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Abstract
The reduced thyroid activity during short-term starvation is associated with a lowered hypothalamic synthesis and secretion of TRH. However, little is known about the cause of the reduced thyroid function during prolonged malnutrition. We have therefore studied the effects of food reduction to one-third of normal (FR33) on the hypothalamus-pituitary-thyroid axis of male and female Wistar rats. After 3 weeks body weights of FR33 rats were almost 50% lower than those of controls. In both sexes, FR33 caused marked increases in serum corticosterone, and decreases in serum TSH, thyroxine (T4), free T4, tri-iodothyronine (T3) and free T3. While the free T3 fraction (FFT3) in serum decreased, the free T4 fraction (FFT4) tended to increase. Electrophoretic analysis indicated that decreased FFT3 was correlated with an increased thyroxine-binding globulin, while the increase in FFT4 seemed due to a decreased thyroxine-binding prealbumin binding capacity. Total RNA and proTRH mRNA in the hypothalamus were not affected by FR33. Median eminence and posterior pituitary TRH content tended to increase in FR33 rats, suggesting that hypothalamic TRH release is reduced in FR33 rats. Anterior pituitary TSH content was decreased by FR33 in both sexes, but pituitary TSHβ mRNA and TRH receptor status were not affected except for increased pituitary TSHβ mRNA in female FR33 rats. Although FR33 had no effect on pituitary weight, pituitary RNA and membrane protein content in FR33 rats were 50–70% lower than values in controls.
In conclusion, prolonged food reduction suppresses the pituitary-thyroid axis in rats. In contrast to short-term food deprivation, the mechanism whereby serum TSH is suppressed does not appear to involve decreases in proTRH gene expression, but may include effects on pituitary mRNA translation. Our results further support the hypothesis that TSH release may be lowered by increased corticosterone secretion, although the mechanism of this effect may differ between acute starvation and prolonged food reduction.
Journal of Endocrinology (1996) 150, 169–178
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ABSTRACT
Follicle-stimulating hormone release on the morning of oestrus was examined by using two different techniques which eliminate LH-releasing hormone (LHRH) stimulation of the pituitary gland. Cyclic female rats were given a potent LHRH antagonist (ALHRH) or were subject to electrolytic lesions of the medial basal hypothalamus (MBH) before or after the pro-oestrous phase of FSH release. Administration of ALHRH at 14.00, 15.30 and 17.00 h or lesioning of the MBH between 11.30 and 13.00 h on pro-oestrus entirely blocked the preovulatory LH surge and both phases of FSH release. Ovulation was abolished in all of these animals. However, when ALHRH was given at 20.30, 22.00 and 23.30 h or lesions of the MBH made between 20.00 and 21.30 h on pro-oestrus after the prooestrous FSH and LH surges had occurred, the oestrous phase of FSH release was indistinguishable from that of saline-treated control rats. Ovulation occurred in all of these animals, and the mean number of ova shed was eight/rat. The conclusions are that (1) the pro-oestrous phase of FSH release is dependent upon the hypothalamic hormonal stimulation by LHRH and (2) the oestrous phase of FSH release is entirely independent of direct LHRH stimulation, or any hypothalamic stimulus.
J. Endocr. (1985) 106, 361–366
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The activity of corticotrophin releasing factor (CRF) in extracts of the stalk median eminence (SME) complex proper (average protein content, 30·6 μg) of male rats was assayed by monolayer cultures of anterior pituitary cells using the release of immunoreactive ACTH. Extracts which were equivalent to 0·025 SME of control rats usually had detectable CRF activity, while there was no detectable activity in extracts of 0·4 SME equiv. taken 8 days after complete surgical isolation of the medial basal hypothalamus (MBH). The activity of CRF in extracts from rats with an anterolateral cut around the MBH was at least ten times less than that in the control rats. One day after placing an anterolateral cut around the MBH the ACTH releasing activity of the SME was not significantly different from that of the control animals but activity decreased significantly 3 days after the operation and was at least ten times less than in the control animals on day 7 after the operation.
It is suggested that most of the CRF activity of the SME is contained in nerve fibres entering the neurohaemal region from outside the MBH and that transection of these fibres produced the fall in CRF content of the SME in rats with partial or total surgical isolation of the MBH.
