Corticotrophin-releasing factor-41, vasopressin and oxytocin release into hypophysial portal blood in the rat: effects of electrical stimulation of the hypothalamus, amygdala and hippocampus

1991 ◽  
Vol 129 (1) ◽  
pp. 99-107 ◽  
Author(s):  
L. A. Tannahill ◽  
W. J. Sheward ◽  
I. C. A. F. Robinson ◽  
G. Fink
Keyword(s):  
Electrical Stimulation ◽  
Plasma Concentrations ◽  
Direct Proof ◽  
Brain Regions ◽  
Portal Blood ◽  
Male Rats ◽  
Unilateral Stimulation ◽  
Oxytocin Release ◽  
Hypophysial Portal ◽  
Stimulation Of

ABSTRACT The role of the paraventricular nuclei (PVN), amygdala and hippocampus in the control of the hypothalamic-pituitary-adrenal axis has been studied by determining the effect of electrical stimulation of the PVN, amygdala and hippocampus on the release of corticotrophin-releasing hormone (CRF-41) and arginine vasopressin (AVP) into hypophysial portal blood and ACTH and corticosterone into peripheral blood. Adult female Wistar rats were anaesthetized with sodium pentobarbitone and stimulation was carried out through previously implanted bipolar, glass-insulated platinum electrodes. Hypophysial portal blood was collected 30 min before and 30 min during the application of the stimulus which consisted of trains (30 s on and 30 s off) of biphasic rectangular pulses with a frequency of 50 Hz, pulse width 1 ms and amplitude 1 mA. Bilateral stimulation of the PVN increased while unilateral stimulation of the amygdala decreased the release of CRF-41 into hypophysial portal blood. The threefold increase in release of CRF-41 induced by PVN stimulation correlated with a marked increase in peripheral plasma concentrations of ACTH and corticosterone. Stimulation of the hippocampus had no significant effect on CRF-41 release, and stimulation of each of the three brain regions had no effect on AVP release into portal blood. These findings were extended in a second study to compare the effects of unilateral bipolar electrical stimulation of the PVN and of the supraoptic nucleus (SON) on the release of CRF-41, AVP and oxytocin. This study was carried out on adult male rats, anaesthetized with sodium pentobarbitone, in which the stimulus was applied through previously implanted concentric stainless-steel electrodes. Unilateral stimulation of the PVN resulted in a significant increase in the release of CRF-41 and a massive increase in oxytocin release into portal blood. Increased release of oxytocin also occurred after unilateral stimulation of the SON, but CRF-41 secretion was unaffected. The secretion of AVP was unaffected by electrical stimulation of either the SON or PVN. These results (i) provide the first direct proof for the fact that the PVN is the major source of CRF-41 in hypophysial portal blood, and (ii) suggest that the release of CRF-41 may be inhibited by the amygdala. Journal of Endocrinology (1991) 129, 99–107

Concentrations of dopamine and noradrenaline in hypophysial portal blood in the sheep and the rat

1989 ◽  
Vol 121 (1) ◽  
pp. 141-147 ◽  
Author(s):  
G. B. Thomas ◽  
J. T. Cummins ◽  
G. A. Smythe ◽  
R. M. Gleeson ◽  
R. C. Dow ◽  
...  
Keyword(s):  
Plasma Concentrations ◽  
Portal Blood ◽  
Female Rats ◽  
Male Rats ◽  
Gas Chromatography Mass Spectrometry ◽  
Intact Male ◽  
Peripheral Plasma ◽  
Portal Plasma ◽  
Urethane Anaesthesia ◽  
Hypophysial Portal

