Psychotropic drug influences on brain acetylcholine utilization

Domino, Edward F.; Wilson, Ann

doi:10.1007/bf00421968

Cited by 84 publications

(16 citation statements)

References 13 publications

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“…Amitriptyline decreases ACh levels without altering the TR,,,:,, in the cortex and striatum. Imipramine decreases whole brain ACh levels (Hrdina 1974) and increases whole brain TI?,,?,, (Domino and Wilson 1972). The antipsychotic agent clozapine, which has a high affinity for the muscarinic receptor (Miller and Hiley 1974;Snyder et nl.…”

Section: Gut Firnhria-fornixmentioning

confidence: 98%

The effects of muscarinic receptor blockers on the turnover rate of acetylcholine in various regions of the rat brain

Wood¹,

Cheney²

1979

Can. J. Physiol. Pharmacol.

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The actions of antimuscarinic agents (benztropine, trihexyphenidyl, and scopolamine) on the dynamics of acetylcholine (ACh) in central cholinergic neurons were examined in various rat brain areas. It was found that the pattern of changes in ACh turnover (TRACh) elicited by these drugs exhibited marked regional variations. After administration of the anticholinergic drugs, the TRACh in hippocampus and thalamus was increased, in cortex it was decreased, and in striatum it was unchanged. ACh concentration in the cortex and striatum was decreased while in hippocampus and thalamus ACh levels were unaltered. Further analysis of the cholinergic septo-hippocampal pathway using lesions of the fimbria-fornix and local drug injections into the septum argue against an in vivo action of these drugs on presynaptic or cell body muscarinic autoreceptors. Moreover, the data suggest that muscarinic receptor blockers cause an increased TRACh only in those areas where a feedback loop is operative, possibly by inhibiting a neuronal feedback loop involving at least one noncholinergic interneuron.

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Section: Gut Firnhria-fornixmentioning

confidence: 98%

The effects of muscarinic receptor blockers on the turnover rate of acetylcholine in various regions of the rat brain

Wood¹,

Cheney²

1979

Can. J. Physiol. Pharmacol.

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“…An increase in endogenous brain ACh levels at central neuronal synapses evoke a pressor response which is antagonized by atropine (Domino and Wilson 1972) or by depletion of brain ACh with hemicholinium (HC-3), which inhibits ACh synthesis (Yamamura and Snyder 1973). In the present study atropine pretreatment completely abolished VX-induced pressor responses suggesting that the hypertensive effect of VX is mediated through muscarinic receptors.…”

Section: Figurementioning

confidence: 50%

Cardiorespiratory and Neuromuscular Effects of O-Ethyl S-[2- (Diisopropylamino) Ethyl] Methylphosphonothioate (VX) in Rats

Dube

Mazumder

Kumar

et al. 1997

Bulletin of Environmental Contamination and Toxicology

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The exposure to chemical warfare agents is not restricted to the battlefield but as humans may be poisoned with nerve gases either from a chemical warfare stockpile or even in a public place. The recent use of nerve gas Sarin in a subway of Japan by a fanatic group has triggered global consternation about the extremists and homemade weapons of mass destruction. Nerve agents are organophosphorus (OP) compounds that exert acute toxic manifestations principally by inhibiting the enzyme acetylcholinesterase (AChE) resulting in a variety of physiological alterations and ultimately death from respiratory failure (Brimblecombe 1977). However, pharmacological studies indicate that nerve agents have plethora of actions other than inhibition of AChE (Worek and Szinicz 1995, Corbier and Robineau 1989, Robineau and Guittin 1987.Several studies have revealed that acute intravenous (i.v.) administration of an OP agent increased blood pressure in cat, dog and rat (Brezenoff and Giuliano 1982, Lang andRush 1973), while subcutaneous (s.c.) administration produced marked hypotension (Preston and Heath 1972). In a recent communication from this laboratory, it has been reported that i.v. administration of DFP/sarin produced a dose-dependent hypertension involving cholinergic-catecholaminergic interaction in rats. Subcutaneous administration of DFP/ sarin was found to produce a dose-responsive hypotension mediated through muscarinic receptors (Dube et al 1993). However, the mechanism of cardiovascular toxicity induced by nerve agents still remains obscure. Therefore, the effects on blood pressure, heart rate, tracheobronchial response, neuromuscular transmission, and modulatory role of various pharmacological agents were studied after systemic administration of VX (O-ethyl S-[2-(diisopropylamino) ethyl ] methyl phosphonothioate) to delineate the distinction in mechanism of action from other OP compounds.

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“…It is p ossible that th e multipl e effects of PCP could expl ain th e wide ran ge of symptomatology and adver se re a cti on s seen with PCP . Other studies h av e sh own th at th e m a rabolism of serotonin (5-lIT), NE and dop amine (DA) are affec te d by PCP (Leonard 1972 ;Hirzcma nn , Loh & Dom in o 1973 ;Domino & Wilson 1972) . Garey a n d Heath (1976) h ave rec ently demonstrated th at PCP is a competitive inhibitor of DA uptake in th e st ri a t u m a n d NE uptake in the hypoth alamus.…”

Section: H Isto Rymentioning

confidence: 98%