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expression, 20-week-old male homozygous BCATm-deficient mice (KO; n =5) or WT littermates ( n =10) were rapidly killed, trunk blood was collected, and brains were isolated. Samples of mediobasal hypothalamus containing principally arcuate nucleus were
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ABSTRACT
The administration of thyrotrophin-releasing hormone (TRH) causes a variety of dopamine-related biological events. To understand the specific role of TRH on rat hypothalamic dopamine neurones, we examined the in-vivo effects of intraventricular (i.c.v.) infusion of TRH on the release and synthesis of prolactin in the rat pituitary gland and on the changes in binding of [3H]MeTRH and dopamine turnover rates in rat hypothalamus. We have also examined the in-vitro effects of TRH on the release of [3H]dopamine from dispersed tuberoinfundibular dopamine neurones.
Female rats were treated with i.c.v. infusions of 1 μmol TRH/l daily for 1, 3 and 7 days using Alzet osmotic pumps. Following 7 days of treatment the serum prolactin concentrations were significantly decreased. A reduction in hypothalamic TRH-binding sites (Bmax) was also apparent but the dissociation constant (K d) was unaffected. Northern blot analysis of total RNA isolated from the pituitary glands of control animals using 32P-labelled prolactin cDNA as a probe indicated the presence of three species of prolactin gene transcripts of approximately 3·7, 2·0 and 1·0 kb in size, and these were decreased by TRH treatment. We examined the turnover rate of dopamine in the rat hypothalamus when TRH was administered i.c.v. for 7 days. There was a significant increase in 3,4-dihydroxyphenylacetic acid/dopamine ratio with TRH treatment. Moreover, exposure to TRH stimulated [3H]dopamine release from rat tuberoinfundibular neurones in a time- and dose-dependent manner. Dopamine receptor antagonists such as SCH23390 and (−)sulpiride, and other neuropeptides such as vasoactive intestinal peptide and oxytocin did not affect TRH-stimulated [3H]dopamine release.
These data suggest that i.c.v. administration of TRH might decrease both prolactin secretion and accumulation of prolactin gene transcripts in the pituitary by stimulating dopamine release from tuberoinfundibular neurones.
Journal of Endocrinology (1992) 133, 59–66
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SUMMARY
1. The relative radioactivity of different parts of the pituitary and hypothalamus has been assessed with a flow counter, and, more satisfactorily, both visually and by granule-counts in autoradiographs. These experiments have involved 103 rats killed between 15 sec and 97 hr after the administration of 35S dl-cysteine, dl-methionine and sodium sulphate.
2. Subarachnoid injections proved more satisfactory than intraperitoneal or intracarotid ones. They were followed by the rapid localization of radioisotope in the adenohypophysis as well as in nervous tissue.
3. The early and marked uptake of radioisotope shown by the cell bodies of neurones in various nuclear regions, and in particular in the supraoptic nuclei, has been interpreted as evidence of active protein synthesis; this pattern of uptake was observed after the injection of labelled cysteine and methionine, but not sodium sulphate.
4. A similar, early, but less marked uptake of radioisotope was noted in the pars distalis after the injection of both cysteine and methionine. Only after the injection of methionine was there a marked uptake in the pars intermedia, and this was confined to its lateral border.
5. Uptake by the infundibular process of the neurohypophysis became greater than that in pars distalis or in the superjacent hypothalamus 9½ hr and longer after injection of labelled cysteine, but not methionine. This pattern of uptake was confirmed by granule counts in twenty-five animals.
6. It is suggested that the late neurohypophysial uptake of radioisotope reflects the storage in the nerve-terminals of the gland of slowly metabolizing proteins or polypeptides synthesized in the supraoptic and paraventricular nuclear regions. These substances probably include the posterior pituitary principles, since the latter are rich in cystine, but lack methionine.
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Introduction Cortisol is the primary glucocorticoid in teleosts and is released from interrenal cells (adrenal gland homolog) during stress following activation of the hypothalamus–pituitary–interrenal (HPI) axis. During stress, afferent inputs to
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ABSTRACT
We have previously reported a lack of effect of a depolarizing concentration of K+ on the release of vasoactive intestinal polypeptide (VIP) from the perifused rat hypothalamus, and suggested that this was due to the presence of an endogenous inhibitor of the release of VIP. In this study we report that the VIP response to K+ was restored if the hypothalami were obtained from animals killed during the dark phase of the light–dark cycle. Adrenaline blocked the K+-stimulated release of VIP when used at a concentration of 0·1 μmol/l; however, at a higher concentration (10 μmol/l) adrenaline stimulated the basal release of VIP. The use of specific receptor antagonists indicated that this dual effect of adrenaline was mediated through two distinct receptors, a stimulatory β-receptor and an inhibitory α2-receptor. The suggestion that adrenaline might be the endogenous inhibitor of the release of VIP, mediating the diurnal variation in the effect of K+, was supported by studies where 50 mmol K+/l was perifused concomitantly with an α2-antagonist, restoring the VIP response to K+ in light-phase hypothalami. In conclusion, adrenaline has a dual role in the control of VIP release and may function to inhibit the K+-stimulated release of VIP in our system.