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ABSTRACT
Giving a subcutaneous oestradiol implant during anoestrus to ovariectomized ewes inhibits pulsatile LH secretion. This effect results from an increased negative feedback of oestradiol and depends on the synthesis of biogenic amines, mainly from the mediobasal hypothalamus. In the present study, we examined the effect of oestradiol on the extracellular levels of amines and their metabolites. Eight ewes were sampled by microdialysis from the lateral retrochiasmatic area, including the dopaminergic A15 nucleus, during inhibition of LH secretion by long days. Two dialysis sessions were carried out on each ewe; one after a 10-day oestradiol treatment and the other one after 10 days without oestradiol treatment. Half of the ewes were first oestradiol-treated then untreated, the other half received the treatment in the reverse order.
Oestradiol caused a decline in pulsatile LH secretion without affecting the secretion of prolactin. This steroid also led to a significant increase in the levels of amine metabolites: 3,4-dihydroxyphenylacetic acid, homovanillic acid and 5-hydroxyindolacetic acid in the extracellular medium. These results demonstrate the effect of oestradiol on aminergic activity as related to changes in hormonal secretions during long days (16 h of light per 24 h). Thus our data support the hypothesis that amines inhibit gonadotrophic secretion during anoestrus in the ewe and suggest that there is an activation of the aminergic neurones from the retrochiasmatic area in this regulatory mechanism.
Journal of Endocrinology (1992) 135, 421–430
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SUMMARY
Adult, male hamsters exposed to a photoperiod of 1 h light: 23 h darkness for either 2, 3, 4, 6, 8, or 10 weeks exhibited significantly lower testicular weights than did controls after 3 and 4 weeks of exposure to 14 h light: 10 h darkness. Liver Δ4-reductase activity was significantly decreased by 4 weeks of exposure to the short photoperiod. Exogenous melatonin decreased Δ4-reductase activity when incubated with either hamster liver (at 10−7 and 10−5 mol melatonin/l) or hamster hypothalamus (at 10−6 mol melatonin/l). In contrast, exogenous melatonin stimulated Δ4-reductase activity in preparations of rat liver (at 10−7 and 10−6 mol/l) and rat hypothalamus (at 10−9, 10−8, 10−7, and 10−6 mol/l). The possible role of melatonin in influencing the testosterone: dihydrotestosterone ratio is discussed in relation to possible regulation of gonadotrophin release.
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SUMMARY
The rat hypothalamus in vitro preparation was used to investigate the effect of bilateral adrenalectomy, with and without replacement therapy, on the release of corticotrophin-releasing factor (CRF). Corticotrophin-releasing factor was estimated using 48 h basal hypothalamic lesioned assay rats and corticosterone production of excised adrenals was used as the end point.
Bilateral adrenalectomy resulted in depletion of hypothalamic CRF content within the first 2 h after the operation but this effect was prevented by replacement therapy with corticosterone. Thereafter, the hypothalamic CRF content returned to values not significantly different from the intact control level. Bilateral adrenalectomy caused an increase in both basal and acetylcholine-induced release of CRF and it is suggested that corticosteroids exert a negative feedback effect on the hypothalamus.
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ABSTRACT
Much controversy exists concerning the role of catecholamines in the control of ACTH secretion. In this study, noradrenaline (0·1 nmol–0·1 μmol/l) stimulated the release of both immunoreactive corticotrophin-releasing factor-41 (ir-CRF-41) and ir-arginine vasopressin (ir-AVP) from the rat hypothalamus in vitro. The stimulatory effect of noradrenaline on CRF-41 release was blocked by propranolol, whilst that on AVP release was blocked by phentolamine. γ-Aminobutyric acid (GABA; 10 nmol/l) inhibited the acetylcholine-induced release of both AVP and CRF-41 in vitro, and the effect was blocked by picrotoxin (0·1 μmol/l). Neither substance had any effect on the basal secretion of either neuropeptide. The results indicate that noradrenaline stimulates and GABA inhibits the release of both peptides from the rat hypothalamus in vitro.
