Kainate acts at presynaptic receptors to increase GABA release from hypothalamic neurons. J Neurophysiol 1999 Aug;82(2):1059-62
Date
08/13/1999Pubmed ID
10444697DOI
10.1152/jn.1999.82.2.1059Scopus ID
2-s2.0-0032794086 (requires institutional sign-in at Scopus site) 41 CitationsAbstract
Recent reports suggest that kainate acting at presynaptic receptors reduces the release of the inhibitory transmitter GABA from hippocampal neurons. In contrast, in the hypothalamus in the presence of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptor antagonists [1-(4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine (GYKI 52466) and D,L-2-amino-5-phosphonopentanoic acid (AP5)], kainate increased GABA release. In the presence of tetrodotoxin, the frequency, but not the amplitude, of GABA-mediated miniature inhibitory postsynaptic currents (IPSCs) was enhanced by kainate, consistent with a presynaptic site of action. Postsynaptic activation of kainate receptors on cell bodies/dendrites was also found. In contrast to the hippocampus where kainate increases excitability by reducing GABA release, in the hypothalamus where a much higher number of GABAergic cells exist, kainate-mediated activation of transmitter release from inhibitory neurons may reduce the level of neuronal activity in the postsynaptic cell.
Author List
Liu QS, Patrylo PR, Gao XB, van den Pol ANAuthor
Qing-song Liu PhD Professor in the Pharmacology and Toxicology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsAnti-Anxiety Agents
Benzodiazepines
Cells, Cultured
Excitatory Amino Acid Antagonists
Hypothalamus
In Vitro Techniques
Kainic Acid
Neurons
Patch-Clamp Techniques
Rats
Rats, Sprague-Dawley
Receptors, Presynaptic
gamma-Aminobutyric Acid
