TY - JOUR
T1 - Hypothalamic paraventricular, but not supraoptic neurons, mediate the serotonergic stimulation of oxytocin secretion
AU - Van De Kar, Louis D.
AU - Rittenhouse, Peter A.
AU - Li, Qian
AU - Levy, Andrew D.
AU - Brownfield, Mark S.
N1 - Copyright:
Copyright 2015 Elsevier B.V., All rights reserved.
PY - 1995
Y1 - 1995
N2 - The purpose of the present studies was to determine whether cells in the hypothalamic paraventricular (PVN) or supraoptic (SON) nuclei mediate the serotonergic stimulation of oxytocin secretion. The serotonergic stimulus consisted of injection of the 5-HT-releasing drug p-chloroamphetamine (8 mg/ kg, IP). The validity of this approach was verified by comparing this drug with another 5-HT releaser, d-fenfluramins (5 mg/kg, IP). Both 5-HT releasers increased plasma oxytocin concentration. Furthermore, the 5-HT uptake blocker fluoxetine (10 mg/ kg, IP) blocked the effects of both p-chloroamphetamine and d-fenfluramine on plasma oxytocin concentrations, suggesting that both 5-HT releasers must be taken up through the 5-HT transporter into 5-HT nerve terminals to increase oxytocin secretion. In the lesion experiments, cells in the hypothalamic PVN or SON were destroyed by injection of the cell-selective neurotoxin ibotenic acid. The PVN lesions reduced basal levels and inhibited the effect of p-chloroamphetamine (8 mg/kg, IP) on plasma oxytocin concentration. In contrast, SON lesions did not alter basal oxytocin levels and did not reduce the oxytocin response to p-chloroamphetamine, suggesting that the SON is not involved in the serotonergic stimulation of oxytocin secretion. Site specificity of the PVN lesions was confirmed when injections of ibotenic acid into the hypothalamic dorsomedial nucleus (DMN), immediately caudal to the PVN, potentiated the oxytocin response to p-chloroamphstamine, suggesting that the DMN exerts an inhibitory influence on the secretion of oxytocin. Taken together, the deft suggest that the serotonergic stimulation of oxytocin secretion involves PVN, but not SON, oxytocin neurons.
AB - The purpose of the present studies was to determine whether cells in the hypothalamic paraventricular (PVN) or supraoptic (SON) nuclei mediate the serotonergic stimulation of oxytocin secretion. The serotonergic stimulus consisted of injection of the 5-HT-releasing drug p-chloroamphetamine (8 mg/ kg, IP). The validity of this approach was verified by comparing this drug with another 5-HT releaser, d-fenfluramins (5 mg/kg, IP). Both 5-HT releasers increased plasma oxytocin concentration. Furthermore, the 5-HT uptake blocker fluoxetine (10 mg/ kg, IP) blocked the effects of both p-chloroamphetamine and d-fenfluramine on plasma oxytocin concentrations, suggesting that both 5-HT releasers must be taken up through the 5-HT transporter into 5-HT nerve terminals to increase oxytocin secretion. In the lesion experiments, cells in the hypothalamic PVN or SON were destroyed by injection of the cell-selective neurotoxin ibotenic acid. The PVN lesions reduced basal levels and inhibited the effect of p-chloroamphetamine (8 mg/kg, IP) on plasma oxytocin concentration. In contrast, SON lesions did not alter basal oxytocin levels and did not reduce the oxytocin response to p-chloroamphetamine, suggesting that the SON is not involved in the serotonergic stimulation of oxytocin secretion. Site specificity of the PVN lesions was confirmed when injections of ibotenic acid into the hypothalamic dorsomedial nucleus (DMN), immediately caudal to the PVN, potentiated the oxytocin response to p-chloroamphstamine, suggesting that the DMN exerts an inhibitory influence on the secretion of oxytocin. Taken together, the deft suggest that the serotonergic stimulation of oxytocin secretion involves PVN, but not SON, oxytocin neurons.
KW - 5-HT release
KW - Fluoxetine
KW - Ibotenic acid
KW - Oxytocin
KW - Serotonin
KW - Supraoptic
KW - d-Fenfluramine
KW - p-Chloroamphetamine
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UR - http://www.scopus.com/inward/citedby.url?scp=0027995423&partnerID=8YFLogxK
U2 - 10.1016/0361-9230(94)00161-S
DO - 10.1016/0361-9230(94)00161-S
M3 - Article
C2 - 7882048
AN - SCOPUS:0027995423
SN - 0361-9230
VL - 36
SP - 45
EP - 50
JO - Brain Research Bulletin
JF - Brain Research Bulletin
IS - 1
ER -