Kainate acts at presynaptic receptors to increase GABA release from hypothalamic neurons
Open accessAbstract
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.
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Agonism of presynaptic kainate receptors in hypothalamic neurons facilitates inhibitory GABAergic signaling.
“Similarly, agonism of presynaptic kainate receptors in hypothalamic neurons facilitates inhibitory GABAergic signaling (Liu et al., 1999).”
From Glutamate receptors in domestication and modern human evolution (2020) · cites this paper as Liu et al., 1999
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Segerstråle, M. (2011) · Työväentutkimus Vuosikirja
- Authors
- Liu, Q.-S., Patrylo, P. R., Gao, X.-B., & van den Pol, A. N.
- Affiliations
- Yale University (US)
- Department of Neurosurgery, Yale University Medical School, New Haven, Connecticut 06520
- Venue
- Journal of Neurophysiology
- Publisher
- American Physiological Society
- Published
- 1999-08-01
- Volume
- 82
- Issue
- 2
- Pages
- 1059-1062
- ISSN
- 0022-3077 (ISSN-L)
- 1522-1598
- OpenAlex
- W2216130557
- Cited by
- 40
- References
- 26
- Citations by year
- 2021: 2 · 2019: 2 · 2018: 1 · 2015: 1 · 2013: 1 · 2012: 1
- FWCI
- 1.33
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neurophysiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Science Foundation
- Yale University (CT 06520)
- National Institutes of Health (1r01ns031573-01a3)
- National Institute of Neurological Disorders and Stroke (NS37788, NS31573, NS 34887, R01NS037788, R01NS034887)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Keywords
- kainate receptors, presynaptic inhibition, GABA release, hypothalamic neurons, inhibitory postsynaptic currents, miniature IPSCs, tetrodotoxin, neuronal excitability
- MeSH terms
- Animals, Benzodiazepines, Cells, Cultured, gamma-Aminobutyric Acid, Hypothalamus, Kainic Acid, Neurons, Anti-Anxiety Agents, Rats, Sprague-Dawley, Receptors, Presynaptic, Patch-Clamp Techniques, Excitatory Amino Acid Antagonists, Rats, In Vitro Techniques
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