摘要:

This review focuses on the central regulation of thermoregulatory responses with special attention to the participation of thyrotropin-releasing hormone (TRH) in both autonomous and endocrine responses to a cold environment. Besides a direct projection of TRH neurons from paraventricular nuclei (PVN) to the median eminence, and the subsequent activation of the thyroid axis, there are direct projections from the PVN to the autonomic preganglionic neurons controlling autonomous responses. These projections convey information to peripheral targets involved in thermogenesis through the dorsal vagal complex and the spinal cord, for parasympathetic and sympathetic neurotransmissions respectively. Furthermore, cold exposure increases TRH mRNA levels in the PVN but also in dorsal motor and caudal raphe nuclei, thus providing strong evidence for a functional link between autonomous and neuroendocrine systems involved in thermoregulation.

ISSN:0028-3835    

DOI:10.1159/000127126

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

To clarify the relationship between neuronal cell degeneration and MHC class-I complex expression, we have immunohistochemically examined the distribution of β2-microglobulin in the hypophysectomized rat hypothalamus. In the sham-operated control rats, positive stainings were distributed only in blood vessels in the hypothalamic areas where magnocellular neurons were localized. Three days after hypophysectomy, positive stainings appeared in a large number of magnocellular neurons in the paraventricular and supraoptic nuclei. Most of such β2-microglobulin-positive cells were simultaneously stained with antivasopressin serum. The pattern of distribution of positive cells and the intensity of the stainings remained unchanged at least until the 14th day. These morphological findings suggest that the process of degeneration of hypothalamic magnocellular neurons after hypophysectomy is a useful model to investigate the role of MHC class I complex in the brai

ISSN:0028-3835    

DOI:10.1159/000127127

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

The effect of the intracerebroventricular (icv) and intravenous (iv) injection of nerve growth factor (NGF) on peripheral immunity was studied in the rat. Icv administration of NGF (5, 25, 50, 250 and 500 ng/rat) significantly enhanced phytohemagglutinin (PHA)-induced splenocyte proliferation 30 min after treatment. Icv pretreatment with an anti-NGF antibody completely prevented the effect, while iv injection of anti-NGF antibody did not block the effect of icv NGF. On the contrary, NGF at doses of 0.5, 2.5, 5, 25 and 50 ng/rat decreased splenocyte natural killer (NK) activity. When injected iv, NGF enhanced splenocyte proliferation only at doses of 50 and 500 ng/rat, while it did not affect NK activity. These effects on immunity do not appear mediated by activation of the hypothalamus-pituitary-adrenal axis, since NGF did not modify plasma corticosterone concentrations at the doses used. These results indicate that NGF participates in the complex network of neuroimmune interactions.

ISSN:0028-3835    

DOI:10.1159/000127128

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

Cholecystokinin (CCK) is detected in pituitary tumors but its role remains unknown. On the hypothesis that CCK may facilitate the cell growth in pituitary tumors, we have examined the effect of CCK on cell growth using a rat pituitary tumor cell line, GH3, cultured in a serum-free, chemically defined medium. Addition of sulfated CCK-(26-33) (CCK-8) in two different concentrations (0.5 ∼ 1 nM) caused a significant increase in the number of GH3 cells. The antagonist (1 µM) for CCK-B receptor, but not CCK-A receptor, significantly inhibited the number of GH3 cells. Northern blot analysis revealed a significant expression of CCK-B receptor mRNA in GH3 cells, but not in normal rat pituitary glands. In addition, immunoreactive CCK/gastrin was detected by RIA in the GH3 cell extracts as well as the serum-free culture medium. In GH3 cell extracts, both CCK-8 and gastrin like peptides were identified by gel chromatography. These findings provided the first evidence for an autocrine/paracrine role of CCK and gastrin on stimulation of GH3 cell growth through the CCK-B recept

