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Tachykinins Potentiate N ‐Methyl‐ D ‐Aspartate Responses in Acutely Isolated Neurons from the Dorsal Horn
Author(s) -
Rusin K. I.,
Bleakman D.,
Chard P. S.,
Randic M.,
Miller R. J.
Publication year - 1993
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 - 10.1111/j.1471-4159.1993.tb03242.x
Subject(s) - nmda receptor , neurokinin a , kainate receptor , substance p , staurosporine , chemistry , glutamate receptor , ampa receptor , protein kinase c , long term potentiation , excitatory postsynaptic potential , receptor , medicine , endocrinology , biology , biochemistry , kinase , neuropeptide
Substance P and neurokinin A both potentiated N ‐methyl‐ d ‐aspartate (NMDA)‐induced currents recorded in acutely isolated neurons from the dorsal horn of the rat. To elucidate the mechanism underlying this phenomenon, we measured the effects of tachykinins and glutamate receptor agonists on [Ca 2+ ] i in these cells. Substance P, but not neurokinin A, increased [Ca 2+ ] i in a subpopulation of neurons. The increase in [Ca 2+ ] i was found to be due to Ca 2+ influx through voltage‐sensitive Ca 2+ channels. Substance P and neurokinin A also potentiated the increase in [Ca 2+ ] i produced by NMDA, but not by α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid, kainate, or 50 m M K + . Phorbol esters enhanced the effects of NMDA and staurosporine inhibited the potentiation of NMDA effects by tachykinins. It is concluded that activation of protein kinase C may mediate the enhancement of NMDA effects by tachykinins in these cells. However, the effects of tachykinins on [Ca 2+ ] i can be dissociated from their effects on NMDA receptors.