Inhibitory influence of the nuclei of the posterior hypothalamus on the pro-oestrous surge of LH

1984 ◽  
Vol 105 (4) ◽  
pp. 433-440 ◽  
Author(s):  
C. Beltramino ◽  
S. Taleisnik
Keyword(s):  
Posterior Hypothalamus ◽  
Female Rats ◽  
Hypothalamic Nucleus ◽  
Inhibitory Influence ◽  
Medial Basal Hypothalamus ◽  
Mammillary Bodies ◽  
Ventromedial Hypothalamic Nucleus ◽  
Hypothalamic Nuclei ◽  
Posterior Hypothalamic Nucleus ◽  
Lh Release

Abstract. The effect of transecting caudal afferents to the medial basal hypothalamus on the pro-oestrous surge of LH was studied in cyclic female rats. Rats with transverse cuts placed just in front of the mammillary bodies and caudal to the ventromedial hypothalamic nucleus showed an earlier time of onset of pro-oestrous surge of LH. Conversely, rats with transverse cuts placed 2 mm more caudally or with cuts along the lateral edges of the hypothalamus showed no altered release of LH. Advanced release of LH occurred also in rats in which the ventral premammillary nuclei or the posterior hypothalamic nuclei were bilaterally destroyed but not in those sham operated or with lesions in the dorsal premammillary nuclei. The number of ova ovulated was higher in rats bearing lesions of any of these nuclei but enhanced LH release was seen only in animals with lesions of the posterior hypothalamic nuclei. Electrochemical stimulation (anodic d.c., 100 μA, 15 s) applied at noon of pro-oestrus to the ventral premammillary nucleus, dorsal premammillary nucleus or posterior hypothalamic nucleus prevented ovulation and the preovulatory discharge of LH. It is concluded that inputs from nuclei of the posterior hypothalamus are inhibitory for LH release and could participate in determining the timing and magnitude of the pro-oestrous surge of the hormone.

Electrical stimulation of the posterior and ventromedial hypothalamic nuclei causes specific activation of shivering and nonshivering thermogenesis

1994 ◽  
Vol 72 (1) ◽  
pp. 89-96 ◽  
Author(s):  
J. A. Thornhill ◽  
I. Halvorson
Keyword(s):  
Adipose Tissue ◽  
Electrical Stimulation ◽  
Brown Adipose Tissue ◽  
Posterior Hypothalamus ◽  
Hypothalamic Nucleus ◽  
Ventromedial Hypothalamic Nucleus ◽  
Hypothalamic Nuclei ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Stimulation Of

Experiments were designed to determine in the same animal whether electrical stimulation of the posterior hypothalamus and ventromedial hypothalamic nucleus could specifically evoke shivering and nonshivering (brown adipose tissue) thermogenesis, respectively, in anesthetized, normothermic rats. Urethane-anesthetized, male Long–Evans rats, kept at 37 °C, had colonic (Tc), gastrocnemius muscle (Tm), intrascapular brown adipose tissue (TIBAT), and tail (Tt) temperatures measured via thermistor probes, and electromyogram activity (differential multiunit activity from bipolar recording electrodes within gastrocnemius muscle) recorded, before and after unilateral electrical stimulation (monophasic 0.5-ms pulses of 200 μA at 50 Hz for 30 s) of the posterior hypothalamus and ventromedial hypothalamic nucleus (via stereotaxically implanted concentric stimulating electrodes). Each rat showed shivering (increased electromyogram activity) following posterior hypothalamic stimulation, which caused an immediate rise in Tm values with no change in TIBAT or Tt values. Electrical stimulation of the ventromedial hypothalamic nucleus of the same animals elicited no shivering activity, but significant increases in TIBAT values occurred with no change in Tm or Tt values. Results confirm that stimulation of the posterior and ventromedial hypothalamic nuclei in rodents specifically activates shivering and nonshivering (brown adipose tissue) effector mechanisms, respectively, to raise core temperature.Key words: posterior hypothalamus, shivering thermogenesis, ventromedial hypothalamus, intrascapular brown adipose tissue thermogenesis.