ISSN:0028-3835    

DOI:10.1159/000127129

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

Increased gap junctional intercellular communication induced by agents that stimulate the adenylyl cyclase/cAMP pathway was observed in the GnRH-secreting neuronal cell line, GT1-7, and possible underlying mechanisms were examined. A 24-hour treatment of GT1-7 neurons with 100 µM dibutyryl cAMP + 100 µM IBMX or with 2 µM forskolin increased by greater than 2-fold the percentage of cells that were dye coupled, using the noninvasive dye coupling assay, fluorescent recovery after photobleaching (FRAP). Longer treatment times (48 h) and higher concentrations of dibutyryl cAMP (500 µM) did not further increase the percentage of dye-coupled cells, while there was no increase in dye coupling observed between untreated cells and cells treated for 2 h or less. The increase in dye coupling induced by dibutyryl cAMP/IBMX was inhibited by octanol or dieldrin, agents known to block gap junction-mediated intercellular coupling in other cell types. Western blot analysis of total protein or membrane protein-enriched extracts revealed no apparent difference in the cellular levels of connexin 26, a connexin subtype previously shown to be expressed by GT1-7 cells, between untreated cells and cells treated for 24 h with dibutyryl cAMP/IBMX or forskolin. In addition, expression of connexin 32 or 43 protein before or after treatment was not detected. On the other hand, a dramatic increase in both the number of neurites and neurites that immunostained positive for connexin 26 was observed in dibutyryl cAMP/IBMX-treated cells. We hypothesize that the observed increase in dye coupling between GT1-7 neurons following stimulation of the adenylyl cyclase/cAMP pathway results from an augmentation of cell-cell contacts due to an increased number of neurites containing gap junctional plaques, possibly through an effect on cellular differentiat

ISSN:0028-3835    

DOI:10.1159/000127130

出版商:S. Karger AG    

年代:1996

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000127131

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

The mediobasal hypothalamus of rats contains gonadotropin-releasing hormone (GnRH) receptors. These hypothalamic neurons also express the GnRH corresponding gene. Under these circumstances, the possibility exists that these GnRH receptors could be localized in other neurons, which are GnRH-receptive, unknowing the neurotransmitter quality. Therefore, we studied the in vitro effects of the GnRH agonist buserelin on GnRH, glutamate, γ-amino-butyric acid (GABA) and taurine release from explanted superfused hypothalami of untreated and buserelin-pretreated (down-regulated) male rats. When buserelin was added to the superfusion medium it inhibited promptly the release of GnRH and the excitatory amino acid neurotransmitter glutamate, but stimulated the release of the inhibitory neurotransmitters, GABA and taurine. Hypothalamic release of GnRH from hypothalami collected from buserelin-treated (30 µg/100 g b.w. twice daily for 4 days) male rats released significantly less GnRH, glutamate and more GABA and taurine. The inhibitory effect of buserelin was maintained when the superfusion medium continuously contained the GnRH analog. When superfusion of hypothalami from buserelin-pretreated animals was performed in the absence of buserelin, GnRH and glutamate release increased significantly within 45–60 min, whereas GABA and taurine release decreased at this time point. When buserelin was added to the superfusion medium 2 h after buserelin-free superfusion, GnRH and glutamate release decreased whereas GABA and taurine release increased instantaneously. Buserelin-treated rats showed significantly low values of LH and testosterone than the untreated rats. These results suggest that GnRH receptors may not only be present in GnRH axon terminals in the median eminence, but also on glutamatergic, GABAergic and taurinergic neurons by which GnRH may exert an autoinhibitory ultrashort loop feedback on its own secretion. This effect appears to be connected with glutamatergic, GABAergic and taurinergic neur

ISSN:0028-3835    

DOI:10.1159/000127132

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

In order to evaluate the possible participation of the hypothalamic excitatory and inhibitory amino acid neurotransmitter systems in the GnRH release response to GABAergic drugs, hypothalami (preoptic and mediobasal area) of immature (26 days of age) and adult male rats were perifused with GABA-A and -B agonists and antagonists. GnRH and amino acid neurotransmitter concentrations (glutamate, taurine, GABA) were measured in perfusate samples collected every 15 min during 150 min. In immature rats, muscimol and baclofen (GABA-A and GABA-B agonists, respectively) increased GnRH, glutamate and GABA release and decreased taurine output, while in adults these agonists showed opposite effects on GnRH and glutamate release, and increased GABA and taurine output. On the other hand, in immature rats bicuculline and phaclofen (GABA-A and GABA-B antagonists, respectively) decreased GnRH, glutamate and GABA release, increasing taurine outflow. In adult animals, these antagonists enhanced GnRH and glutamate release, decreasing taurine and GABA outflow. These results indicate that GABA stimulates GnRH release in immature male rats and confirm the inhibitory role of this amino acid neurotransmitter in adult animals. This effect might be associated, at least partially, with the modifications observed in the excitatory and inhibitory amino acid release. On the other hand, in immature rats, stimulation of GABA-A and GABA-B receptors increased GABA release. Although ultrastructural studies have not produced any evidence of GABA-GABA neurointeractions, our results suggest the existence of a positive feedback mechanism of GABA autoregulation active during the prepubertal stage. Participation of this mechanism in the onset of puberty cannot be discarded.

