RELEASE OF [3H]GABA FROM IN VITRO PREPARATIONS: COMPARISON OF THE EFFECT OF DABA AND β‐ALANINE ON THE K+ AND PROTOVERATRINE STIMULATED RELEASE OF [3H]GABA FROM BRAIN SLICES AND SYNAPTOSOMES

J. P. Hammerstad, M. L. Cawthon, C. R. Lytle

Research output: Contribution to journalArticle

26 Scopus citations

Abstract

It has been proposed that the major portion of [3H]GABA released from rat cortical slices upon exposure to high K+ comes from a neuronal pool. Using carrier mediated exchange diffusion of DABA or β‐alanine in the superfusion medium for GABA in the slice as a technique for manipulating neuronal and glial pools of GABA, it was found that DABA but not β‐alanine substantially reduced the K+ stimulated release of [3H]GABA. The present study using synaptosomes as an in vitro model of the nerve ending was undertaken to ascertain whether this neuronal pool of releasable [3H]GABA was associated with a specific transmitter pool in nerve endings. A continuous superfusion system employing a Ca2+ pulse to produce a calcium coupled release (Levyet al, 1973) was used to study the effect of two concentrations (20 μm, 1 mm) of DABA and β‐alanine on the release of [3H]GABA from synaptosomes. In contrast to the results in slices, DABA at both concentrations had no effect on the release of [3H]GABA from synaptosomes in spite of evidence that exchange diffusion was occurring. With protoveratrine as the releasing agent there was no effect of DABA on the release of [3H]GABA from either slices or synaptosomes. The results suggest that the major portion of [3H]GABA released from cortical slices by high K+ comes from a non‐transmitter pool in the neuron. Use of K+ stimulated release of amino acids from cortical slices as a criterion for neurotransmitter function must be viewed with caution.

Original languageEnglish (US)
Pages (from-to)195-202
Number of pages8
JournalJournal of neurochemistry
Volume32
Issue number1
DOIs
StatePublished - Jan 1979

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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