J. Endocr. (1988) 116, 335–341
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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
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ABSTRACT
The present study was performed to examine the effect of the cyclo-oxygenase inhibitor, indomethacin, and that of various prostaglandins on the release of vasopressin and β-endorphin-like immunoreactivity (β-EI) from the rat neurointermediate lobe of the hypophysis, which was superfused in vitro. Indomethacin (2·8 and 28 μmol/l) changed neither basal secretion of vasopressin nor that evoked by electrical stimulation, whereas the resting release of β-EI was enhanced by indomethacin (28 μmol/l). Prostaglandin (PG) E2 did not influence resting release of vasopressin but markedly inhibited (by about 50%) electrically induced release of vasopressin (least effective concentration: 300 nmol/l) as well as spontaneous secretion of β-EI (least effective concentration: 100 nmol/l) in the presence of indomethacin (28 μmol/l). Prostaglandin F2α (5 μmol/l) also inhibited the evoked release of vasopressin, whereas PGD2 (5 μmol/l) did not. Prostaglandin F2α (5 μmol/l), D2 and I2 (1·5 μmol/l each) produced no effects on β-EI release. As observed in the neurohypophysis, PGE2 inhibited the electrically induced release of vasopressin from the medial basal hypothalamus in vitro. We conclude that prostaglandins (especially PGE2) can inhibit (1) the stimulated release of vasopressin when acting on vasopressin-containing nerve terminals of either neurosecretory system (neurohypophysis, median eminence region), and (2) the secretion of β-EI and, as can be inferred, α-MSH, by a direct action on intermediate lobe cells.
J. Endocr. (1985) 106, 189–195
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SUMMARY
Thirty ewes with regular oestrous cycles were divided into six groups for slaughter relative to the time of first acceptance of the ram. The slaughter times were: 0 h (in practice within 40 min of onset of oestrus), 6, 12 and 36 h after onset and days 10 and 16 of the cycle. The hypothalamus was removed and the luteinizing hormone (LH) releasing factor activity extracted with 0·1 m-HCl. The extracts were tested for LH releasing activity by adding them to the medium in which anterior pituitary tissue from castrated male sheep was incubated. The LH content of the medium was measured by the ovarian ascorbic acid depletion method (Parlow, 1958).
The activity of the extract from the group slaughtered on day 16 of the cycle was high (minimal effective dose (MED) = 0·00625 hypothalamic equivalents (HE)). The potency declined with the onset of oestrus and remained low at 6 and 36 h after onset (MED in each case 0·025 HE) with intermediate potencies at 12 h and 10 days after onset (MED in each case 0·0125 HE). These changes are compared with changes in the LH content of the pituitary gland (bioassay) and of the plasma (radioimmunoassay) and with parameters of the ovarian activity of the animals.
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SUMMARY
The effect of incubating the hypothalamus of adult male rats with various neurotransmitters upon the release of corticotrophin-releasing hormone (CRH) was studied. The CRH activity in the incubation medium was assayed in 48 h median eminence-lesioned rats and the corticosteroidogenesis of excised adrenals in vitro was used as the end-point. 5-Hydroxytryptamine (100 pg/ml–10 ng/ml) caused a dose-dependent release of CRH which was antagonized by methysergide (30–100 ng/ml). The response to 5-hydroxytryptamine was also inhibited by hexamethonium and atropine which indicated that it was acting through a cholinergic interneurone. Melatonin (10 ng) did not alter the basal release of CRH but inhibited the action of both 5-hydroxytryptamine (10 ng) and acetylcholine (3 pg). Thus it appears that both 5-hydroxytryptamine and melatonin play a role in the control of CRH release. Noradrenaline blocked the release of CRH induced by both acetylcholine and 5-hydroxytryptamine and presumably this inhibition was caused by direct action on the CRH neurone. γ-Aminobutyric acid (GABA) also inhibited the release of CRH and may also be involved in the regulation of CRH secretion. The inhibitory neurotransmitters, noradrenaline, GABA and melatonin, act via independent receptor mechanisms. A model based on the above data is presented.
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SUMMARY
The frequency characteristics of the neuronal activity in the hypothalamus, septum and preoptic area of the forebrain were recorded with stereotaxically orientated steel microelectrodes in adult female rats under light urethane anaesthesia.
An exponential type of relationship was observed between the mean discharge rate of units and the frequency with which they were encountered in all areas. Thus, 40–60 % of units had firing rates of less than 1 spike/sec. and only 10–15% had rates exceeding 6/sec. However, units with a mean discharge rate of 2–4/sec. contributed most to the total spike activity. The form of the interspike interval distributions was found to vary with mean firing rate, and the variability of the interspike interval decreased as the firing rate of the unit increased.
The levels of 'spontaneous' activity in the anterior hypothalamic, preoptic and septal areas of rats with light-induced persistent oestrus were lower than those observed after ovariectomy. The administration of 10 μg. oestradiol benzoate/day to the ovariectomized animals depressed the levels of activity towards those observed in the persistently oestrous animals. Reciprocal effects were observed in the lateral hypothalamic area, i.e. decreased activity in the ovariectomized rats.
The results are discussed in relation to unit recording procedures and the feedback effects of oestrogen.
