丘脑下部促黄体素释放激素

在极为复杂的生殖过程中,垂体功能的重要性,早已为大家所熟悉。而垂体前叶促性腺激素受到丘脑下部激素的控制,是在最近几年来才研究较多,而且进展很快。本文综合国际上有关丘脑下部促黄体素释放激素的研究资料,和国内研究情况,作一简单的介绍。早在1945年英国的哈里斯(Harris)根据生理实验提出,     

磁场对丘脑下部一氧化氮含量的影响及与丘脑下部神经内分泌核团的关系

应用硝酸还原酶反应—分光光度法测定和NADPH-d组织化学技术,对磁场处理后丘脑下部一氧化氮量的变化及其可能的原因进行了研究,发现磁场可促使丘脑下部一氧化氮量(OD值)显著升高,并具有显著滞后效应。NADPH-d阳性神经细胞及NADPH-d和血管加压素(AVP)双染阳性神经细胞集中分布在丘脑下部室旁核、室周核和视上核,但不存在 于视交叉上核,提示室旁核、室周核和视上核一氧化氮能神经细胞是丘脑下部的一氧化氮的主要来源。磁场处理后大鼠丘脑下部一氧化氮含量(OD值)较正常对照组显著升高应归因于这些神经细胞受磁场作用表达增强。一氧化氮和血管加压素的共存可能对磁场调节内分泌具有一定意义。     

甲孕酮和甲地孕酮植入家兔丘脑下部的抗排卵作用

甾体避孕药是目前比较满意的口服避孕药,但其避孕机制尚未完全解决。有较多的学者认为系抑制排卵(吴熙瑞,1964;Pincus,1964;和Fridlander,1964)。1956年Pincus等(1956)即报道19-去甲基睾丸酮类衍生物能阻断家兔排卵。以后临床研究也证明它们     

刺激猫丘脑下部对内脏大神经放电的影响

刺激猫丘脑下部对内脏大神经放电的影响张小鹏,章翔,易声禹,胡三觉（第四军医大学,西京医院神经外科生理学教研室西安７１００３２）重型颅脑损伤可并发急性胃肠粘膜病变,推测其发病机理与交感神经（ＳＮ）强烈兴奋使血管痉挛胃肠粘膜缺血所致。神经动作电位（ＡＰ）...     

睾丸酮改变丘脑下部功能对大鼠胰脏内移植卵巢的影响

过去的实难证明,切除大鼠、小鼠等动物的性腺能引起其垂体促性腺激素分泌的增加。在这种激素不平衡的情况下,如将卵巢移植到门脉系统,可以发展成为肿瘤。若于移植卵巢后给与较大剂量的性腺激素,能抑制卵巢肿瘤的发生。关于性腺激素与垂体激素的相互关系,以往的解释都着重于直接的反馈作用,近年来许多工作表明,垂体促性腺激素的分泌是受丘脑下部的制约,因此探计丘脑下部的功能状态对诱发卵巢肿瘤的影响,     

丘脑下部促黄体素-释放激素(LRH)对水貂诱发排卵的初步试验

水貂(Mustela vison)是小型珍贵毛皮兽类,属诱发性非卵动物。当前,水貂的繁殖还存在不少问题,因而,对水貂生产有一定的影响。为了探讨水貂不育原因,以提高水貂繁殖率,增加皮张生产,我们于1973 年冬季在北京动物园貂场的大力协助下,与工人同志们一起用合成的LRH在非配种季节,对水貂进行了诱发排卵试验。同时也用两种垂体促性腺激素(促滤泡素和促黄体素,简称FSH和 LH)作了对比实验。     

合成丘脑下部促黄体生成素释放激素(LRH)的类似物对家鱼的催情产卵

人工合成LRH类似物(焦谷·组·色·丝·酪·D-丙·亮·精·脯乙基酰胺)对家鱼有很高的生物活性,微克量即能促使性成熟的池养青鱼、草鱼、鲢鱼、鳙鱼、团头鲂等催情产卵或排精。所产之卵受精、化苗正常。用LRH类似物催产副作用小、成本低。LRH类似物可大量合成,能满足鱼苗生产迅速发展的需要。它是一种比较理想的鱼用催产剂。LRH类似物对雌鱼和雄鱼都有催熟作用。文中还讨论了LRH及其类似物对家鱼催产的机制。     