ABSTRACT The concentrations of dopamine, noradrenaline and their respective primary neuronal metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and 3,4-dihydroxyphenylethyleneglycol (DHPG) were measured in the hypophysial portal and peripheral plasma of sheep and rats by combined gas chromatography–mass spectrometry. Hypophysial portal and jugular blood samples were taken at 5- to 10-min intervals for 3–7 h from six conscious ovariectomized ewes. Blood was also collected for 30 min under urethane anaesthesia from the cut pituitary stalk from 16 pro-oestrous female and five intact male rats. In ovariectomized ewes, noradrenaline concentrations were higher in hypophysial portal plasma than in peripheral plasma (6·6 ± 0·8 vs 2·2 ± 0·4 nmol/l). In contrast, dopamine was undetectable (<1 nmol/l) in the portal and peripheral plasma of all ewes. Plasma levels of DOPAC and DHPG in portal and jugular samples were similar. In all pro-oestrous female rats, plasma concentrations of dopamine were higher in portal blood than in jugular blood (8·0±1·4 vs 4·8± 0·6 nmol/l). Detectable concentrations of dopamine were measured in the portal plasma of two out of five male rats. Noradrenaline concentrations were higher in portal plasma than in peripheral plasma of both female (8·3 ± 1·7 vs 3·7 ± 0·6 nmol/l) and male (14·8± 2·7 vs 6·1± 1·2 nmol/l) rats. These data show that noradrenaline, but not dopamine, is secreted into the long portal vessels in sheep. The results suggest that there are species differences in the secretion of hypothalamic dopamine into hypophysial portal blood. Journal of Endocrinology (1989) 121, 141–147

Vasoactive intestinal peptide in rat hypophysial portal blood: effects of electrical stimulation of various brain areas, the oestrous cycle and anaesthetics

1985 ◽  
Vol 106 (3) ◽  
pp. 275-280 ◽  
Author(s):  
A. K. Brar ◽  
G. Fink ◽  
M. Maletti ◽  
W. Rostene
Keyword(s):  
Electrical Stimulation ◽  
Vasoactive Intestinal Peptide ◽  
Peripheral Blood ◽  
Oestrous Cycle ◽  
Portal Blood ◽  
Female Rats ◽  
Female Wistar Rats ◽  
Consistent Increase ◽  
Hypophysial Portal ◽  
Stimulation Of

ABSTRACT Vasoactive intestinal peptide (VIP) was measured by radioimmunoassay in hypophysial portal and peripheral blood from adult male and female Wistar rats. The results confirmed that the concentration of VIP in hypophysial portal blood was significantly greater than in peripheral blood and showed that VIP release into portal blood was not affected by removal of the gut, the largest peripheral source of VIP. Electrical stimulation of the median eminence, several hypothalamic nuclei, the amygdala or hippocampus had no significant effect on the release of VIP into portal blood, possibly because under the conditions of the experiment the spontaneous release of VIP is already at a maximum. In female rats, the VIP released into portal blood collected between 13.00 and 18.30 h of each day of the 4-day oestrous cycle varied under different anaesthetics, and there was no consistent increase in VIP release on pro-oestrus suggesting that VIP is not involved in the pro-oestrous surge of prolactin. J. Endocr. (1985) 106, 275–280

Oxytocin and vasopressin in rat hypophysial portal blood: experimental studies in normal and Brattleboro rats

1985 ◽  
Vol 104 (2) ◽  
pp. 211-NP ◽  
Author(s):  
A. M. Horn ◽  
I. C. A. F. Robinson ◽  
G. Fink
Keyword(s):  
Electrical Stimulation ◽  
Peripheral Blood ◽  
Wistar Rats ◽  
Plasma Concentrations ◽  
Portal Blood ◽  
Brattleboro Rats ◽  
External Layer ◽  
Portal Plasma ◽  
Hypophysial Portal ◽  
Uptake Blockers

