摘要:

Effects of the centrally acting α-adrenergic agonist, clonidine, on growth hormone (GH) secretion was studied in conscious male rats pretreated with monosodium glutamate (MSG) during the neonatal period. GH secretory profiles in individual adult rats were obtained by repeated blood samplings every 10–20 min from 10.00 to 17.00 h. GH secretion was pulsatile with mean peak values at around 12.40 and 15.20 h in control rats. When clonidine (15 µg/100 g body weight) was injected intravenously into control rats at 14.00 h in the interval between two anticipated spontaneous GH bursts, plasma GH was increased with a mean peak value 20 min after the injection, and the following anticipated spontaneous GH burst was not observed during the experiment. In the rats neonatally treated with MSG (4 mg/g body weight, s.α), which causes selective destruction of the hypothalamic arcuate nucleus, plasma GH response to clonidine as well as the spontaneous GH bursts were considerably blunted, whereas prostaglandin Ei (5 µg/100 g body weight, i.v.) caused an abrupt increase in plasma GH levels in these animals. These results suggest that clonidine stimulates rat GH secretion, possibly by acting within the hypothalamus to stimulate GH releasing factor ne

ISSN:0028-3835    

DOI:10.1159/000123857

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The neurotransmitter and andrenoceptors involved in the inhibition of luteinizing hormone (LH) release induced by stimulating the locus ceruleus nucleus (LC) have been characterized in ovariectomized, estrogen-primed rats in which the release of LH was triggered by electrical stimulation of the medial preoptic area. Blockade of norepinephrine synthesis by the injection of the dopamine β-hydroxylase inhibitors, diethyldithiocarbamate or fusaric acid, prevented the inhibition of LH release, whereas blockade of epinephrine synthesis by injecting the phenylethanolamine N-methyltransfe-rase inhibitor, 2,3-dichloro-methylbenzylamine, had no effect. In addition, the inhibition of LH release was prevented by systemic injection of propranolol but not of phenoxybenzamine. This inhibition was also suppressed in rats in which the ventral premammillary (PM) nucleus ipsilateral to the stimulated LC was lesioned, or in animals with a transverse cut placed just in front of the PM. A similar response was seen in rats in which propranolol but not phenoxybenzamine was applied to the PM ipsilateral to the stimulated LC. The present results indicate that norepinephrine, acting through β-adreno-ceptors mediates the transmission of impulses which, originating in the LC, inhibit the release of LH. The LC adrenergic fibers synapse in the PM before the neural information they convey is transfered to the gonadotropin-releasing hormone containing neuron

ISSN:0028-3835    

DOI:10.1159/000123858

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Lesions of the medial preoptic area (MPOA) induce nocturnal prolactin surges similar to those initiated by cervical stimulation (CS). These same lesions can abolish diurnal prolactin surges previously initiated by CS. Based on these results the MPOA has been suggested to contain two functionally dissimilar sets of neurons, one inhibitory for the nocturnal surge and the other stimulatory for the diurnal surge. The present study sought to demonstrate the existence of these neural elements by electrically stimulating the MPOA of conscious ovariectomized female rats during those times of day when these neurons would be most active. Serial blood samples were collected via cannula before, during and after the stimulation. Stimulation of the MPOA (01.00–05.00 h) on day 2 after CS inhibited the nocturnal surge of prolactin while sham MPOA stimulation of CS females did not disturb the nocturnal surge. MPOA stimulation in non-CS females had no effect upon prolactin secretion. Application of MPOA stimulation (15.00–19.00 h) to CS females also suppressed the diurnal surge of prolactin. Sham-stimulated CS females, however, secreted a diurnal surge peaking at 17.00 h. Basal prolactin levels were unaffected by MPOA stimulation (15.00–19.00 h) in non-CS females. The results from these experiments suggest that the MPOA contains neurons inhibitory for both the nocturnal and diurnal prolactin surges. In a further attempt to show a stimulatory role for the MPOA in prolactin regulation, MPOA stimulation was applied (15.00–19.00 h) to pentobarbital anesthetized non-CS females. Pentobarbital treatment allowed the MPOA stimulation to trigger two prolactin peaks, one at 16.00 h and the other at 19.00 h. The anesthesia did not alter prolactin release in the sham controls. From these stimulation studies and previous lesion experiments we conclude that the MPOA exerts monophasic inhibitory control over the nocturnal prolactin surge and biphasic, stimulatory and inhibitory control over the diurnal prolactin surge. CS must then act upon the MPOA to depress its inhibitory and activate its stimulatory elements for the secretion of the nocturnal and diurnal surges of prolactin t