Journal of Endocrinology (1989) 122, 719–723
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Abstract
It has been surmised that GH exerts feedback action on the hypothalamus and thereby regulates its own secretion. Our previous studies suggested that GH acts on somatostatin neurons in the hypothalamic periventricular nucleus (PeV) and neuropeptide Y (NPY) neurons in the hypothalamic arcuate nucleus (ARC). However, there remains uncertainty whether GH acts directly or indirectly through the generation of IGFs on the hypothalamus to regulate its own secretion. To examine this, rat GH (rGH) or human IGF-I was injected directly into a defined area of the hypothalamus, and the blood GH profile was observed in conscious male rats. In the rats given 0·5 μg rGH into the ARC or PeV bilaterally, GH secretion was inhibited, and the inhibition lasted for 12 h. During the period of inhibition, the duration and amplitude of GH pulses were significantly decreased and the episodic secretion of GH appeared irregularly compared with the vehicle-injected control rats. In control rats given the vehicle or those given rGH into the lateral hypothalamus, the blood GH profile did not change and pulsatile GH secretion was produced every 3 h. When 0·1 μg IGF-I was injected into the ARC or PeV bilaterally, the blood GH secretory pattern was not affected. Together with the results of our previous studies showing that c-fos gene expression was induced by systemic administration of GH and that GH receptor mRNA was contained in somatostatin neurons in the PeV and NPY neurons in the ARC, the data of the present study indicate that GH, but not IGF-I, acts on the cells in the ARC and the PeV or in their vicinity to inhibit its own secretion, presumably by activating the somatostatin and NPY neurons.
Journal of Endocrinology (1997) 153, 283–290
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ABSTRACT
The presence of multiple forms of somatostatin-like immunoreactivity (SSLI) in the rat hypothalamus was confirmed using a sensitive radioimmunoassay in conjunction with gel filtration chromatography and high performance liquid chromatography (HPLC). Gel filtration chromatography of hypothalamic extracts revealed the presence of four forms of SSLI with estimated molecular weights of 1500, 3000, 6000 and 10000. Analysis by HPLC indicated that the 1500 and 3000 mol. wt forms of SSLI corresponded respectively to somatostatin-14 (SS14) and somatostatin-28 (SS28) whereas the 6000 and 10 000 mol. wt forms eluted together as a composite peak of high molecular weight somatostatin (HMW-SS). The proportions of SS14 (63%), SS28 (12%) and HMW-SS (25%) present in the hypothalamus were similar to those in the amygdala (59, 9 and 32% respectively). In contrast, the median eminence contained a greater proportion of SS28 than the other tissues: SS14, SS28 and HMW-SS were present in the proportions 40:24:26%. These results show that the rat median eminence differs from the hypothalamus as a whole in containing SS14 and SS28 in almost equimolar concentrations. The localized abundance of SS28 in the nerve terminals of the median eminence suggests a specific role for this peptide in the hypothalamic regulation of growth hormone secretion.
J. Endocr. (1985) 105, 383–389
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ABSTRACT
Using an in-vitro superfusion system, the relative importance of three distinct subtypes of the opiate receptor in the control of the secretion of LHRH from the mediobasal hypothalamus of the cockerel was investigated. Basal release of LHRH was increased by the antagonist naloxone, which shows some μ-receptor selectivity, in a manner which was reversed by the μ-receptor specific agonist [d-Ala2, N-Phe4-Gly-ol5]-enkephalin (DAGO) and the μ- and δ-specific agonist [d-Ala2,N-Phe4,Met(0)ol5]-enkephalin (FK 33–824). The †-specific agonist [d-Thr2,l-Leu5]-enkephalyl-Thr (DTLET) and the κ-specific agonist 1-methyl-2(3-thienylcarbonyl)-aminomethyl-5-(2-fluorophenyl)-H-2,3-dihydro-1,4-benzodiazepine (KC 6128; (+)-titfluadom) did not reverse the effect of naloxone. The δ-specific antagonist N,N-diallyl-Tyr-α-aminoisobutyricacid-Phe-Leu-OH (ICI 174,864) failed to influence basal release. Release of LHRH stimulated by increasing the potassium ion concentration of the superfusate to 48 mmol/l was reduced by DAGO in a manner which was reversed by naloxone, and by FK 33–824 in a manner which was reversed by both naloxone and ICI 174,864. The agonists DTLET and titfluadom did not affect stimulated release of LHRH. These results support the proposal that spontaneous release of LHRH is tonically inhibited by agonists acting through the μ-receptor whilst, in response to a stimulus, the δ-receptor, in addition to the δ-receptor, may be involved.
J. Endocr. (1987) 114,111–117