ABSTRACT Oxytocin (OT) and vasopressin (VP) were measured by radioimmunoassay in hypophysial portal and peripheral blood from male Wistar rats and heterozygous and homozygous Brattleboro rats anaesthetized with urethane. In Wistar rats the concentrations of OT and VP were about 50 times greater than the concentrations in peripheral blood, whether or not the pituitary gland was left in situ during collection, and also considerably greater than the reported concentrations of the peptides in the cerebrospinal fluid. The release of both peptides was increased significantly by a lesion of the supraoptico-hypophysial tract that led to diabetes insipidus, but which left intact the external layer of the median eminence (ME). Concentrations of VP were undetectable in plasma from homozygous Brattleboro rats, but the portal plasma concentrations of VP in heterozygous Brattleboro rats were not significantly lower than in Wistar rats. The concentrations of OT in portal plasma from both types of Brattleboro rat were significantly higher than in Wistar rats. The output of VP and OT into hypophysial portal blood of Wistar rats was not significantly affected by electrical stimulation of the suprachiasmatic, supraoptic or paraventricular nuclei or the ME using two types of stimuli, one of which produced an increase in peripheral plasma concentrations of VP and OT in intact rats and a significant increase in the release of LH-releasing hormone into hypophysial portal blood. The output of VP and OT into portal blood was also not significantly affected by either adrenalectomy with or without injection of dexamethasone or the injection of either the 5-hydroxytryptamine (5-HT) synthesis blocker, parachlorophenylalanine, or the 5-HT uptake blockers, alaproclate or zimelidine. These results show that large amounts of OT as well as VP are released into hypophysial portal blood from fibres of the hypothalamo-neurohypophysial system that terminate in the external layer of the ME. Although distinct from the fibres that terminate in the pars nervosa (PN), the findings in Brattleboro rats show that the VP fibres of the ME system originate in neurones with a genomic mechanism for VP synthesis similar to that of the VP neurones that project to the PN. The lack of effect of adrenalectomy and the administration of 5-HT synthesis and uptake blockers must be interpreted with caution since the results obtained with electrical stimulation suggest that when the pituitary stalk is cut the release of OT and VP into portal blood approaches a maximum and may therefore be difficult to alter by experimental manipulation. The concentrations of OT and VP in portal blood are sufficiently high for these peptides to play a significant role in neural control of the anterior pituitary gland. J. Endocr. (1985) 104, 211–224

Hypothalamic release of atrial natriuretic factor and β-endorphin into rat hypophysial portal plasma: relationship to oestrous cycle and effects of hypophysectomy

1991 ◽  
Vol 131 (1) ◽  
pp. 113-125 ◽  
Author(s):  
W. J. Sheward ◽  
A. Lim ◽  
B. Alder ◽  
D. Copolov ◽  
R. C. Dow ◽  
...  
Keyword(s):  
Plasma Concentrations ◽  
Portal Blood ◽  
Female Rats ◽  
Male Rats ◽  
Blood Collection ◽  
Peripheral Plasma ◽  
Portal Plasma ◽  
Hypophysectomized Rats ◽  
Hypophysial Portal

ABSTRACT The release of β-endorphin and atrial natriuretic factor (ANF) into hypophysial portal plasma was investigated in male and female Wistar rats. The principal aim of the study was to investigate the possible role of β-endorphin and ANF in the hypothalamic control of LH and prolactin secretion. In male rats, anaesthetized with urethane, the concentrations of β-endorphin in portal blood collected immediately after hypophysectomy were within the same range as those in peripheral plasma. Furthermore, electrical stimulation of the median eminence did not increase the portal plasma concentrations of β-endorphin. In female rats, anaesthetized with alphaxalone, the portal plasma concentrations in long-term (6–8 weeks) or acutely hypophysectomized rats were significantly greater than those in peripheral plasma. In acutely hypophysectomized female rats the concentrations and contents of β-endorphin in portal plasma collected at 10.00–11.30 h of pro-oestrus were significantly (approximately sixfold) greater than at dioestrus or at 20.00–21.00 h of pro-oestrus, but these changes were not consistently seen in all experiments. In female rats in which the pituitary gland was not removed for portal blood collection, portal plasma contents of ANF remained unchanged throughout the day of pro-oestrus, suggesting that it is unlikely that ANF is involved in the spontaneous LH or prolactin surge. The effects of ovarian steroids on the secretion of hypothalamic ANF and β-endorphin were determined by measuring the portal plasma concentration of ANF and β-endorphin on the morning of presumptive pro-oestrus in rats ovariectomized 24 h previously and injected with either oil or oestradial benzoate (OB). Portal plasma contents of ANF were significantly lower in OB- compared with oil-treated rats, suggesting that oestradiol inhibits ANF release into rat hypophysial portal plasma. In contrast, there were no significant between-group differences in the content or concentration of β-endorphin in portal plasma. Thus, the increased β-endorphin in the portal plasma of some of the intact animals during the morning of pro-oestrus is not due to the preovulatory surge of oestradiol-17β. The output of β-endorphin into portal blood in long-term hypophysectomized rats was lower than in dioestrous or pro-oestrous rats in which the pituitary gland was removed immediately before portal blood collection. Taken together, these results suggest that β-endorphin release into portal plasma may depend upon normal physiological levels of pituitary and pituitary-dependent hormones in the circulation, and that β-endorphin release into portal blood is not controlled by short- or long-loop negative feedback. In sum, these data confirm that in adult female rats, ANF and β-endorphin are released into hypophysial portal plasma and show (i) that the secretion of ANF, but not of β-endorphin, can be affected by oestradiol, (ii) that the concentrations of ANF in portal plasma are sufficient to affect the release of pituitary hormones but are not related to plasma concentrations of LH and prolactin during the afternoon of pro-oestrus, (iii) that whilst there is no simple inverse relationship between βendorphin overflow into portal plasma and LHRH secretion, the increased release of β-endorphin during the morning of pro-oestrus may be consistent with a role for this peptide in triggering the pro-oestrous surge of pro-lactin, and (iv) that a sex difference in β-endorphin release into portal plasma is suggested by the absence of β-endorphin in the portal plasma of male rats. Journal of Endocrinology (1991) 131, 113–125

