Source:Brain Research Bulletin
Author(s): Makoto Takahashi, Yasushi Hayashi, Junichi Tanaka
The present study was carried out to investigate whether glutamatergic receptor mechanisms modulate the release of noradrenaline (NA) in the region of the median preoptic nucleus (MnPO) using intracerebral microdialysis techniques in freely moving rats. Perfusion of N-methyl-D-asparatate (NMDA, 10 and 50μM) through the microdialysis probe significantly enhanced dialysate NA concentration in the region of the MnPO. Local perfusion of the NMDA antagonist dizocilpine (MK801, 10 and 50μM) did not change the basal release of NA in the MnPO area. MK801 (10μM) administered together with NMDA antagonized the stimulant effect of NMDA (50μM). Perfusion of the non-NMDA agonist quisqualic acid (QA, 10 and 50μM) or kainic acid (KA, 10 and 50μM) significantly increased the NA release in the MnPO area. Perfusion of the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 and 50μM) had no effect on the NA release. CNQX (10μM) administered together with either QA (50μM) or KA (50μM) in the MnPO area prevented the stimulant effect of the agonists on the NA release. Nonhypotensive hypovolemia following subcutaneous injections of polyethylene glycol (PEG, 30%, 5ml) significantly elevated the NA level in the MnPO area. The PEG-induced elevation in the NA release was attenuated by perfusion of either MK801 (10μM) or CNQX (10μM). The present results suggest that glutamatergic synaptic inputs may act to enhance the release of NA in the MnPO area through both NMDA and non-NMDA receptors, and imply that these glutamatergic receptor mechanisms may be involved in the noradrenergic reguratory system for the body fluid balance.
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