Non-Nicotinic Chemical Stimulation of Automatic Ganglia

Haefely, W.

doi:10.1007/978-3-642-67397-9_12

Cited by 4 publications

(1 citation statement)

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“…The quaternary ammonium compound, neostigmine, exerts additional postsynaptic actions at autonomic ganglia (Haefely, 1980) and muscle endplate (Taylor, 1990); some of these actions appear mediated directly by nicotinic AChRs (Haefely, 1980;Fiekers, 1985). Tetrahydroaminoacridine (THA; tacrine) possesses a complex pharmacological profile, with AChE-independent actions reported on muscarinic receptors and on certain enzymes and voltage-gated ion channels (Freeman & Dawson, 1991).…”

Section: Introductionmentioning

confidence: 99%

Blockade of nicotinic responses by physostigmine, tacrine and other cholinesterase inhibitors in rat striatum

Clarke¹,

Reuben

El‐Bizri

1994

British J Pharmacology

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1 The acetylcholinesterase inhibitors physostigmine, neostigmine, tetrahydroaminoacridine (tacrine; THA) and diisopropylfluorophosphate (DFP) were 6 Physostigmine, neostigmine, tacrine and DFP (all at 30 gM) each produced near-total (>96%) inhibition of AChE activity. However, DFP at a concentration (60 gM) that produced a degree of AChE inhibition equal to that of physostigmine 30 gM, did not significantly reduce nicotine-induced dopamine release.7 It thus appears that physostigmine blocks CNS nicotinic receptors in an insurmountable and pharmacologically selective manner, independent of its ability to inhibit acetylcholinesterase. Tacrine reduced nicotinic responses, quite possibly by an indirect mechanism. The possibility of direct or indirect blockade of nicotinic receptor-mediated actions may complicate the interpretation of preclinical studies that have employed physostigmine and tacrine.

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