Activation of GABAB receptors at individual release boutons of the crayfish
opener neuromuscular junction, produces presynaptic inhibition.
Fischer, Yacov and Itzchak Parnas.
The Otto Lowei Center for Cellular and Molecular Neurobiology, Department
of Neurobiology, the Hebrew University, Jerusalem 91904, Israel.
APStracts 2:0307N, 1995.
SUMMARY AND CONCLUSIONS
1. Presynaptic inhibition in crustaceans involves the activation of GABAA
receptors that produce an increase in chloride conductance at excitatory axon
terminals. Such inhibition produced by single inhibitory pulses is blocked by
picrotoxin, a GABAA antagonist. 2. Presynaptic inhibition produced by bath
application of GABA was not blocked by picrotoxin. Measurements of the
membrane resistance of the excitatory axon terminals revealed that substantial
presynaptic inhibition still persisted after 50 SYMBOL 109 \f "Symbol"M
picrotoxin had completely blocked the increase in conductance produced by 10
SYMBOL 109 \f "Symbol"M GABA. 3. Baclofen, a GABAB agonist, reduced release
from the excitatory nerve terminals and 2OH-Saclofen, a GABAB antagonist,
blocked the effect of baclofen and the presynaptic inhibition produced by 10
SYMBOL 109 \f "Symbol"M GABA. 4. 2OH-Saclofen, alone, did not block
presynaptic inhibition produced by 100 SYMBOL 109 \f "Symbol"M GABA and the
combined action of both 2OH-Saclofen and picrotoxin was required to block such
effects. 5. The excitatory nerve terminals seem to contain GABAA and GABAB
receptors. The GABAB receptors are preferentially activated at lower GABA
concentrations (at the SYMBOL 109 \f "Symbol"M range), whereas both the
GABAA and GABAB receptors are activated at high GABA concentrations.
Received 3 August 1995; accepted in final form 19 October 1995.
APS Manuscript Number J501-5.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95