Paraventricular alpha1- and alpha2-adrenergic receptors mediate hindbrain lipoprivation-induced suppression of luteinizing hormone pulses in female rats.
Acute central lipoprivation suppresses pulsatile luteinizing hormone (LH) release and increases blood glucose levels through noradrenergic input to the hypothalamic paraventricular nucleus (PVN) in female rats. The present study was conducted to identify adrenergic receptor subtypes involved in central lipoprivation-induced suppression of pulsatile LH secretion and increases in plasma glucose levels in female rats. Acute hindbrain lipoprivation was produced by injection into the fourth cerebroventricle (4V) of 2-mercaptoacetate (MA), an inhibitor of fatty acid oxidation, in estradiol-implanted ovariectomized rats. Two min before MA injection, alpha1-, alpha2- or beta-adrenergic receptor antagonist was injected into the PVN. Injection of MA into the 4V suppresses pulsatile LH release in PVN vehicle-treated rats, whereas pretreatment of animals with injection of alpha1- or alpha2-adrenergic antagonist into the PVN blocked the effect of the 4V MA injection on LH pulses. beta-Adrenergic antagonist did not affect MA-induced suppression of LH pulses. The counter-regulatory increase in plasma glucose levels after 4V MA injection was also partially blocked by pretreatment with alpha1- and alpha2-adrenergic receptor antagonists. These results suggest that alpha1- and alpha2-adrenergic receptors in the PVN mediate hindbrain lipoprivation-induced suppression of LH release and counter-regulatory increases in plasma glucose levels in female rats.
Sajapitak
Somchai
S
Laboratory of Animal Reproduction, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan.
Uenoyama
Yoshihisa
Y
Yamada
Shunji
S
Kinoshita
Mika
M
Iwata
Kinuyo
K
Bari
Farida Yeasmin
FY
I'anson
Helen
H
Tsukamula
Hiroko
H
Maeda
Kei-Ichiro
K
D058668:Adrenergic alpha-1 Receptor Antagonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D003345:Corticosterone / Q000097:blood; D004734:Energy Metabolism / Q000502:physiology; D004958:Estradiol / Q000494:pharmacology; D005227:Fatty Acids / Q000378:metabolism; D005260:Female; D007276:Injections, Intraventricular; D007986:Luteinizing Hormone / Q000378:metabolism*; D009434:Neural Pathways; D009638:Norepinephrine / Q000037:antagonists & inhibitors; D010052:Ovariectomy; D010286:Paraventricular Hypothalamic Nucleus / Q000166:cytology / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology*; D018341:Receptors, Adrenergic, alpha-2 / Q000502:physiology*; D012249:Rhombencephalon / Q000166:cytology / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology; D013864:Thioglycolates / Q000494:pharmacology
D058668:Adrenergic alpha-1 Receptor Antagonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D001786:Blood Glucose; D005227:Fatty Acids; D018340:Receptors, Adrenergic, alpha-1; D018341:Receptors, Adrenergic, alpha-2; D013864:Thioglycolates; D004958:Estradiol; C017487:2-mercaptoacetate; D007986:Luteinizing Hormone; D003345:Corticosterone; D009638:Norepinephrine