多巴胺拮抗物PIM增强丘脑下部促黄体素释放激素类似物诱导大鳞副泥鳅排卵效应的研究

在注射低剂量LRH-A的同时注射多巴胺拮抗物pimozide(PIM),能显著增强LRH-A诱导的排卵效应,排卵率达到100％。 LRH-A+PIM能促进脑垂体GtH细胞的合成和分泌,而注射多巴胺能抑制LRH-A诱导的GtH释放活动。     

多巴胺拮抗物PIM增强丘脑下部促黄体素释放激素类似物诱导大鳞副泥鳅排卵效应的研究

在注射低剂量LRH—A的同时注射多巴胺拮抗物pimozide(PIM),能显著增强LRH-A诱导的排卵效应,排卵率达到100％。LRH—A PIM能促进脑垂体GtH细胞的合成和分泌,而注射多巴胺能抑制LRH—A诱导的GtH释放活动。     

丘脑下部促黄体素释放激素类似物(LRH-A)的作用机制Ⅰ.脑垂体组织生理学的研究

真骨鱼脑垂体的组织学和组织化学的研究,有一些学者报道过。如Sokol(1961),Baker(1974)描述过鱼类脑垂体的组织结构;Matty等(1959)用组织学方法对六种真骨鱼脑垂体进行分类及激素分泌的定位工作;施琼芳(1964)对草、鲢鱼脑垂体同性腺发育的组织学变化,进行过详细观察。但是,罗非鱼脑垂体的组织生理学的研究,至今,未见报道。     

Molecular mechanism of effect of rotating constant magnetic field on organisms

The effect of RCMF-magnetic therapy apparatus on signal substances was studied. The radioimmunoassay (RIA) suggested that the magnetic field increased β-endorphin markedly in plasma. ELISA indicated that the magnetic field inhibited vomiting reaction induced by chemotherapy drug, with reversible decrease of serotonin (5-HT) level in brains, small intestine tissue and serum. Furthermore, the bioeffect of magnetic fields on 5-HT level presented a typical window effect and post-effect, and the inhibitory effect of magnetic field on the emesis was parallel to the decrease level of 5-HT. This result implied that the decrease of 5-HT might be the basis of rotating constant magnetic field (RCMF) inhibiting drug-induced emesis. The nitric acid reductase-spectrophotometry and nicotinamide adenine dinucleotide-diaphorase/arginine-vasopressin (AVP) cytochemistry technique showed that the magnetic field induced nitric oxide (NO) increase in hypothalamus and the high NO(A) level lasted for 3 hours. The results suggested that NO(A) increases after the treatment of the magnetic field in hypothalamus, which may result from strong expression of NO-ergic neuron in paraventricular hypothalamic nucleus (PVN), periventricular hypothalamic nucleus (PEN) and supraoptic nucleus (SON). The coexistence of NO and AVP may play an important role in the regulation of endocrine and neuroendocrine by the magnetic field. And our data also confirmed that the magnetic field increased the content of NO so strongly that high NO level lasted for 3 hours, also made neuropeptide Y (NPY) cell in medulla stained heavily.     

Molecular mechanism of effect of rotating constant magnetic field on organisms

The effect of RCMF-magnetic therapy apparatus on signal substances was studied. The radioimmunoassay (RIA) suggested that the magnetic field increased p-endorphin markedly in plasma. ELISA indicated that the magnetic field inhibited vomiting reaction induced by chemotherapy drug, with reversible decrease of serotonin (5-HT) level in brains, small intestine tissue and serum. Furthermore, the bioeffect of magnetic fields on 5-HT level presented a typical window effect and post-effect, and the inhibitory effect of magnetic field on the emesis was parallel to the decrease level of 5-HT. This result implied that the decrease of 5-HT might be the basis of rotating constant magnetic field (RCMF) inhibiting drug-induced emesis. The nitric acid reductase-spec-trophotometry and nicotinamide adenine dinucleotide-diaphorase/arginine-vasopressin (AVP) cytochemistry technique showed that the magnetic field induced nitric oxide (NO) increase in hypo-thalamus and the high NO(A) level lasted for 3 hours. The results sugg     

BiP mRNA expression is upregulated by dehydration in vasopressin neurons in the hypothalamus in mice

The immunoglobulin heavy chain binding protein (BiP) is an endoplasmic reticulum (ER) chaperone that facilitates the proper folding of newly synthesized secretory and transmembrane proteins. Here we report that BiP mRNA was expressed in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of the hypothalamus in wild-type mice under basal conditions. Dual in situ hybridization in the SON and PVN demonstrated that BiP mRNA was expressed in almost all the neurons of arginine vasopressin (AVP), an antidiuretic hormone. BiP mRNA expression levels were increased in proportion to AVP mRNA expression in the SON and PVN under dehydration. These data suggest that BiP is involved in the homeostasis of ER function in the AVP neurons in the SON and PVN.     

