Elsevier

Brain Research

Volume 607, Issues 1–2, 2 April 1993, Pages 177-184
Brain Research

Potentiation by choline of basal and electrically evoked acetylcholine release, as studied using a novel device which both stimulates and perfuses rat corpus striatum

https://doi.org/10.1016/0006-8993(93)91504-LGet rights and content

Abstract

We examined the release of acetylcholine (ACh) and dopamine (DA) using a novel probe through which striatal neurons could be both superfused and stimulated electrically in both anesthetized and freely moving awake animals. Optimal stimulation parameters for eliciting ACh release from cholinergic neurons differed from those required for eliciting DA release from dopaminergic terminals: at 0.6 ms pulse duration, 20 Hz and 200 μA, ACh release increased to357±30% (P < 0.01) of baseline and was blocked by the addition of tetrodotoxin (TTX). Pulse durations of 2.0 ms or greater were required to increase DA release. Unlike ACh release, DA release showed no frequency dependence above 5 Hz. The mmximal evoked releases of ACh and DA were556±94% (P < 0.01)and254 ±38% (P < 0.05) of baseline, respectively. Peripheral administration of choline (Ch) chloride (30–120 mg/kg) to anesthetized animals caused dose-related (r = 0.994, P < 0.01) increases in ACh release; basal release rose from117±7%to141±5% of initial baseline levels (P < 0.05) and electrically evoked ACh release rose from386±38%to600±34% (P < 0.01) in rats given 120 mg/kg. However, Ch failed to affect basal or evoked DA release although neostigmine (10 μM) significantly elevated basal DA release (from 36.7 fmol/10 min to 71.5 fmol/10 min;P < 0.05). In Awake animals, Ch (120 mg/kg) also elevated both basal (from106±7%to154±17%; P < 0.05) and electrically evoked (from146±13to262±19%; P< 0.01) ACh release. These experiments demonsrates that ACh and DA release can both be reliably evoked from rat striatum and that an intraperitoneal (i.p.) injection of Ch can increase both basal and evoked striatal ACh release.

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