Plasma LH levels following electrochemical stimulation of the deafferented medial basal hypothalamus

1980 ◽  
Vol 94 (1) ◽  
pp. 11-17
Author(s):  
A. J. Carrillo ◽  
N. Hagino ◽  
G. Setalo
Keyword(s):  
Median Eminence ◽  
Jugular Vein ◽  
External Jugular Vein ◽  
Female Rats ◽  
Medial Basal Hypothalamus ◽  
Blood Samples ◽  
Ether Anaesthesia ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Stimulation Of

Abstract. We have investigated the capability of a completely deafferented medial basal hypothalamus (MBH) pituitary complex to support LH release following electrochemical stimulation (ECS) of the arcuate-median eminence (ARC-ME) region. In adult female rats the MBH was completely deafferented (CD) on the morning of pro-oestrus (08.00-10.00 h of day 0). In the first experiment the animals were divided into 5 groups depending on the day of ECS (14.00–16.00 h) and oestradiol benzoate (Oe) treatment (08.00–10.00 h): group No. 1) ECS on day 0; 2) no ECS; 3) ECS on day 1; 4) Oe on day 0 and ECS on day 1; 5) Oe on day 4 and ECS on day 5. Blood samples were collected from the external jugular vein under ether anaesthesia for LH determinations just before and 1 and 2 h after ECS. ECS on day 0 resulted in a significant (P<0.01) rise in plasma LH at 1 and 2 h, while the rats subjected to CD, but not ECS failed to show any changes in plasma LH levels. ECS on days I and 5 (groups 3 and 5) failed to alter plasma LH levels, however, ECS on day 1 in Oe treated rats produced a significant (P < 0.01) elevation in plasma LH that was comparable to that of day 0. In a second experiment Oe was injected on days 1–5 and ECS of the ARC-ME was done bilaterally. ECS on day 5 resulted in a significant (P < 0.05) rise in plasma LH levels in rats with a completely deafferented MBH. In animals with an incomplete deafferentation ECS resulted in a much greater (P < 0.005) rise in plasma LH at l and 2 h. Since LH was released several days after complete hypothalamic deafferentation, these data suggest that LRH secreting cells may be present within the MBH of the rat. In a third experiment injection of LRH (400 ng) on days 0, 1 and 5 with Oe on days 0, 4 or 1–5 resulted in a significant (P < 0.001) rise of plasma LH at 30 and 60 min in all groups. Rats injected on day 0 showed the greatest elevation at 60 min in all groups. Saline injected rats did not show any changes in plasma LH levels.

scholarly journals Sex-dimorphic neuroestradiol regulation of ventromedial hypothalamic nucleus glucoregulatory transmitter and glycogen metabolism enzyme protein expression in the rat

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Md. Main Uddin ◽  
Mostafa M. H. Ibrahim ◽  
Karen P. Briski
Keyword(s):  
Protein Expression ◽  
Glycogen Synthase ◽  
Metabolic Stress ◽  
Glycogen Metabolism ◽  
Female Rats ◽  
Hypothalamic Nucleus ◽  
Energy Yield ◽  
Intact Male ◽  
Energy Deficiency ◽  
Ventromedial Hypothalamic Nucleus

