EXCITATION OF SUPRAOPTIC VASOPRESSIN CELLS BY STIMULATION OF THE A1 NORADRENALINE CELL GROUP - FAILURE TO DEMONSTRATE ROLE FOR ESTABLISHED ADRENERGIC OR AMINO-ACID RECEPTORS

被引:53
作者
DAY, TA
RENAUD, LP
SIBBALD, JR
机构
[1] MONTREAL GEN HOSP,RES INST,NEUROSCI UNIT,MONTREAL H3G 1A4,QUEBEC,CANADA
[2] UNIV OTAGO,DEPT PHYSIOL,DUNEDIN,NEW ZEALAND
[3] UNIV OTAGO,CTR NEUROSCI,DUNEDIN,NEW ZEALAND
基金
英国医学研究理事会;
关键词
Excitatory amino acid; Neurosecretory cell; Noradrenaline; Noradrenergic neuron A1; Supraoptic nucleus; Vasopressin cell; γ-Adrenoceptor;
D O I
10.1016/0006-8993(90)90901-M
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The effects of adrenergic and excitatory amino acid antagonists on supraoptic nucleus (SON) neurosecretory cell responses to stimulation of the A1 noradrenaline (NA) cell group were examined in anaesthetized male rats. As in previous studies, delivery of cathodal pulses (100 μA, 1 ms pulses, 1 Hz) to the A1 region of the caudal ventrolateral medulla excited spontaneously active, antidromically identified neurosecretory cells, the majority of which were identified as arginine vasopressin (AVP) secreting on the basis of basal discharge patterns and responses to abrupt increases in arterial blood pressure. Administration of α- and β-adrenoreceptor antagonists, by systemic or intracerebroventricular delivery of a bolus, or by direct pressure injection into the SON, did not alter neurosecretory cell responses to A1 stimulation, even when doses applied exceeded that required for blockade of excitations elicited by local application of NA. Application of the broad spectrum excitatory amino acid antagonist kynurenic acid (5-40 mM) blocked the excitatory effects of locally applied glutamate (100 μM) and transiently inhibited spontaneous activity, but failed to alter the excitatory effects of A1 region stimulation on SON cells. Identical effects were obtained with a selective kainate/quisqualate receptor antagonist. These data indicate that neurosecretory cell responses to activation of the A1 cell group are unaltered by antagonists of α- and β-adrenoreceptors, or excitatory amino acid receptors. Several alternative explanations are plausible: (i) that the effects of A1 region stimulation are not due to a direct A1 cell projection to SON cells; (ii) intimacy of NA release sites and post-junctional receptors restricts antagonist access; (iii) neurally released NA interacts with a novel receptor, such as the postulated γ-adrenoreceptor; (iv) A1 cells utilize a neurotransmitter other than NA or an excitatory amino acid. © 1990.
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页码:91 / 98
页数:8
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