Enhancement of Immunoreactive Somatostatin Release into Hypophysial Portal Blood by Electrical Stimulation of the Preoptic Area in the Rat*

Endocrinology ◽  
1979 ◽  
Vol 105 (6) ◽  
pp. 1416-1418 ◽  
Author(s):  
KAZUO CHIHARA ◽  
AKIRA ARIMURA ◽  
CARLOS KUBLI-GARFIAS ◽  
ANDREW V. SCHALLY
Keyword(s):  
Electrical Stimulation ◽  
Preoptic Area ◽  
Portal Blood ◽  
Hypophysial Portal ◽  
Stimulation Of

OVULATORY DISCHARGE OF GONADOTROPHINS INDUCED BY HYPOTHALAMIC STIMULATION IN CASTRATED MALE RATS BEARING A TRANSPLANTED OVARY

1966 ◽  
Vol 51 (2) ◽  
pp. 281-289 ◽  
Author(s):  
J. Moll ◽  
G. H. Zeilmaker
Keyword(s):  
Electrical Stimulation ◽  
Preoptic Area ◽  
Hypothalamic Stimulation ◽  
Male Rats ◽  
Corpora Lutea ◽  
Histological Changes ◽  
Experimental Animals ◽  
Cumulus Oophorus ◽  
Dc Current ◽  
Stimulation Of

ABSTRACT Castrated young adult inbred male rats bearing ovarian transplants were subjected to electrical stimulation of the hypothalamus. This was done in order to investigate whether discharge of ovulatory amounts of gonadotrophins could be induced in such male animals by this procedure. Bilateral stimulations with unipolar electrodes and a DC current of 1.5 mA applied during 10 seconds induced in the ovarian grafts histological changes indicating the discharge of ovulatory amounts of gonadotrophins. In animals killed one day after stimulation these changes consisted of displacement of the ova towards the centre of the follicles with loosening of the cumulus oophorus. In one animal the ova had left the follicles. In animals killed three days after stimulation numerous young corpora lutea could be observed. These results were obtained with electrode tips either close to the median eminence, or in the preoptic area. Shamstimulations were ineffective. Some of the experimental animals received progesterone pretreatment. This rendered the stimulations ineffective, if continued until the day preceding stimulation, but seemed without effect on the results of stimulation, if two or three days without progesterone preceded the stimulations.

