Facilitation of Ca2+ store-dependent noradrenaline release after an N-methyl-D-aspartate receptor antagonist in the rat supraoptic nucleus.
J Neuroendocrinol
; 13(10): 894-904, 2001 Oct.
Article
em En
| MEDLINE
| ID: mdl-11679058
ABSTRACT
We examined the role of N-methyl-d-aspartate (NMDA) receptors in the control of noradrenaline release in the supraoptic nucleus (SON) using a microdialysis method in urethane-anaesthetized rats. Local application of 0.5 mm NMDA into the SON by retrodialysis decreased noradrenaline content in the dialysate from the SON. On the other hand, MK-801, a channel blocker of NMDA receptors, or D(-)2-amino-5-phosphonopentanoic acid (AP-5), a competitive NMDA receptor antagonist, increased the basal noradrenaline content. Tetrodotoxin did not completely block the noradrenaline increase after NMDA antagonists. Infusion of Ca2+-free solution containing Ni2+ and Cd2+, or a mixture of omega-agatoxin IVA and omega-conotoxin GVIA, voltage-sensitive Ca2+ channels blockers, did not block noradrenaline increase after AP-5, but blocked noradrenaline increase after high K+. Infusion of intracellular Ca2+ blockers, thapsigargin or TMB-8, impaired noradrenaline increase after AP-5 but not that after high K+. These data are consistent with the hypothesis that activation of an NMDA receptor inhibits an intracellular Ca2+ store-dependent noradrenaline release from nerve terminals in the SON.
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Base de dados:
MEDLINE
Assunto principal:
Núcleo Supraóptico
/
Norepinefrina
/
Cálcio
/
Receptores de N-Metil-D-Aspartato
/
Antagonistas de Aminoácidos Excitatórios
/
Sinalização do Cálcio
Limite:
Animals
Idioma:
En
Ano de publicação:
2001
Tipo de documento:
Article