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Prostaglandin E 2 Inhibits Spontaneous Inhibitory Postsynaptic Currents in Rat Supraoptic Neurones via Presynaptic EP Receptors
Author(s) -
Niema Ibrahim,
Izumi Shibuya,
Narutoshi Kabashima,
Sutarmo Sv,
Yoichi Ueta,
Hiroshi Yamashita
Publication year - 1999
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1046/j.1365-2826.1999.00404.x
Subject(s) - excitatory postsynaptic potential , inhibitory postsynaptic potential , agonist , postsynaptic potential , medicine , endocrinology , supraoptic nucleus , chemistry , prostaglandin e , receptor , postsynaptic current , biology , central nervous system
Prostaglandin E2 (PGE 2 ) has been implicated in the excitatory regulation of magnocellular neurones in the supraoptic nucleus (SON). We have recently reported that PGE 2 excited SON neurones by directly activating postsynaptic PGE 2 receptors (EP receptors) of a subclass other than EP 1–3 , but did not affect excitatory postsynaptic currents (EPSCs). In the present study, we examined presynaptic effects of PGE 2 on rat SON neurones by measuring spontaneous inhibitory postsynaptic currents (IPSCs) by a slice patch‐clamp technique. PGE 2 inhibited spontaneous IPSCs in a dose‐dependent and reversible manner. PGE 2 selectively suppressed the frequency of IPSCs without affecting the amplitude of IPSCs in the presence of tetrodotoxin, a blocker of Na + channels, indicating that the effects were presynaptic. The inhibitory effects of PGE 2 on the frequency of IPSCs were mimicked by the EP 1 /EP 3 agonists, 17PT‐PGE 2 and sulprostone, and the EP 2 /EP 3 agonist, misoprostol, whereas the EP 2 agonist, butaprost, or the FP agonist, fluprostenol, had little effect. The effects of PGE 2 on IPSCs were unaffected by the selective EP 1 antagonist, SC‐51322. They were unaffected also by antagonists of GABA B and α 2 adrenergic receptors, which are present at presynaptic terminals of GABA neurones in the SON and cause suppression of spontaneous IPSCs. The inhibitor of PG synthesis, indomethacin, had little effect on spontaneous IPSCs and on the inhibitory effects of PGE 2 as well as of the GABA B agonist, baclofen, and noradrenaline. These results suggest that PGE 2 inhibits release of GABA from the GABAergic terminals innervating SON neurones by activating presynaptic EP receptors, presumably of the EP 3 subclass, and that such a presynaptic mechanism may play a role in the excitatory regulation of SON neurones by PGE 2 .