Age-related changes in oxytocin-, arginine vasopressin- and nitric oxide synthase-expressing neurons in the supraoptic nucleus of the rat

Many histochemical investigations indicated that the oxytocin (OXY), the arginine vasopressin (AVP) and the nitric oxide synthase (NOS) have been synthesized in the supraoptic nucleus (SON) neurons. The objective of this study was to examine the age-related expression of the OXY, the AVP and the NOS in the SON of the young adult (2-month-old) and the aged (24-month-old) rats. The histochemistry for reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d; marker for the NOS) and the double labeling histochemistry for the OXY/NADPH-d or the AVP/NADPH-d were employed, and the quantitative analysis was performed with a computer-assisted image processing system. In comparison of the young adult and the aged group, the cell number, the cell size and the reactive density of the NOS-expressing neurons showed a significant increase along with age, and these evidences suggested the age-related increase of the nitric oxide (NO) production. The age-related significant increase was not detected in the number of the OXY/NOS-expressing neurons in the dorsal part, but was detected in the number of the AVP/NOS-expressing neurons in the ventral part. Based on our histochemical findings and reports demonstrated by other authors, we attempted to discuss the physiological role of NOS for the secretion of posterior pituitary hormones along with age.     

Genomic Effects of Cold and Isolation Stress on Magnocellular Vasopressin mRNA-Containing Cells in the Hypothalamus of the Rat

We assessed the effects of cold and isolation stress on arginine vasopressin (AVP) mRNA in the paraventricular (PVN) and supraoptic (SON) nuclei of the hypothalamus. Vasopressin mRNA levels were determined by in situ hybridization histochemistry at the cellular level. In posterior magnocellular neurons of the PVN isolation stress for 7 or 14 days increased vasopressin mRNA levels 28 and 29%, respectively, compared to group-housed controls. No significant alterations in vasopressin gene expression were observed in the SON after 7 or 14 days of isolation stress. Scattered magnocellular AVP mRNA-expressing cells of the medial parvocellular PVN showed increases of 19 and 34% after 7 and 14 days of isolation, respectively. We also studied the effect of cold or combined cold and isolation stress on vasopressin gene expression in the PVN and SON. Cold stress for 3 h daily for 4 consecutive days increased AVP mRNA levels in the posterior magnocellular PVN by 15%. Cold-isolated animals showed an increase of 21%. No significant effect on AVP mRNA levels in the SON was observed. In contrast to the posterior magnocellular PVN, cold or cold-isolation stress increased AVP mRNA in magnocellular neurons of the medial parvocellular region of the PVN by 25 and 43%, respectively, relative to control rats. These results suggest that psychological and metabolic stress may be added to the list of stressors that activate the hypothalamo-neurohypophysial system.     

Fos protein expression in mouse hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei upon osmotic stimulus: colocalization with vasopressin, oxytocin, and tyrosine hydroxylase

The quantity and topography of activated vasopressin (AVP), oxytocin (OXY), and tyrosine hydroxylase (TH) neurons were studied immunohistochemically in the anterior, middle, and posterior portions of the PVN and SON in mice 60 min after a single injection of hypertonic saline (HS, 400 microl 1.5M, i.p.). Fos-neuropeptide double-stainings revealed: (1) Fos expression in each portion of the PVN and SON; (2) maximal number of Fos-AVP (79 cells) and Fos-OXY (50 cells) double-labelings in the middle portion of the PVN; (3) low number of Fos-TH perikarya in the PVN and their lack in the SON; (4) similar incidence (around 50%) of Fos-AVP and Fos-OXY perikarya in the SON; and (5) presence of activated AVP, OXY, and TH neurons in the periventricular, subependymal, and sub-PVN zones of the PVN. Topographic analysis revealed that the majority of AVP neurons expressing Fos occupied the dorsolateral and central part of the middle portion of the PVN. In the same PVN portion, Fos-OXY neurons occurred in similar frequency, however, they were primarily distributed along the lateral and medial margins of the PVN. In the SON, Fos-OXY cells occupied mainly its dorsal, while Fos-AVP cells predominated in its ventral part. The data clearly indicate that HS is not a selective stimulus neither for PVN nor SON itself and provide evidence that both PVN and SON AVP and OXY cells play important role in the mediation of signals induced by HS. In addition, the limited number of AVP, OXY, and TH neurons activated by HS may account for their differential functional specializations selective for stress/osmotic circuits activated by HS.     

