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Cocaine nerve terminals

Although this drug is categorized as a local anesthetic, I have chosen to put it in with the hallucinogens because of the psychotomimetic effects that it produces. Cocaine is not a phenylethyl-amine, but it produces central nervous system arousal or stimulant effects which closely resemble those of the amphetamines, the methylenedioxyamphetamines in particular. This is due to the inhibition by cocaine of re-uptake of the norepinephrine released by the adrenergic nerve terminals, leading to an enhanced adrenergic stimulation of norepinephrine receptors. The increased... [Pg.66]

Transmitter reuptake after release Cocaine, tricyclic antidepressants Adrenergic nerve terminals Inhibit uptake increase transmitter effect on postsynaptic receptors... [Pg.124]

Because neuronal uptake is necessary for the hypotensive activity of guanethidine, drugs that block the catecholamine uptake process or displace amines from the nerve terminal (see Chapter 6) block its effects. These include cocaine, amphetamine, tricyclic antidepressants, phenothiazines, and phenoxybenzamine. [Pg.230]

A particularly devastating substance that affects neurotransmission is the illicit drug cocaine, which blocks catecholamine uptake at nerve terminals. Addictive cocaine is particularly dangerous because it can cross the blood-brain barrier readily. [Pg.220]

Although cocaine can function as a local anesthetic, most of its actions relate to a second mechanism. Cocaine increases synaptic concentrations of catecholamines (i.e., dopamine and norepinephrine) in the brain by blocking their reuptake mechanisms. Normally, when these transmitters are released from nerve terminals, they are rapidly removed from the synaptic cleft by specific energy-dependent transporter proteins that carry them back into the terminal. By blocking these transporter systems, cocaine prolongs the time the catecholamines remain in the synapse and intensifies their actions. This increase in dopamine concentration in the CNS appears to be the basis for the various euphoric and related changes that occur in people who use cocaine. A similar mechanism has been suggested for methamphetamine. [Pg.201]

Staley JK, Talbot JZ, Ciliax BJ, Miller GW, Levey AI, Kung M-P, Kung HF, Mash DC (1997) Radioligand binding and immunoautoradiographic evidence for a lack of toxicity to dopaminergic nerve terminals in human cocaine overdose victims. Brain Res 747 219-229. [Pg.570]

Postmortem studies show a correlation between PD and DAT concentrations in the striatum (Niznik et al., 1991). Molecular imaging techniques have been used to determine DAT levels using DAT radiotracers such as 2P-carbomethoxy-3 -(4-iodophenyl) tropane ([ I] P-CTT) and [ C] cocaine (Shih et al., 2006). These techniques are useful for the evaluation and diagnosis of patients with PD and to monitor the progression of the disease (Shih et al., 2006). The delivery of DA to surviving nerve terminals by treatment with l-DOPA helps alleviate some of the early symptoms of PD (Nutt, 2002). Unfortunately, the ameliorating effects of... [Pg.185]

Interactions of sympathomimetics with other vasoactive drugs are complex. Some drugs block the reuptake mechanism for noradrenaline in adrenergic nerve terminals and potentiate the pressor effects of noradrenaline e.g. cocaine, tricyclic antidepressants or highly noradrenaline-selective reuptake inhibitors such as roboxetine. Others deplete or destroy the intracellular stores within adrenergic nerve terminals (e.g. reserpine and guanethidine) and thus block the action of indirect S5unpathomimetics. [Pg.448]

CO-beneldopa benserazide levodopa. cocaine (ban, usan] (cocaine hydrochloride (jan, usan)) is an ester of benzoic acid and methylecgonine and the principal alkaloid of Erythroxylum coca and other Erythroxylum spp. (Erythroxylaceae). It is a LOCAL ANAESTHETIC (used topically because of toxicity), and has pronounced indirect-acting SYMPATHOMIMETIC actions by virtue of being an UPTAKE INHIBITOR (interferes with Uj active uptake of noradrenaline into noradrenergic nerve terminals). It is a VASOCONSTRICTOR and can be used as a topical mydriatic and ocular diagnostic agent. It is a powerful CNS stimulant (similar in action to amphetamine), with considerable abuse potential, cocaine hydrochloride cocaine. [Pg.82]

Additional radioligands have recently been developed for probing the DA transporter proteins that are highly characteristic gene products of DA neurons and nerve terminals in the basal ganglia. Cocaine(53 Fig. 12.1 l)bindsto the DA transporter (DAT) and other monoamine transporters, but radiolabeled cocaine... [Pg.735]

