septal hippocampal nerve fibers do not bind the labeled benzilate, whereas postsynapclc muscarinic sites do bind It. [Pg.68]

Figure 2 Targets of neurotoxic agents acting on PNS cholinergic nerve fibers (upper portion), terminals (lower midportion) and neuromuscuiar synapses (iowest portion). Ach, acetyichoiine AChase, acetylcholinesterase CAT, choline acetyltransferase. (From Spencer PS and Schaumburg H (eds.) (2000) Experimental and Clinical Neurotoxicology, 2nd edn. New York Oxford University Press Oxford University Press, inc. Used by permission of Oxford University Press, inc.)... Figure 2 Targets of neurotoxic agents acting on PNS cholinergic nerve fibers (upper portion), terminals (lower midportion) and neuromuscuiar synapses (iowest portion). Ach, acetyichoiine AChase, acetylcholinesterase CAT, choline acetyltransferase. (From Spencer PS and Schaumburg H (eds.) (2000) Experimental and Clinical Neurotoxicology, 2nd edn. New York Oxford University Press Oxford University Press, inc. Used by permission of Oxford University Press, inc.)...
E. Nonadrenergic, Noncholinergic (NANC) Transmission Some nerve fibers in autonomic effector tissues do not show the histochemical characteristics of either cholinergic or adrenergic fibers. Some of these are motor fibers that cause the release of ATP and possibly other purines related to it. Purine-evoked responses have been identified in the bronchi, gastrointestinal tract, and urinary tract. Other motor fibers are peptidergic, ie, they release peptides as the primary transmitters (see list above under Cotransmitters). [Pg.49]


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See also in sourсe #XX -- [ Pg.165 ]




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