Abstract Background Ventromedial hypothalamic nucleus (VMN) gluco-regulatory transmission is subject to sex-specific control by estradiol. The VMN is characterized by high levels of aromatase expression. Methods The aromatase inhibitor letrozole (LZ) was used with high-resolution microdissection/Western blot techniques to address the hypothesis that neuroestradiol exerts sex-dimorphic control of VMN neuronal nitric oxide synthase (nNOS) and glutamate decarboxylase65/67 (GAD) protein expression. Glycogen metabolism impacts VMN nNOS and GAD profiles; here, LZ treatment effects on VMN glycogen synthase (GS) and phosphorylase brain- (GPbb; glucoprivic-sensitive) and muscle (GPmm; norepinephrine-sensitive) variant proteins were examined. Results VMN aromatase protein content was similar between sexes. Intracerebroventricular LZ infusion of testes-intact male and ovariectomized, estradiol-replaced female rats blocked insulin-induced hypoglycemic (IIH) up-regulation of this profile. LZ exerted sex-contingent effects on basal VMN nNOS and GAD expression, but blocked IIH-induced NO stimulation and GAD suppression in each sex. Sex-contingent LZ effects on basal and hypoglycemic patterns of GPbb and GPmm expression occurred at distinctive levels of the VMN. LZ correspondingly down- or up-regulated baseline pyruvate recycling pathway marker protein expression in males (glutaminase) and females (malic enzyme-1), and altered INS effects on those proteins. Conclusions Results infer that neuroestradiol is required in each sex for optimal VMN metabolic transmitter signaling of hypoglycemic energy deficiency. Sex differences in VMN GP variant protein levels and sensitivity to aromatase may correlate with sex-dimorphic glycogen mobilization during this metabolic stress. Neuroestradiol may also exert sex-specific effects on glucogenic amino acid energy yield by actions on distinctive enzyme targets in each sex.

Brown adipose tissue thermogenesis evoked by medial preoptic stimulation is mediated via the ventromedial hypothalamic nucleus

1994 ◽  
Vol 72 (9) ◽  
pp. 1042-1048 ◽  
Author(s):  
J. Thornhill ◽  
A. Jugnauth ◽  
I. Halvorson
Keyword(s):  
Blood Pressure ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Hypothalamic Nucleus ◽  
Marked Rise ◽  
Sterile Saline ◽  
Ventromedial Hypothalamic Nucleus ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Posterior Hypothalamic Nucleus

Experiments were designed to determine if a functional ventromedial hypothalamic nucleus was required for the activation of brown adipose tissue thermogenesis evoked by medial preoptic stimulation. Male, urethane-anesthetized Long–Evans rats, maintained at 37 °C, had temperatures (thermistor probes for gastrocnemius, Tm; intrascapular brown adipose tissue, 7IBAT; colonic, Tc; and tail, Tt), gastrocnemius electromyogram activity (via stainless steel recording electrodes), and systemic blood pressure and heart rate (via a femoral arterial catheter) measured before and after a series of unilateral medial preoptic electrical stimulations (monophasic 0.5-ms pulses of 300 μA at 50 Hz for 30 s). Measurements were made (i) after an initial control medial preoptic electrical stimulation, (ii) after medial preoptic stimulation was applied 1 min following an intracranial injection of 300 nL of sterile saline or buffered 2% Lidocaine into the ipsilateral posterior hypothalamic nucleus or the ipsilateral ventromedial hypothalamic nucleus, and (iii) after recovery medial preoptic stimulation 45 min after Lidocaine was injected into the ventromedial hypothalamic nucleus. TIBAT and blood pressure rose significantly (p < 0.05) above the corresponding prestimulation control values with all protocols, except when Lidocaine was injected into the ventromedial hypothalamic nucleus prior to medial preoptic stimulation. Shivering (electromyogram) activity was not evoked following medial preoptic stimulation and Tm and Tt did not significantly change from the corresponding prestimulation values. A recovery medial preoptic stimulation 45 min after Lidocaine treatment of the ventromedial hypothalamic nucleus again evoked significant increases in TIBAT above the core temperature, similar to the rise in TIBAT seen after the first control medial preoptic stimulation. Pretreatment with Lidocaine into the posterior hypothalamic nucleus before medial preoptic stimulation caused no suppression of blood pressure compared with treatments after the control medial preoptic stimulation; however, TIBAT was reduced (p < 0.05) from the marked rise in TIBAT seen after the control stimulation. Results indicate that a functional ventromedial hypothalamic nucleus is required for medial preoptic stimulation to activate brown adipose tissue thermogenesis.Key words: brown adipose tissue thermogenesis, medial preoptic stimulation, thermoregulation, heat production.

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