Phasically active neurosecretory neurons in the paraventricular nucleus (PVN) of urethane-anesthetized rats displayed orthodromic excitation, inhibition or no response following electrical stimulation of the anteroventral third ventricle (AV3V) region, and exhibited orthodromic excitation or no response following electrical stimulation of the A1 noradrenergic region of the ventrolateral medulla. Of the 14 neurons that responded to both the stimuli, A1 region stimulation at the subthreshold current significantly enhanced the excitation induced by AV3V region stimulation, and the enhancement was abolished by iontophoretically applied phentolamine, an alpha-adrenoceptor antagonist, but not by timolol, a beta-adrenoceptor antagonist. These results suggest that A1 noradrenergic projections may act to potentiate the excitatory inputs from the AV3V region to vasopressinergic PVN neurons through alpha-adrenoceptor mechanisms.
Extracellular recordings were obtained from 34 phasically active neurosecretory cells in the hypothalamic paraventricular nucleus (PVN) of male rats under urethane anesthesia. Intracarotid injections of hypertonic saline (0.2 M NaCl solution, 0.05 ml) caused an increase in neuronal activity of 27 PVN cells. Pretreatment with saralasin (Sar, 10(-10) M), a specific angiotensin II (ANG II) antagonist, into the median preoptic nucleus (MnPO) diminished the excitatory response to the osmotic stimulation in 13 of 17 cells tested. Pretreatment with Sar in the vicinity of the MnPO or the third ventricle did not cause a marked change. These results suggest that the ANGergic system in the MnPO could contribute to the mechanism of osmotic activation of PVN neurosecretory cells.
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