FAILURE OF HISTAMINE TO INDUCE THE RELEASE OF LUTEINIZING HORMONE IN CASTRATED RATS PRIMED WITH SEX STEROIDS

1978 ◽  
Vol 78 (3) ◽  
pp. 447-448 ◽  
Author(s):  
A. O. DONOSO ◽  
A. M. BANZAN
Keyword(s):  
Luteinizing Hormone ◽  
Positive Feedback ◽  
Sex Steroids ◽  
Third Ventricle ◽  
Male Rats ◽  
Intraventricular Injection ◽  
Mediobasal Hypothalamus ◽  
Feedback Effects ◽  
The Third

Instituto de Investigaciones Cerebrales, Facultad de Ciencias Médicas, Universidad Nacional de Cuyo, Mendoza, Argentina (Received 10 March 1978) Injection of histamine into the third ventricle causes the release of luteinizing hormone (LH) in ovariectomized, steroid-primed and pro-oestrous rats (Donoso, Banzan & Borzino, 1976; Donoso, 1978). In oestrous rabbits, intraventricular injection of large doses of histamine or injection of histamine into the mediobasal hypothalamus induces ovulation and secretion of progesterone by the ovaries (Sawyer, 1955; Endröczi & Hilliard, 1965). However, histamine has no effect on the concentration of LH in the plasma of male rats (Donoso & Banzan, 1976). Together, these results suggest that histamine is able to induce the release of LH both before ovulation and in the presence of an adequate hormonal background. The positive feedback effects of oestradiol and progesterone on the release of gonadotrophins are absent in male rats. Injection of oestradiol, progesterone or testosterone into steroid-primed

scholarly journals Tanycyte Pyroglutamyl Peptidase II Contributes to Regulation of the Hypothalamic-Pituitary-Thyroid Axis through Glial-Axonal Associations in the Median Eminence

Endocrinology ◽  
2009 ◽  
Vol 150 (5) ◽  
pp. 2283-2291 ◽  
Author(s):  
Edith Sánchez ◽  
Miguel Angel Vargas ◽  
Praful S. Singru ◽  
Isel Pascual ◽  
Fidelia Romero ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Median Eminence ◽  
Anterior Pituitary ◽  
Cellular Localization ◽  
Third Ventricle ◽  
Male Rats ◽  
Mediobasal Hypothalamus ◽  
External Zone ◽  
The Third ◽  
In Cells

Pyroglutamyl peptidase II (PPII), a highly specific membrane-bound metallopeptidase that inactivates TRH in the extracellular space, is tightly regulated by thyroid hormone in cells of the anterior pituitary. Whether PPII has any role in the region where axons containing hypophysiotropic TRH terminate, the median eminence, is unknown. For this purpose, we analyzed the cellular localization and regulation of PPII mRNA in the mediobasal hypothalamus in adult, male rats. PPII mRNA was localized in cells lining the floor and infralateral walls of the third ventricle and coexpressed with vimentin, establishing these cells as tanycytes. PPII mRNA extended in a linear fashion from the tanycyte cell bodies in the base of the third ventricle to its cytoplasmic and end-feet processes in the external zone of the median eminence in close apposition to pro-TRH-containing axon terminals. Compared with vehicle-treated, euthyroid controls, animals made thyrotoxic by the ip administration of 10 μg l-T4 daily for 1–3 d, showed dramatically increased accumulation of silver grains in the mediobasal hypothalamus and an approximately 80% increase in enzymatic activity. PPII inhibition in mediobasal hypothalamic explants increased TRH secretion, whereas ip injection of a specific PPII inhibitor increased cold stress- and TRH-induced TSH levels in plasma. We propose that an increase in circulating thyroid hormone up-regulates PPII activity in tanycytes and enhances degradation of extracellular TRH in the median eminence through glial-axonal associations, contributing to the feedback regulation of thyroid hormone on anterior pituitary TSH secretion.

REVERSAL BY ARGININE-VASOTOCIN OF THE EFFECTS OF PINEALECTOMY ON THE AMOUNT OF 5-HYDROXYTRYPTAMINE IN THE HYPOTHALAMUS AND THE CONCENTRATIONS OF LUTEINIZING HORMONE AND FOLLICLE-STIMULATING HORMONE IN THE PLASMA OF IMMATURE MALE RATS

1980 ◽  
Vol 84 (1) ◽  
pp. 159-161 ◽  
Author(s):  
S. PAVEL ◽  
NOEMI LUCA ◽  
MARIA CALB ◽  
R. GOLDSTEIN
Keyword(s):  
Luteinizing Hormone ◽  
Wistar Rats ◽  
Third Ventricle ◽  
Follicle Stimulating Hormone ◽  
Arginine Vasotocin ◽  
Male Rats ◽  
The Third ◽  
Immature Male ◽  
Receptor Sites ◽  
Male Wistar Rats

Pinealectomy in immature (25-day-old) male Wistar rats significantly decreased the content of 5-hydroxytryptamine (5-HT) in the hypothalamus and increased concentrations of plasma LH and FSH 3 days after surgery. Extremely small amounts (10−4 pg) of arginine-vasotocin (AVT) injected into the third ventricle (pineal recess) 5 min after pinealectomy completely prevented the decrease in the hypothalamic content of 5-HT and the increase in the concentration of LH and FSH in the plasma. It is suggested that AVT prevented the increase of plasma levels of LH and FSH after pinealectomy by increasing levels of 5-HT at postsynaptic receptor sites.

