a(CHEBI:Mecamylamine)

Entity

Name

Mecamylamine

Namespace

chebi

Namespace Version

20180906

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/chebi-names.belns

In antagonism tests, (-)-nicotine failed to block the stimulus effects of mecamylamine PubMed:28391535

During attention tasks, the nicotinic antagonist, mecamylamine, impaired accuracy or reaction time (151, 152) and nicotinic agonists improved accuracy (153). PubMed:17009926

The discovery that nicotine, a ligand acting at nAChRs, and its mimetics can protect neurons against Abeta toxicity (Kihara et al., 1998) is of interest, especially in view of the observation that nicotine also enhances cognition (Rusted et al., 2000). Nicotinic receptors play a particularly prominent role in nicotine protection. The protective effect is blocked by the nicotinic antagonists dihydro-beta-erythroidine and mecamylamine (Kihara et al., 2001; Takada- Takatori et al., 2006). PubMed:19293145

In a work that evaluated the function of the cholinergic system in mediating the response to stress it was found that treatment of rats with the antagonist of the nicotinic receptor, mecamylamine, attenuates the activation of the HPA axis in response to a stressor agent PubMed:26813123

Administration of the nicotinic antagonist mecamylamine to elderly subjects and AD patients has produced cognitive impairment (Newhouse and Kelton 2000) PubMed:11230871

early studies indicated that acute nicotine administration improved performance of patients with Alzheimer’s disease in cognitive tasks, whereas acute administration of the non-competitive (channel blocker) antagonist mecamylamine resulted in dose-dependent impairment of performance in a battery of cognitive tasks137–141 PubMed:19721446

This conclusion is based on the fact that the stimulus effects of nicotine are convincingly blocked by (a) mecamylamine, a voltage dependent noncompetitive channel blocker at nicotinic receptors (Fig. 3; Table 4) and (b) dihydro-β-erythrodine (DHβE), a nicotinic receptor antagonist that shows high affinity for the nAChR α4β2 subunit (Fig. 3; Table 5) but not by methyllycaconitine (MLA), a α7 nicotinic receptor antagonist (Table 5). PubMed:28391535

Mecamylamine (Inversine®, Vecamyl®; Fig. 3) was developed over 60 years ago and marketed as a ganglionic blocker for the treatment of hypertension (e.g., [127]) PubMed:28391535

In addition, mecamylamine can produce CNS effects that include tremor, mental confusion, seizures, mania, and depression but the mechanisms by which these effects are produced are unclear PubMed:28391535

In addition, mecamylamine can produce CNS effects that include tremor, mental confusion, seizures, mania, and depression but the mechanisms by which these effects are produced are unclear PubMed:28391535

In addition, mecamylamine can produce CNS effects that include tremor, mental confusion, seizures, mania, and depression but the mechanisms by which these effects are produced are unclear PubMed:28391535

In addition, mecamylamine can produce CNS effects that include tremor, mental confusion, seizures, mania, and depression but the mechanisms by which these effects are produced are unclear PubMed:28391535

In addition, mecamylamine can produce CNS effects that include tremor, mental confusion, seizures, mania, and depression but the mechanisms by which these effects are produced are unclear PubMed:28391535

Also, mecamylamine is sometimes used as an anti-addictive drug to help people stop smoking tobacco products (e.g.,[128, 129]) PubMed:28391535

Biochemical and pharmacological studies have characterized mecamylamine as a nonselective, voltage dependent and noncompetitive receptor antagonist of neuronal nAChRs and it is often referred to as a “nicotine receptor antagonist.” PubMed:28391535

For example, some biochemical studies suggest that mecamylamine is a channel blocker that inhibits most neuronal nAChRs (e.g., [131–133]). PubMed:28391535