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Sodium Pentobarbitone and the Suppression of Luteinizing Hormone Pulses in the Female Rat: the Role of Hypothermia
Author(s) -
Strutton Paul H.,
Coen Clive W.
Publication year - 1996
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.1996.tb00825.x
Subject(s) - endocrinology , medicine , luteinizing hormone , hypothermia , pentobarbital , sodium , hormone , chemistry , organic chemistry
The role of hypothermia in the suppression of pulsatile luteinizing hormone (LH) release by the barbiturate sodium pentobarbitone has been investigated in ovariectomized rats. Each animal was fitted with an intraperitoneal miniature radio transmitter to monitor core temperature and with an indwelling intravenous and intraperitoneal catheter. During the 6‐h sampling period the animal's core temperature was recorded automatically every 5 min and a 25 μl blood sample was obtained concurrently using an automated system. After the initial 3 h of sampling either the drug or the vehicle was administered via the intraperitoneal cannula from outside the cage, thus ensuring minimal disturbance to the animal. Administration of sodium pentobarbitone (40 mg/kg) at an ambient temperature of 21°C resulted in a significant hypothermia throughout the 3‐h post‐injection period. During this period there was a significant reduction in mean LH concentration, and in the frequency and amplitude of the LH pulses. When the drug was administered at an ambient temperature of 35°C there was no reduction in core temperature and no significant change in the LH pulse parameters. Vehicle treatment was without significant effect on core temperature or on the LH pulse parameters when administered at an ambient temperature of either 21°C or 35°C. These results indicate that the effects of this barbiturate on the pulsatile release of LH are secondary to the induced hypothermia and suggest that hypothermia per se may be able to disrupt LH pulses. It is therefore imperative to reassess the significance of previous studies that have implicated particular neurotransmitter systems in the control of LH pulses; unrecognized hypothermic effects of the treatments may have been the primary cause of the pulse suppression, rather than a direct involvement of the neurotransmitter in question in the regulation of LH releasing hormone. The neurophysiological process by which the hypothermic state may inhibit LH pulses remains to be determined.