Central administration of metformin into the third ventricle of C57BL/6 mice decreases meal size and number and activates hypothalamic S6 kinase

2013 ◽  
Vol 305 (5) ◽  
pp. R499-R505 ◽  
Author(s):  
Hyun-Ju Kim ◽  
Eun-Young Park ◽  
Mi-Jeong Oh ◽  
Sung-Soo Park ◽  
Kyung-Ho Shin ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Third Ventricle ◽  
Meal Size ◽  
Dependent Manner ◽  
Central Administration ◽  
Mediobasal Hypothalamus ◽  
S6 Kinase ◽  
The Third

Administration of metformin is known to reduce both body weight and food intake. Although the hypothalamus is recognized as a critical regulator of energy balance and body weight, there is currently no evidence for an effect of metformin in the hypothalamus. Therefore, we sought to determine the central action of metformin on energy balance and body weight, as well as its potential involvement with key hypothalamic energy sensors, including adenosine monophosphate-activated protein kinase (AMPK) and S6 kinase (S6K). We used meal pattern analysis and a conditioned taste aversion (CTA) test and measured energy expenditure in C56BL/6 mice administered metformin (0, 7.5, 15, or 30 μg) into the third ventricle (I3V). Furthermore, we I3V-administered either control or metformin (30 μg) and compared the phosphorylation of AMPK and S6K in the mouse mediobasal hypothalamus. Compared with the control, I3V administration of metformin decreased body weight and food intake in a dose-dependent manner and did not result in CTA. Furthermore, the reduction in food intake induced by I3V administration of metformin was accomplished by decreases in both nocturnal meal size and number. Compared with the control, I3V administration of metformin significantly increased phosphorylation of S6K at Thr389 and AMPK at Ser485/491 in the mediobasal hypothalamus, while AMPK phosphorylation at Thr172 was not significantly altered. Moreover, I3V rapamycin pretreatment restored the metformin-induced anorexia and weight loss. These results suggest that the reduction in food intake induced by the central administration of metformin in the mice may be mediated by activation of S6K pathway.

scholarly journals Classical and Membrane-Initiated Estrogen Signaling in an In Vitro Model of Anterior Hypothalamic Kisspeptin Neurons

Endocrinology ◽  
2015 ◽  
Vol 156 (6) ◽  
pp. 2162-2173 ◽  
Author(s):  
Melinda A. Mittelman-Smith ◽  
Angela M. Wong ◽  
Anupama S. Q. Kathiresan ◽  
Paul E. Micevych
Keyword(s):  
Positive Feedback ◽  
Intracellular Signaling ◽  
Third Ventricle ◽  
Reproductive Function ◽  
Estrogen Signaling ◽  
The Third ◽  
Periventricular Area ◽  
Estrogen Positive Feedback

Abstract The neuropeptide kisspeptin is essential for sexual maturation and reproductive function. In particular, kisspeptin-expressing neurons in the anterior rostral periventricular area of the third ventricle are generally recognized as mediators of estrogen positive feedback for the surge release of LH, which stimulates ovulation. Estradiol induces kisspeptin expression in the neurons of the rostral periventricular area of the third ventricle but suppresses kisspeptin expression in neurons of the arcuate nucleus that regulate estrogen-negative feedback. To focus on the intracellular signaling and response to estradiol underlying positive feedback, we used mHypoA51 cells, an immortalized line of kisspeptin neurons derived from adult female mouse hypothalamus. mHypoA51 neurons express estrogen receptor (ER)-α, classical progesterone receptor (PR), and kisspeptin, all key elements of estrogen-positive feedback. As with kisspeptin neurons in vivo, 17β-estradiol (E2) induced kisspeptin and PR in mHypoA51s. The ERα agonist, 1,3,5-Tris(4-hydroxyphenyl)-4-propyl-1H-pyrazole, produced similar increases in expression, indicating that these events were mediated by ERα. However, E2-induced PR up-regulation required an intracellular ER, whereas kisspeptin expression was stimulated through a membrane ER activated by E2 coupled to BSA. These data suggest that anterior hypothalamic kisspeptin neurons integrate both membrane-initiated and classical nuclear estrogen signaling to up-regulate kisspeptin and PR, which are essential for the LH surge.

scholarly journals Improved visualization of luteinizing hormone releasing hormone pathways by immunocytochemical staining of thick vibratome sections.

