Corticoliberin and somatoliberin activity in the pituitary stalk median eminence of rats after neonatal treatment with monosodium glutamate

1982 ◽  
Vol 93 (2) ◽  
pp. 239-245 ◽  
Author(s):  
Zsuzsanna Ács ◽  
F. A. Antoni ◽  
G. B. Makara

Neurotoxic lesions of the arcuate nucleus by neonatal treatment with monosodium glutamate (MSG) resulted in a decrease of plasma GH levels without affecting plasma corticosterone concentration. The corticoliberin activity of the pituitary stalk median eminence (SME) in MSG-treated animals was similar to that of litter-mate controls. Growth hormone releasing (somatoliberin) activity of the SME, tested after placing an anterolateral cut around the medial basal hypothalamus, was significantly lower in MSG-treated than in control animals. It was concluded that a substantial proportion of the somatoliberin neurones are found in the arcuate nucleus.

1988 ◽  
Vol 48 (6) ◽  
pp. 645-649 ◽  
Author(s):  
Miriam Sterman Dolnikoff ◽  
Claudio Elias Kater ◽  
Mizue Egami ◽  
Iracema Senna de Andrade ◽  
Maria Regina Marmo

Author(s):  
Marton Fekete ◽  
Daniel Szekács ◽  
Miklós Vecsernyés ◽  
Ibolya Bodnár ◽  
Hitoshi Okamura ◽  
...  

1981 ◽  
Vol 240 (4) ◽  
pp. E441-E446 ◽  
Author(s):  
G. B. Makara ◽  
E. Stark ◽  
M. Karteszi ◽  
M. Palkovits ◽  
G. Rappay

The effects of destroying the paraventricular nucleus (PVN) of the rat hypothalamus on pituitary-adrenal function were studied. Four days after PVN lesions were placed with a rotating knife, the basal plasma corticosterone level was normal, but the corticosterone response to electrical stimulation of the medial basal hypothalamus, surgical trauma, and ether-venesection stress was significantly inhibited. Four and 8 days after PVN lesioning and adrenalectomy, the basal plasma ACTH level was lower, and the rise of plasma ACTH level elicited by a 3-min ether inhalation was significantly smaller than in the adrenalectomized controls. Corticotropin-releasing factor (CRF) activity in the stalk-median eminence extracts from PVN-lesioned rats was significantly less than in the control extracts. The weight of the adrenals was decreased by both 2 and 4 wk after PVN destruction, and 2 wk after hemiadrenalectomy, the compensatory adrenal hypertrophy was inhibited. The plasma corticosterone response to ether-venesection stress was inhibited only temporarily because it returned to normal by the end of the 4th postoperative week. The results are consistent with the hypothesis that a substantial portion of CRF-containing fibers in the stalk-median eminence region either originate from or run though the PVN or its immediate vicinity.


1985 ◽  
Vol 104 (1) ◽  
pp. 121-127 ◽  
Author(s):  
I. Kakucska ◽  
M. Antal ◽  
M. Kárteszi ◽  
G. B. Makara

ABSTRACT Plasma and pituitary GH content, in-vitro GH release and somatostatin-like immunoreactivity (SLI) in the stalk-median eminence were studied up to 7 days after making an anterolateral cut (ALC) around the medial-basal hypothalamus. Plasma GH concentration increased within 15 min to a very high level, then fell to a high level which was unchanged for several hours. The GH concentration then steadily decreased between days 2 and 7. The SLI content in the stalk-median eminence decreased to 3·5% of the control value within 3 days. The GH content of the anterior pituitary gland was 58·8% of the control value by 1 week after the operation but the in-vitro sensitivity to somatostatin of the GH cells failed to change. Pentobarbitone injection stimulated GH release in the sham-operated controls but decreased it in the rats with an ALC. These findings suggest that transection of somatostatin-containing fibres is followed by a rapid rise and a lasting high concentration of plasma GH which slowly returns towards lower levels in parallel with a marked depletion of pituitary GH content. In rats with transected somatostatin innervation of the median eminence, sodium pentobarbitone probably decreases GH secretion by depressing the secretion of GH-releasing hormone. J. Endocr. (1985) 104, 121–127


1981 ◽  
Vol 91 (3) ◽  
pp. 415-425 ◽  
Author(s):  
F. A. ANTONI ◽  
G. B. MAKARA ◽  
GY. RAPPAY