ISSN:0028-3835    

DOI:10.1159/000127133

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

As an example of pheromone-induced activation of reproductive function, the ‘male effect’ is well knwon in seasonally anestrous goats. The effect of this male pheromone on the hypothalamic gonadotropin-releasing hormone (GnRH) pulse generator activity was examined by monitoring the characteristic increases in the multiple-unit activity (MUA volleys) of the medial basal hypothalamus which had been associated with the pulsatile secretion of luteinizing hormone in ovariectomized goats carrying estradiol implants under 16L/ 8D condition. Male goat hair was used as the source of male pheromones, and the exposure to the hair was accurately timed to be midway between succeeding MUA volleys. The interval from the pheromone exposure to the subsequent volley was measured, so that the primer pheromone effect was assessed in terms of the stimulation of the GnRH pulse generator activity. Exposure to hair from an intact male goat resulted in occurrence of a MUA volley within a few minutes (1.7 ± 0.2 min, n = 15) with the intervolley interval being apparently shortened as compared with the preexposure period. Hair from castrated male goats, on the other hand, had no such stimulatory effect at all on the hypothalamic GnRH pulse generator activity, but treatment of the castrated goats with testosterone for 2 months resumed the pheromone activity. The present results provide first direct evidence for the central action of the primer pheromone in a mammalian species, and pheromonal stimulation of the reproductive neuroendocrine system is shown to be exerted by instantaneously stimulating the hypothalamic GnRH pulse generator acti

ISSN:0028-3835    

DOI:10.1159/000127134

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

In cultured pituitary cells of tilapia, gonadotropin-releasing hormone (GnRH; IO11M 4-24 h), elevation of cyclic AMP (by 10 µM forskolin or 0.2 mM3-isobutyl-1-methylxanthine: IBMX 0.5-36 h) or activation of protein kinase C (PKC; by 12.5 nM tetradecanoyl phorbol-13-acetate: TPA, 0.5–24 h) all increased gonadotropin (GtH) IIβ steady state mRNA levels by three- to fourfold. The involvement of PKA and PKC in the GnRH stimulatory effect on both GtH release and GtH IIβ mRNA levels was corroborated by use of the PKA and PKC inhibitors, H89 and GF109203X, respectively (100 nM) which attenuated the GnRH effect. Incubation with actinomycin D (8 µM, 4–21 h) after preexposure for 24 h to either forskolin (10 µM) or TPA (12.5 nM), revealed that rates of transcript degradation were slower in forskolin-treated cells (T½ = 14.1 h) than in control or TPA-treated cells (T½ = 8.47 or 8.38 h), suggesting a stabilizing effect on the mRNA. Dopamine (DA; 10 µM, 4–36 h) had no apparent effect on steady state mRNA levels of GtH Ilβ, but reduced GtH release by as much as 75%. Steady state levels of growth hormone (GH) mRNA were not affected by exposure to GnRH (10 nM, 4–24 h), although GH release was more than doubled. Similarly, activation of PKC (by TPA 12.5 nM, 1.5–36 h), which was shown to be essential for the GnRH-stimulatory effect on GH release, did not alter levels of the GH transcript, but increased GH release by more than fivefold. DA (10 µM, 4–24 h) moderately increased GH transcript levels (160%) with similar kinetics but lower potency than direct elevation of cAMP (by 10 µM forskolin or 0.2 mM f IBMX, 0.5-36 h) which increased transcript levels by more than fourfold. The involvement of PKA in the DA effect was confirmed when the PKA inhibitor H89 (100 nM, 15 min prior to DA exposure) attenuated the DA effect on GH mRNA levels. Exposure of cells to actinomycin D (8 µM, 2–16 h) after treatment with forskolin (10 µM, 24 h) led to a slower rate of transcript degradation than in control cells (T½ = 6.5 h vs. T½ = 4.36 h), suggesting that cAMP also elicits a stabilizing effect on GH mRNA. Somatostatin (100 nM, 0.5-36 h) had no clear effect on GH transcript levels, but reduced GH release by as much as 90%. These results suggest that activation of either cAMP-PKA or PKC pathways can, possibly by different mechanisms, stimulate mRNA levels of the GtH IIβ gene, but that only the cAMP-PKA pathway stimulates GH mRNA levels. It would appear therefore that GnRH, although stimulating GH release, does not regulate

ISSN:0028-3835    

DOI:10.1159/000127135

出版商:S. Karger AG    

年代:1996

数据来源: Karger