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 language||English (US)|
|Number of pages||8|
|Journal||Journal of neurochemistry|
|State||Published - Jan 1979|
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience