摘要:

The effects of pretreatment with drugs on drug-induced yawning and penile erection in intact and chronically castrated rats were investigated. Naloxone partially blocked yawning in intact rats and in castrated rats pretreated with dihydro-testosterone propionate (DHTP) but not in control castrates. In contrast, naloxone potentiated apomorphine-induced penile erections in intact rats. Morphine, haloperidol and atropine blocked yawning and penile erections. Methyl naloxone, methyl atropine and domperidone at doses which are selectively peripheral-acting had no effect on drug-induced yawning or penile erection indicating that both effects are mediated centrally. Pretreatment with morphine did not change the naloxone effects in intact rats. The results indicate a naloxone-androgen interaction in drug-induced yawning but the results with morphine are not consistent with a role of opiates in this interaction. The penile erection data support a direct opiate-dopamine receptor interaction in this response. The haloperidol and atropine effects support a cholinergic-dopaminergic interaction in both yawning and penile erections.

ISSN:0028-3835    

DOI:10.1159/000124438

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Serotonin and dopamine neurons have been shown to exert a stimulatory and inhibitory control, respectively, over pituitary release of β-endorphin-like immunoreactivity (β-END-LI). In the present study we sought to determine whether an interaction exists between these two reciprocal mechanisms regulating β-END-LI in the rat. The intraperitoneal (i.p.) administration of 5 mg/kg quipazine, a serotonin receptor agonist, or 2.5 mg/kg haloperidol, a dopamine receptor antagonist, each elevated circulating levels of β-END-LI 5-fold over control levels by 30 min post-injection. Pretreatment (1 h) with 5 mg/kg, i.p., cinanserin, a serotonin receptor antagonist, completely blocked the quipazine-induced rise in β-END-LI without affecting the elevated levels of β-END-LI in haloperidol-treated animals. Conversely, pretreatment (2 h) with 1 mg/kg, i.p., bromocriptine, a dopamine receptor agonist, had no effect on quipazine-induced release of β-END-LI but did completely prevent the rise in plasma β-END-LI due to haloperidol treatment. Gel filtration chromatography revealed that quipazine and haloperidol treatments elevated plasma levels of both β-END-size immunoreactivity and β-lipotropin (β-LPH)-sized immunoreactivity though to different relative degrees. However, since circulating levels of β-LPH serve as a marker for anterior lobe (AL) β-END-LI secretion, serotonin and dopamine appear to exert stimulatory and inhibitory control, respectively, over AL β-END-LI release. Further, the quipazine-induced rise in total plasma β-END-LI primarily resembled β-LPH in size and was blocked by cinanserin but not bromocriptine pretreatment. And conversely, bromocriptine but not cinanserin prevented the haloperidol-induced rise in circulating β-END-LI. In comparison to quipazine, haloperidol had a considerably more marked effect on plasma levels of β-END-sized immunoreactivity. Together, these findings support the conclusion that dopamine and serotonin neurons exert reciprocal and independent control over pituitary β-END-LI

ISSN:0028-3835    

DOI:10.1159/000124439

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

A series of studies was designed to determine the effects of protein kinase C activators on TSH, LH, and GH release from anterior pituitary cells. A 15-min incubation of cultured pituitary cells with synthetic diacylglycerol or phorbol myristate acetate, stimulators of protein kinase C, increased GH, LH, and TSH release. Similarly phospholipase C, which liberates endogenous diacylglycerol, stimulated GH, LH, and TSH secretion. The potentiation of the effects of protein kinase C activators is achieved by calcium mobilization in various cell types. The results of the present studies show that calcium ionophore A23187 or calcium channel activator maitotoxin potentiate diacylglycerol-, phorbol ester-, or phospholipase C-induced GH, LH, or TSH release. These findings suggest that activation of protein kinase C by diacylglycerol and mobilization of calcium may be synergistically involved in the regulation of GH, LH, and TSH release.

