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ABSTRACT
GH administered centrally or peripherally inhibits basal or secretagogue-induced GH secretion in domestic fowl. Since the release of pituitary GH is neurally regulated by the hypothalamus, GH autoregulation may be mediated by changes in the content or metabolism of hypothalamic monoamines. When chicken GH (500 μg/kg body weight) was injected i.v. into laying hens, tissue catecholamine (adrenaline, noradrenaline and dopamine) concentrations in the preoptic area (POA) and medial basal hypothalamus (MBH) were depleted for 2–24 h, as were concentrations of dihydroxyphenylacetic acid, a dopamine metabolite. The serotonin (5-HT) content of the POA and MBH was unaffected by i.v. GH administration, although a reduction in MBH 5-hydroxyindoleacetic acid suggested a tissue-specific inhibition of 5-HT turnover. Qualitatively similar results were observed in laying hens 24 h after the intracerebroventricular injection of chicken GH (10 μg/bird). These results therefore demonstrate aminergic actions of GH within the chicken hypothalamus which may mediate GH autoregulation. However, as amine metabolism is not only suppressed when endogenous GH secretion is reduced, but also at times when normal GH secretion is restored, these aminergic effects may also reflect other actions of GH on central function.
Journal of Endocrinology (1993) 136, 245–251
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ABSTRACT
Recent findings suggest that placental lactogen has a role in the regulation of hypothalamic function during pregnancy. To explore the mechanisms by which placental hormones may exert effects in the maternal central nervous system, we have examined the binding of rat placental lactogen-I (rPL-I) to brain slices from pregnant rats at mid- and late gestation. The binding of rPL-I to maternal rat brain was compared with that of human GH (hGH). Radiolabelled rPL-I bound specifically to ependymal cells of the choroid plexus in the lateral ventricles and in the roof of the third ventricle. The binding of 125I-labelled rPL-I was inhibited by unlabelled rPL-I, hGH or rat prolactin but not by rat GH, indicating that rPL-I and rat prolactin interact with a common binding site in maternal rat brain. Radiolabelled hGH bound to the choroid plexus and to ependymal cells lining the third ventricle in the region of the arcuate nucleus. In addition, hGH bound specifically to the ventromedial nuclei and to the medial preoptic area of the hypothalamus. The binding of radiolabelled hGH to all brain regions was inhibited by unlabelled rPL-I as well as hGH, indicating that rPL-I competes for lactogenic binding sites in the hypothalamus as well as the choroid plexus of the pregnant rat. These findings suggest potential mechanisms by which placental hormones may exert direct effects on the maternal central nervous system during pregnancy. The precise functions and roles of the PL-I binding sites in maternal choroid plexus and hypothalamus remain to be explored.
Journal of Endocrinology (1993) 139, 235–242
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SUMMARY
Corticotrophin (ACTH) release induced by surgical trauma under pentobarbitone anaesthesia was studied in rats. The plasma corticosterone level was used as an index of 'rapid' ACTH release.
One hour after surgical trauma the plasma corticosterone level had risen in rats with various cuts around the medial basal hypothalamus except in the group with lateral cuts. After stress no significant difference was found between the plasma levels of the controls and those of the rats with anterior, 'low' superior, 'low' anterosuperior, and 'short' posterior cuts. In contrast, in rats with 'high' superior, 'high' anterosuperior, 'long' posterior and lateral cuts the plasma corticosterone level was lower than in the appropriate sham-operated controls.
It is suggested that the nerve fibres initiating ACTH release after surgical trauma ascend the spinal cord to the medulla and mid-brain whence the pathways pass forward in the region of the dorsal longitudinal fasciculus and/or the median forebrain bundle to the lateral hypothalamic area, and from there to the medial basal hypothalamus.
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ABSTRACT
In the photoinhibited castrated male Syrian hamster, removal of the pineal gland or transfer to long photoperiods was followed by a rapid increase in the serum concentration of FSH. Levels were significantly above those of controls within 10 days. Central passive immunization of pineal-intact photoinhibited castrated animals against melatonin had a stimulatory effect on serum FSH levels, comparable with that observed following pinealectomy or transfer to short days. The effects of pinealectomy were blocked by programmed s.c. infusions of melatonin in a time-dependent manner. Serum FSH levels remained low in animals receiving 100 ng melatonin delivered over 10 h but the same mass of melatonin delivered over 4 h had no effect on the response to pinealectomy. Lesions of the anterior hypothalamus had no effect on the pinealectomy-induced increase of serum FSH in animals receiving saline infusions. However, in lesioned animals, programmed infusions of melatonin were no longer able to suppress the rise in FSH following pinealectomy. These results demonstrated that pineal melatonin is the mediator of central photoperiodic control of FSH secretion. The duration of the melatonin signal determines its effectiveness and an intact anterior hypothalamus is necessary for the signal to be read and/or the appropriate neuroendocrine response expressed.
Journal of Endocrinology (1989) 122, 247–254
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SUMMARY
Corticosteroid feedback mechanisms were investigated at the hypothalamic level using the rat hypothalamus in vitro and at the pituitary level using basal hypothalamic-lesioned rats. Both fast and delayed corticosteroid feedback effects were demonstrated at the level of the hypothalamus and pituitary gland with doses of corticosteroids within or near the physiological range. These two phases of feedback were separated temporally by a 'silent period' during which no feedback was apparent.
Studies on the mechanism of action of corticosteroids at the hypothalamic level showed that the fast feedback mechanism acts by inhibition of release whilst the delayed feedback mechanism acts by inhibition of both synthesis and release. The fast feedback action of corticosterone does not appear to act by excitation of neuroinhibitory pathways since neither picrotoxin nor phentolamine prevented the feedback action of corticosteroids in vitro.
Corticosterone inhibition of corticotrophin releasing factor release was overcome by depolarization of the membrane with K+ suggesting that the mechanism of action of the fast feedback of corticosteroids is by membrane stabilization.
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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.
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The ability of the isolated rat hypothalamus, incubated in vitro, to form and secrete corticotrophin releasing factor (CRF) has been assessed. It was found that serotonin (10 ng/ml), when added to the hypothalamus in vitro, caused the release of CRF and an increase in the activity of CRF contained in the tissue. The activity of CRF was estimated by its ability to cause the secretion of ACTH (determined by the cytochemical assay procedure) from anterior pituitary fragments in vitro. Provided a minimum of 10 min 'rest' in serotonin-free medium was allowed between each challenge with the neurotransmitter, the response of the hypothalamus in vitro was maintained for at least 3 h. A detailed examination of the time-course of CRF formation and secretion following a single addition of serotonin showed that the release was well underway within 40 s and continued up to 4 min, but then ceased. On the other hand, the tissue content of CRF was found to be reduced significantly at 20 and 40 s, had returned to basal values at 1 min and continued to increase to reach a maximum at 4 min that was maintained at 6 min. The stimulated release was approximately six times greater than basal and the increase in content approximately ten times basal. Removal of the serotonin-containing medium after 6 min of stimulation was accompanied by a precipitous fall in the CRF contained in the tissue and this was significant 2 min later with CRF content back to basal levels within 4 min. The serotonin-induced increase in CRF content was shown to be greatest in the area of the ventral portion of the medial basal hypothalamus containing the median eminence and its attendant pituitary stalk.
The energy metabolite status of the hypothalamus in vitro under the conditions employed to cause the secretion of CRF was assessed. The rates of oxygen consumption and release of lactate, and the tissue concentrations of K+ and ATP were all determined and found to be comparable to values published for more conventional cerebral slice preparations for up to 2 h in vitro. At 3 h a fall in tissue K+ and an increase in the amount of lactate released into the medium suggested that the preparation was showing signs of becoming compromised metabolically and this trend was more obvious at 4 h when the ATP level had also fallen significantly.
In more limited cognate experiments the changes in ACTH formation and release induced in anterior pituitary fragments in vitro by the addition of hypothalamic extracts were studied. Once again the release of the hormone was accompanied by an increase in the ACTH content of the tissue. The increase in content reached a maximum by 10 min and then declined to basal levels within 10 min of removal of the CRF-containing medium. Thus, it is possible that degrading enzymes play an important role in the control of hormonal output from both tissues.
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SUMMARY
RNA from the anterior hypothalamus and anterior pituitary of rats has been labelled by incubation in vitro with [3H]uridine and characterized by density gradient centrifugation. A study of normal females during the oestrous cycle showed cyclic changes in [3H]uridine incorporation into rapidly labelled RNA (rl-RNA) both in the anterior pituitary and hypothalamus. In both tissues the specific activity of RNA was low at dioestrus and high at oestrus and metoestrus. In androgenized females, incorporation into hypothalamic rl-RNA was less than the oestrus—metoestrus level and similar to that at dioestrus, while incorporation into anterior pituitary rl-RNA was similar to the oestrus—metoestrus level and greater than at dioestrus. [3H]Uridine incorporation into ribosomal RNA (r-RNA) of anterior hypothalamus and pituitary was also demonstrated by incubation for 4 h. Under these conditions there was no effect of androgenization on hypothalamic r-RNA, but the specific activity of pituitary r-RNA was greater than normal.
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SUMMARY
Two hundred rabbits aged from 0 to 21 days were used for studies of the functional activity and maturity of the thyroid and hypothalamo-hypophysial system in the newborn rabbit.
Histological findings showed that there was a rapid increase in the thyroid weight, attributed to somatic growth. The calculated relation between thyroid (Y) and body weight (X) was found to be Y = 0·3404X 0·7726.
The hormonal iodine in the blood and thyroid gland:serum radioactive concentration ratio increased with age. These variations in thyroid gland activity were paralleled by maturation of the hypothalamus (as judged from the appearance of the neurosecretory material). The supraoptic nucleihypophysial system of the rabbit appeared to be morphologically mature at about 7 days after birth.
A differentiation can be made between the 'functional development' of the thyroid gland and its 'basal growth', which is part of the general growth of the body.
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Growth hormone secretory dynamics were studied in rats sampled through chronic indwelling right atrial cannulae at time-intervals ranging from 2 days to 2 months after placing an anterolateral cut (ALC) around the medial-basal hypothalamus (MBH). The episodic secretion normally occurring in the control animals could not be seen in the rats with an ALC. Instead of the usual high bursts and low trough levels occurring between 09.00 and 13.00 h in the controls, the operated animals had fairly constant plasma GH levels with only minor fluctuations at all postoperative time-points studied. These results suggest that (1) the isolated MBH is incapable of maintaining the episodic secretion of GH and (2) the pulsatile hormone release is dependent on neural pathways entering the MBH from an anterolateral direction.