1980 ◽  
Vol 28 (4) ◽  
pp. 361-363 ◽  
Author(s):  
B J Burchanowski ◽  
L A Sternberger
Keyword(s):  
Luteinizing Hormone ◽  
Median Eminence ◽  
Anterior Commissure ◽  
Third Ventricle ◽  
Immunocytochemical Staining ◽  
Luteinizing Hormone Releasing Hormone ◽  
Bed Nucleus ◽  
Releasing Hormone ◽  
The Third ◽  
Diagonal Band

Using 100-micron thick Vibratome sections and a modification of the peroxidase--antiperoxidase method of immunocytochemical staining we achieve a Golgi-like image of luteinizing hormone releasing hormone (LHRH) cells and fibers in mouse brain. Five LHRH pathways are described: 1) A dense projection of fibers from LHRH cells in the medial preoptic and septal areas to the wall of the third ventricle; 2) a projection of fibers from neurons in the bed nucleus of the stria terminalis and the nucleus of the anterior commissure to the subfornical organ; 3) projections of fibers from neurons in the medial septal nucleus and the diagonal band of Broca to the olfactory bulb; 4) fibers which travel within or just lateral to the wall of the third ventricle from the organum vasculosum laminae terminalis to the median eminence; 5) cells and fibers located just dorsal to the optic tracts which project rostrally to the preoptic area and caudally to the level of the median eminence where they course medially to converge and enter the median eminence.

Possible site of negative and positive feedback action of oestrogen on gonadotrophin secretion in normal women

1985 ◽  
Vol 108 (4) ◽  
pp. 440-444 ◽  
Author(s):  
Yasuhito Nagahara ◽  
Akira Miyake ◽  
Keiichi Tasaka ◽  
Yasuhiro Kawamura ◽  
Toshihiro Aono ◽  
...  
Keyword(s):  
Positive Feedback ◽  
Direct Action ◽  
Feedback Effects ◽  
The Third ◽  
Serum Lh ◽  
Gonadotrophin Secretion ◽  
Site Of Action ◽  
The Mean ◽  
Normal Women

Abstract. For determination of the site of action of oestrogen (E) during the negative and positive feedback phases of gonadotrophin secretions, studies were made on the pituitary response to a small amount of LRH and the pulsatility of gonadotrophins after E administration in normal cycling women in the mid-follicular phase. The pituitary responses to an iv bolus of 2.5 μg of synthetic LRH were evaluated by measuring serum LH and FSH 2 h before and 8 h after administration of 20 mg of conjugated E (Premarin). In the next cycle, the pituitary responses to a same dose of LRH were also observed 2 h before and 56 h after E injection. The mean levels of serum LH and FSH and the peak responses to LRH were significantly (P < 0.05) decreased 8 h after E injection, but were significantly (P < 0.05) increased 56 h after E administration. In the third cycle, the pulsatility of gonadotrophins was evaluated by measuring serum LH and FSH every 15 min for 180 min before and 8 h and 56 h after E injection. The pulse frequencies of gonadotrophins were not significantly different before and 8 h and 56 h after E injection. The amplitudes of pulses 56 h after Premarin injection were significantly higher than those before the injection. These findings suggest that the negative and positive feedback effects of E on gonadotrophin secretion may be caused, in part, by its direct action on the pituitary response to LRH.

scholarly journals Integrated Effects of Leptin in the Forebrain and Hindbrain of Male Rats

Endocrinology ◽  
2013 ◽  
Vol 154 (8) ◽  
pp. 2663-2675 ◽  
Author(s):  
Bhavna N. Desai ◽  
Ruth B. S. Harris
Keyword(s):  
Weight Loss ◽  
Food Intake ◽  
Body Fat ◽  
Fourth Ventricle ◽  
Third Ventricle ◽  
Male Rats ◽  
Low Doses ◽  
Sprague Dawley ◽  
The Third ◽  
Stat3 Phosphorylation

Abstract Leptin receptors (ObRs) in the forebrain and hindbrain have been independently recognized as important mediators of leptin responses. It is unclear how leptin activity in these areas is integrated. We tested whether both forebrain and hindbrain ObRs have to be activated simultaneously to change energy balance and to maintain metabolic homeostasis. Previous studies used acute leptin injections in either the third ventricle (1–5 μg) or the fourth ventricle (3–10 μg); here we used 12-day infusions of low doses of leptin in one or both ventricles (0.1 μg/24 h in third, 0.6 μg/24 h in fourth). Male Sprague Dawley rats were fitted with third and fourth ventricle cannulas, and saline or leptin was infused from Alzet pumps for 6 or 12 days. Rats that received leptin into only the third or the fourth ventricle were not different from controls that received saline in both ventricles. By contrast, rats with low-dose leptin infusions into both the third and fourth ventricle showed a dramatic 60% reduction in food intake that was reversed on day 6, a 20% weight loss that stabilized on day 6, and a 50% decrease in body fat at day 12 despite the correction of food intake. They displayed normal activity and maintained energy expenditure despite weight loss, indicating inappropriately high thermogenesis that coincided with increased signal transducer and activator of transcription 3 (STAT3) phosphorylation in the brainstem. Altogether, these findings show that with low doses of leptin, chronic activation of both hypothalamic and brainstem ObRs is required to reduce body fat.

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