The possible role of the neural connections of the medial-basal hypothalamus (MBH) in the maintenance of GH releasing activity of the pituitary stalk median eminence (SME) was investigated. Male rats, subjected to sham-operation and to complete and anterolateral cuts around the MBH were used 7–8 days after surgery. Electrical stimulation of neural structures within the MBH caused an increase of plasma GH in pentobarbitone- as well as in urethane-anaesthetized animals. In sham-operated rats the rise of plasma GH levels was apparent only after completion of 10 min of electrical stimulation, while in animals with complete or anterolateral cuts an increase was already evident during electrical stimulation. The results suggest that depolarization of somatostatin secreting fibres in the median eminence may be responsible for the delay in the rise of GH levels in sham-operated rats, while the increment can be attributed to a GH releasing principle in the hypothalamus. Acidic extracts of the SME of rats with complete or anterolateral cuts stimulated the release of GH by primary cultures of rat anterior pituitary cells. Microinjection of 0·05 SME equivalents of SME extract into the anterior pituitary gland of urethane-anaesthetized rats produced a rise in plasma GH levels within 3 min of injection. These data favour the existence of a GH releasing factor, and suggest that the ventromedial and arcuate hypothalamic nuclei are major sites of production of this releasing hormone.


1983 ◽  
Vol 96 (3) ◽  
pp. 427-432 ◽  
Author(s):  
F. A. Antoni ◽  
B. Kanyicska ◽  
G. B. Makara

The role of nerve cells of the arcuate nucleus and endogenous opioid peptides in the regulation of GH and prolactin secretion has been investigated. Electrical stimulation of the medial-basal hypothalamus (MBH) for 10 min raised plasma levels of both hormones in male rats anaesthetized with pentobarbitone sodium. Plasma hormone levels increased within 5 min after the termination of the stimulus, while no marked changes were found during stimulation. The GH response to the electrical stimulus was substantially reduced in rats with arcuate lesions induced by neonatal treatment with monosodium-l-glutamate (MSG). By contrast, the size of the prolactin response was not altered by MSG treatment. The opiate receptor antagonist naloxone (10 mg/kg, i.v.) failed to influence GH secretion induced by electrical stimulation in either control or MSG-treated animals. The post-stimulus rise of plasma prolactin levels was attenuated by naloxone in control rats, while the same dose of the drug was ineffective in rats which had been exposed to MSG. We conclude that endogenous opioids participate in the increase of prolactin release upon electrical stimulation of the MBH but are not involved in the GH secretory response. Arcuate neurones are important in the maintenance of the GH response to electrical stimulation. By contrast, lesioning of the arcuate nucleus failed to affect the prolactin secretory response elicited by MBH stimulation. However, prolactin release in MSG-treated rats appeared less susceptible to the inhibitory action of naloxone, suggesting a possible supersensitivity towards endogenous opioids.


2001 ◽  
Vol 55 (6) ◽  
pp. 767-774 ◽  
Author(s):  
Ibolya Bodnár ◽  
Pál Göõz ◽  
Hitoshi Okamura ◽  
Béla E Tóth ◽  
Miklós Vecsernyé ◽  
...  

Endocrinology ◽  
2002 ◽  
Vol 143 (9) ◽  
pp. 3268-3275 ◽  
Author(s):  
Hideki Tamura ◽  
Jun Kamegai ◽  
Takako Shimizu ◽  
Shinya Ishii ◽  
Hitoshi Sugihara ◽  
...  

Abstract Ghrelin, an endogenous ligand for the GH secretagogue receptor 1a (GHS-R1a), was originally purified from the rat stomach. Ghrelin mRNA and peptide have also been detected in the hypothalamus and pituitary. Ghrelin is a novel acylated peptide that regulates GH release and energy metabolism. GHS-R1a mRNA is expressed in the pituitary gland as well as in several areas of the brain including the hypothalamus. In this study, we examined whether ghrelin could stimulate GH secretion and feeding in chronic GHRH, neuropeptide Y, and agouti-related protein deficient rats that were neonatally treated with monosodium glutamate (MSG), which destroys the neurons in the hypothalamic arcuate nucleus (ARC). Intravenous (iv) administration of rat ghrelin (10 μg/kg body weight) increased plasma GH levels significantly in the normal adult male rats during a GH trough period of pulsatile GH secretion, while iv injection of ghrelin in MSG-treated rats resulted in a markedly attenuated GH response. When rat ghrelin (10 μg/rat) was administered intracerebroventricular (icv), plasma GH levels were increased comparably in normal control and MSG-treated rats. However, the GH release after icv injection of ghrelin was markedly diminished compared with that after iv administration of a small amount of ghrelin in normal control rats (icv: 10 μg/rat, iv: approximately 4.0 μg/rat), indicating that the GH-releasing activity of exogenous ghrelin is route dependent and at least in part via hypothalamic ARC. The icv administration of 1 μg of ghrelin increased significantly 4-h food intake in normal control, whereas the peptide did not increase food intake in MSG-treated rats, indicating that the feeding response to ghrelin requires intact ARC. Taken together, the primary action of ghrelin on appetite control and GH releasing activity is via the ARC even though it might act on another type of GHS-R besides GHS-R1a.


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