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The influence of melatonin on the hippocampal glutamergic system
Author(s) -
Wieraszko A.,
Hogan M. V.,
ElSherif Y.,
Tesoriero J.,
Raja H.
Publication year - 2002
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.81.s1.11_9.x
Subject(s) - melatonin , glutamate receptor , synaptosome , neurotransmitter , endocrinology , medicine , hippocampal formation , population , neurotransmission , stimulation , receptor , chemistry , biology , biochemistry , central nervous system , environmental health
We have demonstrated previously that melatonin and its analog chloromelatonin depressed evoked potentials (EPSP and the population spike) recorded from hippocampal slices during stimulation of Schaffer collaterals (Hogan et al. J. Pineal Res. 2001, 30 , 87–96). The effect was concentration‐ and receptor‐dependent and occurred within minutes following melatonin application. Since Schaffer collaterals use glutamate as a neurotransmitter, we focused our research on the glutamergic system as a possible target of melatonin action. Experiments were performed on hippocamapal synaptosomes and/or synaptosomal membranes prepared from CD −1 mice. We evaluated the influence of melatonin on the binding of 3H‐glutamate to the glutamergic receptors and synaptosomal uptake of 3H‐ D ‐Aspartate used as a marker of glutamergic neurotransmission. When synaptosomal membranes were incubated with 1 m m melatonin (30 min, 37°C), the binding of 3H‐glutamate increased by 12.5 ± 7% ( n = 7). In uptake studies the synaptosomes were exposed to 1 m m melatonin for 15 min at 37°C, and then the accumulation of 3H‐ D ‐Aspartate was tested at 5, 30, 60, 120 and 300 s. The incubation with 3H‐ D ‐Aspartate was followed by filtration and radioactivity absorbed on the filters was determined. Melatonin increased the uptake of 3H‐ D ‐Aspartate at all time intervals tested by 37.6 ± 5% ( n = 5). Experiments are in progress to further characterize the melatonin actions and to evaluate melatonin effects on the release of 3H‐ D ‐Aspartate from synaptosomes. Supported partially by NIH grant RO1 ES011022‐01A1.