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Potentiation by Angiotensin II of Spontaneous Excitatory Postsynaptic Currents in Rat Supraoptic Magnocellular Neurones
Author(s) -
Ozaki Y.,
Soya A.,
Nakamura J.,
Matsumoto T.,
Ueta Y.
Publication year - 2004
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 - 10.1111/j.1365-2826.2004.01244.x
Subject(s) - excitatory postsynaptic potential , angiotensin ii , long term potentiation , medicine , vasopressin , losartan , endocrinology , inhibitory postsynaptic potential , chemistry , postsynaptic potential , postsynaptic current , angiotensin ii receptor type 1 , biology , receptor
The physiological actions of angiotensin II in the supraoptic (SON) and paraventricular nuclei have been widely demonstrated, including the modulation of firing rate and release of arginine vasopressin and oxytocin. Here, we investigated whether angiotensin II modulates synaptic inputs into the SON. To do this, we measured spontaneous excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs) from rat SON neurones in thin slice preparations using the whole‐cell patch‐clamp technique. Angiotensin II reversibly increased the frequency of spontaneous EPSCs in a dose‐related manner without affecting the amplitude, indicating that angiotensin II potentiated EPSCs via a presynaptic mechanism. Angiotensin II‐induced potentiation of EPSCs was unaffected in the presence of tetrodotoxin. On the other hand, angiotensin II did not cause significant effects on IPSCs. The potentiation of EPSCs by angiotensin II was potently suppressed by previous exposure to the angiotensin type 1 (AT1) receptor antagonist, losartan. Our results suggest that angiotensin II potentiates the excitatory synaptic inputs into SON neurones, via the AT1 receptors.