GABA-dependent firing of glutamate-evoked action potentials at non-NMDA
receptors in developing hypothalamic neurons.
Xiao-Bing Gao, Gong Chen, and Anthony N. van den Pol.
Department of Neurosurgery, Yale University School of Medicine, 333 Cedar
St., New Haven, CT 06520.
APStracts 4:265N, 1997.
ABSTRACT
Although it plays a major inhibitory role in the adult mammalian CNS, GABA may
have an excitatory function in developing neurons. The present study focuses
on the dependence of glutamate on GABA to generate action potentials in
developing hypothalamic neurons. Under conditions where glutamate by itself
could not evoke an action potential, GABA facilitated glutamate-mediated
depolarization to fire action potentials. This facilitation had a broad time
window during the decaying phase of the GABA-mediated depolarization in
developing neurons in culture. The glutamate-mediated depolarization was
shunted only during the peak of GABA-mediated depolarization, but was
facilitated after that. Similar results were obtained in the presence of 2-
amino-5-phosphono-pentanoic acid (AP-5), indicating that GABA can facilitate
glutamate responses independent of relief of the Mg2+ block of the NMDA
receptor. This novel interaction between GABA- and glutamate-mediated
excitation could play a role in strengthening neuronal circuits during early
development, and would exert a maximal effect if GABA and glutamate receptors
were activated after a slight temporal delay.
Received 18 June 1997; accepted in final form 18 September 1997.
APS Manuscript Number J506-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 7 October 1997