Cocaine is a potent CNS stimulant that elicits a state of increased alertness and euphoria with its actions similar to those of amphetamine but of shorter duration. These CNS effects are thought to be largely associated with the ability of cocaine to block dopamine reuptake at nerve synapses and thereby prolong the action of dopamine in the CNS. It is this response that leads to recreational abuse of cocaine. Cocaine also blocks the reuptake of norepinephrine at presynaptic nerve terminals this produces a sympathomimetic response (including an increase in blood pressure, heart rate, and body temperature). Cocaine is effective as a local anesthetic and vasoconstrictor of mucous membranes and is therefore used clinically for nasal surgery, rhinoplasty, and emergency nasotracheal intubation. [Pg.1335]

TERMINATION OF THE ACTIONS OF CATECHOLAMINES The actions of NE and Epi are terminated by (1) reuptake into nerve terminals by NET (2) dilution by diffusion out of the junctional cleft and uptake at end organs and extraneuronal sites by ENT, OCTl, and OCT2. Subsequent to uptake, the catecholamines are subject to metabolic transformation by MAO and catechol-0-methyltransferase (COMT). In addition, catecholamines are metabolized by sulfotransferases (see Chapter 3). Termination of action by a powerful degradative enzymatic pathway, such as that provided by AChE in cholinergic transmission, is absent from the adrenergic system. Inhibitors of neuronal reuptake of catecholamines (e.g., cocaine, imipramine) potentiate the effects of the... [Pg.108]

Mode of action Sympathomimetic agonists may directly activate their adrenoceptors, or they may act indirectly to increase the concentration of catecholamine transmitter in the synapse. Amphetamine derivatives and tyramine cause the release of stored catecholamines these sympathomimetics are therefore mainly indirect in their mode of action. Another form of indirect action is seen with cocaine and the tricyclic antidepressants these drugs inhibit reupmke of catecholamines by nerve terminals and thus increase the synaptic activity of released transmitter. [Pg.78]

The indirect-acting agents (cocaine and tyramine) act through catecholamines in or released from the nerve terminal clonidine acts primarily on the receptor of the presynaptic nerve terminal. The answer is (C). [Pg.86]

Overdoses with amphetamines or cocaine have many signs and symptoms in common. However, the ability of cocaine to block the reuptake of norepinephrine at sympathetic nerve terminals results in greater cardiotoxicity. Tachycardia is the rule, with the possibility of an arrhythmia. infarct, or stroke. The answer is (B). [Pg.294]

Fig. 23.5. Schematic of a dopaminergic nerve terminal. Amphetamine increases synaptic concentration of dopamine primarily by causing its release from presynaptic terminals, whereas cocaine increases synaptic concentration by preventing its reuptake (a). Fig. 23.5. Schematic of a dopaminergic nerve terminal. Amphetamine increases synaptic concentration of dopamine primarily by causing its release from presynaptic terminals, whereas cocaine increases synaptic concentration by preventing its reuptake (a).
Cocaine, in addition to being a local anaesthetic (Chapter 5). is a sympathomimetic because il inhibits the reuplake of norepinephrine by nerve terminals. It has an intense central stimulant effect that has made il a popular drug of abuse (Chapter. 11). [Pg.25]

Cocaine has been shown to inhibit the reuptake of norepinephrine in the sympathomimetic nerve terminal. Local anesthesia probably results from a membrane effect. Small doses cause an increase in respiratory rate whereas large amounts lead to death from respiratory depression or cardiac arrest. [Pg.328]


See other pages where Cocaine nerve terminals is mentioned: [Pg.358]    [Pg.43]    [Pg.8]    [Pg.56]    [Pg.83]    [Pg.85]    [Pg.114]    [Pg.240]    [Pg.114]    [Pg.455]    [Pg.124]    [Pg.358]    [Pg.551]    [Pg.43]    [Pg.113]    [Pg.113]    [Pg.526]    [Pg.196]    [Pg.196]    [Pg.3]    [Pg.180]    [Pg.131]    [Pg.239]    [Pg.358]    [Pg.810]    [Pg.983]    [Pg.1044]    [Pg.69]    [Pg.287]    [Pg.733]   
See also in sourсe #XX -- [ Pg.329 ]




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