Regulation of Apoptosis in Nonapeptidergic Neurons of Rat Hypothalamus by Catecholamines in Experiments in vitro

Effects of noradrenaline (NA) and dopamine (DA) on apoptosis of nonapeptidergic neurons of supraoptic (SON) and paraventricular (PVN) nuclei of hypothalamus of male Wistar rats was studied in experiments in vitro. Incubation of hypothalamic sections in the medium with added NA was shown to induce an increase of the amount of pro-apoptotic protein caspase-9 in the nonapeptidergic neurons of the SON and PVN. A comparison of the level of neuronal NO-synthase with the level of caspase-9 expression in these neurons allows concluding that NA leads to initiation of apoptosis in neurons of the SON with mediation by nitric oxide (NO). In the PVN, the NA-induced initiation of apoptosis does not depend on the NO level. Addition of DA to the incubation medium results in an increase of the caspase-9 amount only in PVN neurons regardless of the NO content. The absence of neuronal death after the NA-induced increase of the caspase-9 level in the cells of SON and PVN seems to be due to increased expression of the anti-apoptotic protein bcl-2. Protection of the PVN neurons from death after addition of DA to the incubation medium is probably independent of the expression level of bcl-2. Thus, in the nonapeptidergic neurons of the SON and PVN, which are related by origin and by performed functions, modulation of the process of apoptosis by elevated concentrations of NA and DA is realized by different mechanisms.     

Neuromedin S exerts an antidiuretic action in rats

We recently identified neuromedin S (NMS) as an endogenous ligand for the FM-4/TGR-1 receptor. Here, we examined the possible involvement of central NMS in regulation of urinary output and vasopressin (AVP) release in rats. Intracerebroventricular (icv) injection of NMS induced a dose-dependent increase in the plasma level of AVP, followed by a decrease of nocturnal urinary output. Expression of cFos after icv injection of NMS was observed in the supachiasmatic nucleus (SCN), arcuate nucleus, paraventricular nucleus (PVN), and supraoptic nucleus (SON). The cFos expressing cells in PVN and SON, but not SCN, were then double-stained using antibodies against the vasopressin. On the other hand, icv injection of neuromedin U, which also binds to the FM-4/TGR-1 receptor, required a concentration ten times higher than that of NMS in order to exert the same antidiuretic potency. These results suggest that central NMS may exert a physiological antidiuretic action via vasopressin release.     

The Notch effector gene Hes1 regulates migration of hypothalamic neurons, neuropeptide content and axon targeting to the pituitary

Proper development of the hypothalamic-pituitary axis requires precise neuronal signaling to establish a network that regulates homeostasis. The developing hypothalamus and pituitary utilize similar signaling pathways for differentiation in embryonic development. The Notch signaling effector gene Hes1 is present in the developing hypothalamus and pituitary and is required for proper formation of the pituitary, which contains axons of arginine vasopressin (AVP) neurons from the hypothalamic paraventricular nucleus (PVN) and supraoptic nucleus (SON). We hypothesized that Hes1 is necessary for the generation, placement and projection of AVP neurons. We found that Hes1 null mice show no significant difference in cell proliferation or death in the developing diencephalon at embryonic day 10.5 (e10.5) or e11.5. By e16.5, AVP cell bodies are formed in the SON and PVN, but are abnormally placed, suggesting that Hes1 may be necessary for the migration of AVP neurons. GAD67 immunoreactivity is ectopically expressed in Hes1 null mice, which may contribute to cell body misplacement. Additionally, at e18.5 Hes1 null mice show continued misplacement of AVP cell bodies in the PVN and SON and additionally exhibit abnormal axonal projection. Using mass spectrometry to characterize peptide content, we found that Hes1 null pituitaries have aberrant somatostatin (SS) peptide, which correlates with abnormal SS cells in the pituitary and misplaced SS axon tracts at e18.5. Our results indicate that Notch signaling facilitates the migration and guidance of hypothalamic neurons, as well as neuropeptide content.