Pentobarbital stimulates the activity of the GnRH pulse generator interacting with opioid neurons in rats in proestrus.
In order to investigate the possibility that i.p. injection of pentobarbital sodium (PB, 32 mg/kg bw) potentiates the GnRH pulse generator activity, effects of i.v. infusions of an opiate receptor antagonist naloxone (NAL, 2 mg/h) on the pulsatile LH secretion were compared in saline (SAL)- and PB-injected rats in proestrus and diestrus 1. In SAL-injected rats in proestrus, NAL infusions significantly increased both the frequency and amplitude of LH pulses, and also the overall mean LH concentration. In PB-injected rats in proestrus, all the parameters of the pulsatile LH secretion were similar to those in SAL-injected rats in proestrus. The NAL infusion in PB-injected rats caused an increase in the frequency, but it was similar to that in SAL-injected rats. But, increases in the amplitude and the overall mean LH observed during NAL infusions in PB-injected rats were greater than in SAL-injected rats. In SAL-injected rats in diestrus 1, NAL infusions increased all the parameters, as in rats in proestrus. In PB-injected rats in diestrus 1, LH secretion was severely suppressed. NAL infusions recovered the pulsatile LH secretion, but the frequency and the overall mean LH of the secretion were smaller than those obtained during NAL infusions in SAL-injected rats. In addition, characteristic increases in the MUA (volleys), which occur in association with the initiation of an LH pulse and thus are considered to represent an increased activity of the GnRH pulse generator, appeared more frequently during NAL infusions in PB-injected rats in proestrus than in SAL-injected rats. These results suggest that the GnRH pulse generator in rats in proestrus, but not in rats in diestrus 1, is refractory to PB and further is potentiated by PB in the response to NAL. Together with the fact that this dosage of PB blocks the surge of LH secretion in rats in proestrus, the concept of the existence of separate neuronal mechanisms responsible for the surge and pulsatile secretion of LH are supported.
Funabashi
T
T
Department of Physiology, Yokohama City University School of Medicine, Yokohama, Japan.
Jinnai
K
K
Sano
A
A
Shinohara
K
K
Kimura
F
F
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001683:Biological Clocks / Q000187:drug effects* / Q000502:physiology; D004031:Diestrus / Q000187:drug effects / Q000502:physiology; D004567:Electrodes, Implanted; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000096:biosynthesis*; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism; D007262:Infusions, Intravenous; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism; D009270:Naloxone / Q000008:administration & dosage / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D009474:Neurons / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D010424:Pentobarbital / Q000494:pharmacology*; D010507:Periodicity; D011359:Proestrus / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar
D009292:Narcotic Antagonists; D007987:Gonadotropin-Releasing Hormone; D009270:Naloxone; D007986:Luteinizing Hormone; D010424:Pentobarbital