GABA modulates the release of dopamine and acetylcholine from rat caudate nucleus slices.

Abstract:

:The effects of GABA on depolarization-induced (26 mM K+) release of radiolabeled dopamine (DA) and acetylcholine (ACh) from slices of rat caudate nucleus were examined with a superfusion method. GABA, in concentrations of 10(-5)--10(-3) M, dose-dependently enhanced the release of DA, either accumulated by high-affinity uptake or synthesized from 14-C-tyrosine. In contrast, the release of ACh was reduced by GABA. This reduction appeared to be caused by the increase in DA-release. These effects of GABA decreased from the caudal to rostral part within the caudate nucleus, an order which parallels the distribution of endogenous GABA and glutamic acid decarboxylase. However, GABA had little, if any, effect in the nucleus accumbens. Since it was difficult to antagonize the effects of GABA on DA and ACh release with bicuculline or picrotoxin, it remains uncertain whether these effects were mediated via GABA receptors. In view of the high endogenous GABA level in the caudate nucleus it is concluded that GABA may be one of the local factors involved in the control of the amount of transmitter that will be released from dopaminergic varicosities upon depolarization.

journal_name

Eur J Pharmacol

authors

Stoof JC,Den Breejen EJ,Mulder AH

doi

10.1016/0014-2999(79)90101-8

subject

Has Abstract

pub_date

1979-07-15 00:00:00

pages

35-42

issue

1

eissn

0014-2999

issn

1879-0712

pii

0014-2999(79)90101-8

journal_volume

57

pub_type

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