ISSN:0028-3835    

DOI:10.1159/000123859

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Extracts of rat stalk-median eminences were chromatographed on Sephadex G-50 and BioGel P2. Effluent fractions were monitored for corticotrophin-releasing factor (CRF) bioactivity, using the perfused isolated pituitary cell column bioassay, and radioimmunoassay for CRF-41, AVP, oxytocin, neurophysin, adrenocorticotrophic hormone (ACTH) and luteinizing hormone-releasing hormone (LHRH). Porcine hypothalami were also chromatographed on Sephadex G-50. Our results suggest that vasopressin and a peptide in the rat related to synthetic ovine CRF are two components of the hypothalamic CRF complex which potentiate each other at the corticotrope to release ACTH. However, these two substances alone do not appear to be wholly responsible for CRF bioactivity of hypothalamic stalk-median eminence extracts and other CRFs may yet be found.

ISSN:0028-3835    

DOI:10.1159/000123860

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Controversy exists concerning the possible involvement of serotonin (5-HT) in the pituitary-adrenocortical response to stress. In the present research, a variety of pharmacological and physiological manipulations were used in male rats to study the role of this neurotransmitter in the adrenocortical response to insulin-induced hypoglycemia. We first examined the effect of insulin stress on hypothalamic 5-HT metabolism and found increased turnover as determined by an enhanced accumulation of 5-HT following monoamine oxidase inhibition. Brain 5-HT depletion by intraventricular injection of 5,7-dihydroxytryptamine significantly attenuated the corticosterone response to insulin, while treatment with the 5-HT receptor blocker methysergide tended to have the same effects. The corticosterone response to insulin was potentiated by prior administration of L-tryptophan, and blocked by pretreatment with valine, an amino acid that competes with tryptophan for transport across the blood-brain barrier. It therefore appears that the pituitary-adrenal response to insulin is mediated at least in part by 5-HT, and may be dependent on increased uptake of tryptophan by the brain.

ISSN:0028-3835    

DOI:10.1159/000123861

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Measurements of serum corticosterone taken at three times in the diurnal cycle (08.00, 18.00, and 23.30 h) showed that aged male Sprague-Dawley rats have higher nonstressed circulating levels at two time points measured. To determine if such elevated levels of steroids were sufficient to interfere with lesion-induced sprouting, the corticosterone peak at 18.00 h of either aged or young adult animals was maintained in young adrenalectomized rats by use of subcutaneous corticosterone pellets. The normal young adult animal levels resulted in mild suppression of the adrenergic sprouting response seen in hippocampus following transection of the fimbria-fornix. Young animals maintained at the elevated corticosterone levels of normal senescent rats had marked suppression of sprouting. The levels of circulating glucocorticoids reached by aged rats are sufficient to retard sprouting, and may therefore interfere with synaptic turnover and the response of the senescent brain to damage.

ISSN:0028-3835    

DOI:10.1159/000123862

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The binding of [3H]-spiperone to partially purified rat anterior pituitary plasma membranes was quantified throughout the estrous cycle in relation with the serum prolactin (PRL) levels. Receptor affinity remained unchanged throughout the cycle (Kd: 0.08–0.16 nM). The number of receptors was constantly high from diestrus I 10.30 h to proestrus 10.30 h, as long as serum PRL remained low. Between 10.30 and 17.30 h on proestrus, there was a rapid and marked decrease in receptor numbers (Bmax, from 180 ± 50 to 48 ± 10 fmol/mg protein: means ± SEM of three independent determinations), which coincided with the preovulatory PRL surge. Subsequently, [3H]-spiperone binding gradually increased (from 48 ± 10 to 110 ± 21 fmol/mg protein, at 21.30 h), while PRL returned to basal levels. On the afternoon of estrus, the number of dopamine receptors was also negatively correlated with the increase in serum PRL. These results show that, while receptor affinity is constant, the number of dopamine binding sites changes significantly and rapidly on the afternoon of proestrus. A rapid decrease in receptor content is temporally correlated with the onset of the preovulatory PRL surge. Therefore, the number of [3H]-spiperone binding sites may be regulated during the estrous cycle. In addition, the proestrus decrease in the number of these receptors might be a decisive component in the initiation or maintenance of the preovulatory PRL surge in t

