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Pre‐ and postsynaptic modulation of the electrical activity of rat supraoptic neurones
Author(s) -
Shibuya Izumi,
Kabashima Narutoshi,
Ibrahim Nuruhadi,
Setiadji Sutarmo V.,
Ueta Yoichi,
Yamashita Hiroshi
Publication year - 2000
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1111/j.1469-445x.2000.tb00018.x
Subject(s) - supraoptic nucleus , postsynaptic potential , excitatory postsynaptic potential , inhibitory postsynaptic potential , neuroscience , postsynaptic current , chemistry , glutamate receptor , vasopressin , hypothalamus , biology , receptor , endocrinology , biochemistry
The release of vasopressin and oxytocin is regulated by the electrical activity of magnocellular neurosecretory cells in the supraoptic and paraventricular nuclei, which is under the control of a great variety of neuro‐transmitters and neuromodulators. The major neural signals to the supraoptic nucleus are from excitatory glutamate inputs and inhibitory GABA inputs. In recent studies, the voltage‐clamp mode of the whole‐cell patch‐clamp technique has been applied to slice preparations from rat hypothalamus to monitor synaptic inputs to supraoptic neurones. Spontaneous excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs) are abolished by CNQX and picrotoxin, respectively, but are insensitive to tetrodotoxin, indicating that they represent quantal release of glutamate and GABA, respectively, from nerve terminals of presynaptic neurones. GABA and glutamate show remarkable suppressive effects on both EPSCs and IPSCs via presynaptic GABA B and mGlu receptors, respectively. Noradrenaline, which excites supraoptic neurones via postsynaptic α 1 ‐receptors, also suppresses IPSCs and potentiates EPSCs. On the other hand, prostaglandin E 2 , which excites supraoptic neurones via postsynaptic prostaglandin E 2 (EP) receptors of the EP 4 subclass, also suppresses IPSCs via EP 3 receptors but has little effect on EPSCs. Thus pre‐ and postsynaptic mechanisms may act cooperatively to excite supraoptic neurones. Nitric oxide, which inhibits supraoptic neurones, potentiates IPSCs without affecting EPSCs. This provides another example for the preferential modulation of IPSCs of supraoptic neurones. On the other hand, PACAP, which causes a long‐lasting increase in the firing frequency via the postsynaptic receptors, has no effect on EPSCs and IPSCs, suggesting that some ligands act only at postsynaptic receptors. Thus multiple patterns for pre‐ and postsynaptic modulation are present in the supraoptic nucleus, and the electrical activity of supraoptic neurones is regulated via complex mechanisms at both pre‐ and postsynaptic sites.