Facilitation of female reproductive behavior from mesensephalic central gray in the rat

1979 ◽  
Vol 237 (5) ◽  
pp. R278-R284 ◽  
Author(s):  
Y. Sakuma ◽  
D. W. Pfaff
Keyword(s):  
Electrical Stimulation ◽  
Mesencephalic Reticular Formation ◽  
Female Rats ◽  
Motor Systems ◽  
Functional Link ◽  
Implanted Electrodes ◽  
Unilateral Stimulation ◽  
Postural Changes ◽  
Central Gray ◽  
Stimulation Of

Electrical stimulation in the mesencephalic central gray (CG) and adjacent subtectum through chronically implanted electrodes in free-moving estrogen-primed ovariectomized female rats elicited a rapid and large facilitation of the lordosis reflex in response to either male mounts or manula cutaneous stimuli. Unilateral stimulation was sufficient for this effect. The facilitation increased in a graded manner to increased stimulus intensity, and was optimally evoked by stimuli delivered at 50--150 Hz. Facilitation disappeared rapidly following the end ot electrical stimulation, and within 15 min, reflex performance returned to the prestimulation level. Lordosis facilitation appeared when no aversive responses occurred; stimulation with comparable parameters at the lateral edge of CG or in the mesencephalic reticular formation often resulted in postural changes or aversive responses but was not able to facilitate lordosis. Lordosis refelx facilitation was probably mediated by projections descending from neurons in and around the CG, and represents stimulation of a functional link between ascending somatosensory and descending motor systems for the control of lordosis behavior.

The release of catecholamines from the adrenal medulla and its modulation by α2-adrenoceptors in the anaesthetized dog

1987 ◽  
Vol 65 (4) ◽  
pp. 550-557 ◽  
Author(s):  
Sylvain Foucart ◽  
Réginald Nadeau ◽  
Jacques de Champlain
Keyword(s):  
Electrical Stimulation ◽  
Adrenal Medulla ◽  
Plasma Concentrations ◽  
Splanchnic Nerve ◽  
Feedback Mechanism ◽  
Adrenal Vein ◽  
Low Frequencies ◽  
Negative Feedback Mechanism ◽  
Frequency Of Stimulation ◽  
Stimulation Of

The adrenal nerve of anaesthetized and vagotomized dogs was electrically stimulated (10 V pulses of 2 ms duration for 10 min) at frequencies of 1, 3, 10, and 25 Hz. There was a correlation between the frequency of stimulation and the plasma concentrations of epinephrine, norepinephrine, and dopamine in the adrenal vein, mainly after the 1st min of stimulation and the maximal concentration was reached sooner with higher frequencies of stimulation. Moreover, the relative percentage of catecholamines released in response to the electrical stimulation was not changed by the frequency of stimulation. To test the hypothesis that a local negative feedback mechanism mediated by α2-adrenoceptors exists in the adrenal medulla, the effects of the systemic administration of clonidine (α2-agonist) and yohimbine (α2-antagonist) on the concentrations of catecholamines in the adrenal vein were evaluated during the electrical stimulation of the adrenal nerve (5 V pulses of 2 ms duration for 3 min) at 3 Hz. Moreover, the effects of the systemic injections of more specific α2-agonist and antagonist (oxymetazoline and idazoxan) were tested on the release of catecholamines in the adrenal vein in response to electrical stimulation of the splanchnic nerve at 1 and 3 Hz frequencies. The injection of 0.5 mg/kg of yohimbine caused a significant increase in the concentrations of epinephrine and norepinephrine in the adrenal vein induced by the electrical stimulation of the adrenal nerve and the injection of 15 μg/kg of clonidine had no effects. In the second series of experiments, the injection of 2 μg/kg of oxymetazoline caused a significant decrease in the release of epinephrine and norepinephrine at 1 Hz, but similarly to clonidine, there were no changes at 3 Hz. In contrast, the release of epinephrine and dopamine in response to electrical stimulation of the splanchnic nerve was increased at 3 Hz after the injection of idazoxan, but not at 1 Hz. It is concluded that the adrenal medulla catecholamines secretion appears to be partly modulated by a presynaptic inhibitory mechanism that involves α2-adrenoceptors. The observation that agonists appear to be more efficient at low frequencies of stimulation while antagonists appear to be more efficient at higher frequencies could be explained by the possibility that adrenal medullary α2-receptors would be saturated at higher frequencies of stimulation.

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