ISSN:0028-3835    

DOI:10.1159/000123863

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The regional distribution of pro-opiocortin-derived peptides and methionine enkephalin was investigated in human brain post-mortem. Sequence-directed radioimmunoassays for β-endorphin, γ-lipotropin, adrenocorticotrophin, corticotrophin-like intermediate lobe peptide (ACTH18–39, CLIP) α-MSH and methionine enkephalin were used and 40 different human brain areas were assayed. The regional distribution of all the pro-opiomelanocortin-derived immunoreactivi-ties were correlated with highest amounts of β-endorphin, γ-lipotropin and ACTH in the hypothalamus, amygdala, peri-ventricular grey, substantia nigra and superior colliculus. The distribution of β-endorphin, γ-lipotropin and ACTH did not parallel the distribution of methionine-enkephalin immunoreactivity which was present in the globus pallidus, nucleus accumbens and substantia nigra. Gel exclusion chromatography (G-50) showed that pro-opiocortin-related peptides in the human hypothalamus and periventricular grey separated in positions consistent with the major immunoreactive forms being β-endorphin, γ-lipotropin, ACT

ISSN:0028-3835    

DOI:10.1159/000123864

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The synthesis and release of dopamine within tuberoinfundibular neurons were studied in rats treated with reserpine and/or pargyline. The effect of reserpine to elevate the serum concentration of prolactin was accompanied by a 70–80% reduction in the concentration of dopamine in pituitary stalk plasma. When rats were given pargyline (75 mg/kg) prior to the administration of reserpine (2.5 mg/kg), the reserpine-induced alterations in serum prolactin and stalk plasma dopamine concentrations were completely prevented. Pargyline treatment alone resulted in a significant elevation of the concentration of dopamine in pituitary stalk plasma and a reduction in the serum concentration of prolactin. The effects of reserpine and pargyline on the synthesis of dopamine in the median eminence were found to be the opposite of their effects on the release of dopamine. Dopamine synthesis (as estimated by the accumulation of dihydroxyphenylalanine after inhibition of decarboxylase activity) was increased after reserpine and decreased after pargyline administration. Thus, these data serve to illustrate the point that, under certain conditions, the release of dopamine from tuberoinfundibular neurons can be dissociated from its rate of synthesis. More importantly, it appears the release of dopamine from these neurons is dependent upon intact dopamine storage function and monoamine oxidase activity, in addition to continued catecholamine synthesi

ISSN:0028-3835    

DOI:10.1159/000123865

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The potential involvement of the endogenous opioid and dopamine (DA) systems in the mechanism(s) mediating arginine vasotocin (AVT)- and arginine vasopressin (AVP)-induced prolactin (PRL) release was investigated in vivo. The injection of AVT (5 µg) into unanesthetized male rats resulted in a 2-fold stimulation of PRL release 15 min later, followed by an inhibition of PRL release 30 min thereafter; both the stimulatory and inhibitory PRL responses to AVT were obviated by naloxone (NAL) (200 µg). Similarly, the administration of either AVT or AVP (5 µg) to urethane-anesthetized rats led to a 3- and 5-fold increase in plasma PRL levels, respectively, 10 min after injection. The PRL stimulatory response to both peptides was completely blocked by pretreating the animals with apomorphine (APO) (5 mg); however, the injection of APO by itself had no effect on PRL secretion in these animals. Both AVT and AVP were also effective in stimulating PRL release 10 min after injection in estrogen (50 µg)-progesterone (25 mg) (EP)-treated rats anesthetized with urethane. APO negated the PRL stimulatory response to these compounds in the EP-treated rat as well. Normal, urethane-treated rats experienced a 7- to 8-fold increase in PRL levels 20 min following the injection of methysergide (MET) (250 µg). Both AVT and AVP caused approximately a 2.5-fold greater PRL response in MET-treated animals than in AVT and AVP controls, respectively; however, only in the MET + AVT-treated rats was the PRL stimulatory response greater than in the MET controls. MET probably stimulated PRL through its DA antagonistic properties. It appears that AVT may stimulate PRL release in vivo via the endogenous opioid system. Furthermore, the mechanism(s) mediating the PRL stimulatory action of both AVT and AVP may also involve an inhibition of hypothalamic DA rel

ISSN:0028-3835    

DOI:10.1159/000123866

出版商:S. Karger AG    

年代:1984

数据来源: Karger