ISSN:0028-3835    

DOI:10.1159/000124440

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

The quantitative autoradiographic deoxyglucose method was used to study the effects of acute dehydration on local cerebral glucose utilization in Long-Evans and homozygous Brattleboro rats. Water-sated Brattleboro rats had high rates of glucose utilization in the subfornical organ, habenular complex, septal triangular nucleus and pituitary neural lobe. Deprivation of water for 16–18 h enhanced glucose utilization in these structures, more intensely in the Brattleboro rats, and activated others, particularly those connected to the subfornical organ. In Long-Evans rats, water deprivation increased metabolic activity in the subfornical organ, in several structures with which it is connected, and in other brain regions putatively involved in maintaining fluid balanc

ISSN:0028-3835    

DOI:10.1159/000124441

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

To pursue the possibility that subdivisions within the amygdaloid complex are differentially involved in adrenocortical function, plasma samples obtained prior to and following electrical stimulation of the amygdala of urethane (1.30 g/kg) anesthetized female rats were assessed for corticosterone concentration. Hippocampal EEG, ECG, heart rate, mean arterial pressure, and respiration routinely were monitored, and timed blood samples (0.2 ml) were obtained from a catheterized artery. Blood samples were taken 0.5 min prior to and at 5, 10, 15, and 30 min after initiation of stimulation. Whereas stimulation of the central and lateral nuclei produced a decrease (p < 0.05) in plasma corticosterone, stimulation of the basomedial, medial and posterior corticomedial nuclei resulted in increased plasma corticosterone levels (p < 0.05). In contrast, no change in corticosterone levels were observed following sham stimulation or stimulation of several nonamygdaloid sites. Collectively, these data support the hypothesis that subdivisions within the amygdaloid complex are differentially involved in adrenocortical function.

ISSN:0028-3835    

DOI:10.1159/000124442

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Somatostatin inhibits growth hormone (GH) and thyrotropin (TSH) secretion in the rat. Previous studies have shown that small discrete lesions of the periventricular hypothalamic (PV) and medial-basal amygdaloid (AMG) nuclei, which contain high concentrations of somatostatin neurons, reduce somatostatin-like immunoreactivity (SLI) in the median eminence (ME) by approximately two thirds and one third, respectively. The present study assessed the function of the PV and AMG somatostatin systems in the regulation of basal episodic GH and TSH secretion. Three experiments were performed in freely behaving, chronically cannulated adult male rats. In experiment 1, bilateral electrolytic lesions (20 mC) were placed in the PV at the level of the paraventricular nucleus. In experiment 2, bilateral thermal lesions (55 °C × 1 min) were placed in the AMG. In experiment 3, thermal lesions were placed in both the PV and AMG (PV/AMG). Blood samples were removed from animals every 15 min for 5.5 h 14–21 days postoperatively. The ME was microdissected for determination of SLI content. PV, AMG and PV/AMG lesions reduced ME SLI by 59, 26, and 91%, respectively. PV or AMG lesions had no effect on the amplitude or frequency of GH secretory peaks, GH trough levels or the total amount of GH secreted, whereas combined PV/AMG lesions reduced GH peak levels. Lesions of the AMG caused a 34% increase in mean plasma TSH levels, while PV or PV/AMG lesions reduced TSH. The latter effect was probably caused by damage to thyrotropin-releasing hormone neurons and/or axons, which are also located in the PV region. These results suggest that PV and AMG somatostatin systems may not have a significant role in the regulation of basal episodic GH secretion and the putative AMG somatostatin system exerts a significant inhibitory influence on TSH secret

ISSN:0028-3835    

DOI:10.1159/000124443

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Cholecystokinin (CCK) and substance P (SP) were measured in discrete areas of the rat brain at different stages of the estrous cycle. Significantly higher levels of CCK were found in the lateral septum during diestrus as compared to proestrus. In the parietal cortex, CCK concentrations were significantly higher in diestrus than in proestrus. In the amygdala, estrous levels of CCK were significantly higher than proestrous levels. SP concentrations were significantly higher in diestrus than in proestrus in the medial and lateral septum, and the medial and lateral preoptic area. In the amygdala and ventral tegmental area, SP concentrations were significantly higher in estrus than in proestrus. These data suggest that certain CCK and SP neuronal systems may play a role in regulating the hypothalamo-pituitary-gonadal axis and/or be involved in steroid-dependent behavior.

ISSN:0028-3835    

DOI:10.1159/000124444

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

The ventromedial nucleus of the hypothalamus (VMN) of male and female rats was examined ultrastructurally at 100 days of age. Axodendritic shaft and spine synapses were counted in two subdivisions of the nucleus, the dorsomedial part (DM-VMN), which contains only a few sex steroid-concentrating neurons, and the ventrolateral part (VL-VMN), which is abundant in such neurons. In normal males, the numbers of shaft and spine synapses were significantly greater in the VL-VMN than in the DM-VMN. In normal females, however, there was no significant difference in the numbers of shaft and spine synapses between the DM-VMN and the VL-VMN. Moreover, the numbers of shaft and spine synapses in the VL-VMN were significantly greater in normal males than in normal females. Castration of males on day 1 significantly reduced the numbers of shaft and spine synapses in the VL-VMN to the level comparable to those of normal females. In contrast, neonatal treatment of females with 1.25 mg testosterone propionate (TP) on day 5 significantly increased the numbers of shaft and spine synapses to the levels comparable to those of normal males. In the DM-VMN, there were no significant differences in the numbers of shaft and spine synapses among normal and experimental animals. These results suggest that the synaptic organization in the VMN is sexually dimorphic but the occurrence of this structural difference is limited to the VL-VMN which is abundant in sex steroid receptors, and is modified by neonatal sex steroid environment.

ISSN:0028-3835    

DOI:10.1159/000124445

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

The distribution of growth hormone-releasing factor (GRF) and tyrosine hydroxylase (TH), a marker for dopamine neurons in this region, was analyzed in the mediobasal hypothalamus with indirect immunofluorescence histochemistry and an elution-restaining procedure. TH-like immunoreactivity was present in most GRF-immunoreactive cells in the ventral part of the arcuate nucleus (ventral A12 dopamine cell group). Dopamine cells in the dorsal A12 group and, for example, in the hypothalamic A14 cell group seemed to lack GRF peptide. Partly overlapping GRF- and TH-immunoreactive fibers in the median eminence were observed, indicating possible coexistence of the two compounds also in nerve endings close to portal vessels. These findings suggest that a subpopulation of A12 dopamine neurons produces, stores and releases a GRF-like peptide. Possible interactions of GRF and dopamine in the control of growth hormone secretion are discussed.

ISSN:0028-3835    

DOI:10.1159/000124446

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

The present study examines the effect of opiates on α-MSH and β-endorphin release from perifused neurointermediate rat pituitaries, as stimulated by various secretagogues for which Ca ions and/or cAMP serve as messengers. α-MSH release stimulated by high K+ concentrations (5-min pulses) and veratridine depolarization, which is closely dependent on Ca2+ ñuxes, was abolished by both Leu-enkephalin and β-endorphin. A dose-response relationship between inhibition of α-MSH secretion and the concentration of Leu-enkephalin, with EDso – 10–9M, was observed. High K+-in-duced release of β-endorphin was likewise blunted by Leu-enkephalin. The stimulatory effect of the Ca2+ ionophore A 23187 was inhibited in a similar way as was that of CRF, which requires both Ca2+ fluxes and cAMP formation. The antagonist naloxone not only reversed the action of opiates, but also enhanced spontaneous hormonal output. In contrast, the effects of /-isoproterenol and forskolin, for which cAMP serves as a primary messenger, were unaffected in the absence of extracellular Ca ions and, also, in the presence of Leu-enkephalin. We conclude that opioid peptides may exert a direct inhibitory influence on the release of both α-MSH and β-endorphin and do so by interfering with the Ca2+ messenger system. In addition, these data also suggest the existence of an opiate-opiate negative feedba

ISSN:0028-3835    

DOI:10.1159/000124447

出版商:S. Karger AG    

年代:1986

数据来源: Karger