摘要:

AbstractThe role of N‐methyl‐D‐aspartate (NMDA) receptor activation in the central regulation of luteinizing hormone (LH) and growth hormone (GH) was tested by administering a bolus intravenous dose of N‐methyl‐D,L‐aspartic acid (NMA), a NMDA receptor agonist, to 24‐week‐old intact (n = 5), estradiol‐treated intact (n = 3) and castrated (n = 3) Holstein bull calves. The calves were bled for 12 h pre‐ and 100 min post‐NMA injection (1.75 mg/kgBW) periods at 10min intervals. Concentrations of LH and GH in plasma were measured by specific RlA. Prior to administration of NMA, the average concentration of LH, but not GH, differed significantly among the 3 groups. As expected, administration of estradiol prevented the normal ontogeny of pulsatile LH secretion, while castration resulted in an increased frequency of LH discharges. Injection of NMA resulted in an acute (P<0.001) release of LH in 3 of 5 intact and 3 of 3 estradiol‐treated intact calves with the peak response being observed at 20 min (3.18 ±1.3 and 5.58 ± 1.3 ng/ml, respectively) following the challenge. Treatment with NMA did not alter the release of LH in castrate calves. Concentrations of GH in plasma increased (P<0.001) within 20 to 30 min after administration of NMA in intact, estradiol‐treated intact and castrate calves with a similar response being observed in each group. Based on these findings, we suggest an involvement of glutamatergic neurotransmission in the hypothalamic or supra‐hypothalamic control of LH and GH secretion, and that the excitatory effects of NMDA receptor activation on LH release are overtly influenced by go

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1993.tb00510.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractAcute glucoprivation profoundly stimulates hypothalamic‐pituitary‐adrenocortical (HPA) and adrenomedullary outflows. Whether these responses reflect a single central mechanism regulated by corticotropin‐releasing hormone (CRH) has been unclear. This study examined the role of endogenous CRH in HPA and adrenomedullary responses to hypoglycemia in Sprague‐Dawley rats, by using anti‐CRH immune serum or a CRH antagonist (α‐helical h/r CRH9–41, and in Lewis rats, a strain characterized by deficient hypothalamic CRH responses during stress. In conscious Sprague‐Dawley rats with indwelling arterial and venous cannulas, insulin (0.3 U/kg) was injected iv, and responses of serum glucose concentrations and plasma levels of corticotropin (ACTH) and catechols (including epinephrine, EPI; norepinephrine, NE; dihydroxyphenylalanine, DOPA; dihydroxyphenylglycol, DHPG; and dihydroxyphenylacetic acid, DOPAC) were assessed, with or without pretreatment with anti‐CRH immune serum (0.5 or 1.0ml iv or 10μI icv) or α‐helical h/r CRH9–41(130 nmol iv or 13 nmol icv). Responses to insulin (1.0 U/kg iv) were also measured in conscious juvenile Lewis and Fischer 344/N rats. Insulin‐induced hypoglycemia markedly increased plasma levels of EPI and ACTH in all groups. Pretreatment iv with 1.0ml of anti‐CRH immune serum blocked the ACTH response to insulin but failed to attenuate the EPI response, α‐helical h/r CRH9_41, whether given iv or icv, failed to alter ACTH or EPI responses to insulin, although the antagonist did block EPI responses to icv CRH. Hypoglycemia elicited similar increments in ACTH levels in Lewis rats and Fischer 344/N control rats; and although Lewis rats had lower baseline EPI and smaller responses of NE, DHPG, DOPA, and DOPAC levels, the groups did not differ in proportionate increments in EPI levels. The results indicate that the ACTH response to hypoglycemia depends on availability of CRH outside the blood‐brain barrier—presumably in the pituitary gland. The findings with icv α‐helical h/r CRH9_41can be explained by failure of the antagonist to reach effective concentrations at central sites of action of endogenous CRH, or by mechanisms other than CRH release determining the adrenomedullary response to hypoglycemia. Lewis rats seem to have less adrenomedullary secretion at baseline and smaller responses of NE synthesis and release during hypoglycemia than do Fischer 344/N rats. Neurochemical evidence for differential adrenomedullary and sympathoneural responses during hypoglycemia in all three rat strains is inconsistent with Cannon's view of a functionally unitary sympathoadrenal system. Since Lewis and Fischer 344/N rats had similar proportionate responses of both ACTH and EPI levels during hypoglycemia, either Lewis rats have deficient CRH responses to some stressors but not to others, or else pituitary‐adrenocortical and adrenomedullary responses in this setting depend on mechanisms other than CRH release in the brain. Both explanations are inconsistent with the doctrine of non‐specificit

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1993.tb00511.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractA double‐label immunocytochemical technique was used to determine whether progesterone receptor‐containing neurons in the female guinea‐pig hypothalamus also contained galanin. Adult ovariectomized guinea‐pigs were primed by estradiol to induce progesterone receptors and injected intracerebroventricularly with colchicine to visualize galanin‐immunopositive neurons. A small proportion of progesterone receptor‐containing perikarya in the medial preoptic area and the mediobasal hypothalamus were found to be immunoreactive for galanin. The medial preoptic, periventricular and arcuate nuclei showed the greatest concentration of double‐labelled cells. Galanin varicosities appeared in close proximity to neurons with progesterone receptor‐containing nuclei. These results provide neuroanatomical evidence that a subset of hypothalamic galanin‐immunoreactive neurons is directly regulate

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1993.tb00512.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractThe neurohypophysial melanin‐concentrating hormone, MCH, plays a role in adaptive colour change in teleost fishes, inducing pallor when the fish is placed in pale‐coloured surroundings. The present study shows that its plasma concentration, measured in groups of white‐adapted fish, is not uniformly high throughout the day but follows a clear diurnal pattern. Over a 24 h cycle, plasma concentrations rise gradually during the morning to reach peak values around the middle of the photophase, after which they decline significantly before night. Lowest concentrations are observed during the dark period. This pattern was observed under a long photoperiod in summer and a short photoperiod in winter. The peak was shifted within a week of changing the onset of either light or dark. When dawn was delayed by 6 h for fish held on a long photoperiod, the usual morning rise in hormone titres was suppressed but, with the advent of light, hormone concentrations rose more rapidly than usual to reach peak values at about the normal time. If the dawn was advanced by 6 h for fish held under short photoperiod conditions, then peak concentrations were attained 6 h precociously. Fish from a long photoperiod placed in constant light showed a pattern of MCH release which approximated to the normal over the first 24 h period but plasma values then became raised and periodicity was no longer discernible. Plasma hormone concentrations were much reduced in trout kept in black coloured tanks in which nocturnal and daytime values differed, but significant differences during the photophase were not demonstrable. The results suggest that an illuminated white background can initiate the early morning release of MCH, and that an endogenous pacemaker underlies the pattern of MCH secr

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1993.tb00513.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractIncreases in plasma VP in response to osmotic stimulation are critical for water conservation, while VP released into the pituitary portal circulation is an important regulator of ACTH secretion and does not contribute to plasma VP levels. The role of the adrenal medulla in the specificity of these responses was studied in rats subjected to osmotic and non‐osmotic stress two months following adrenal demedullation or sham operation. Basal and stimulated plasma corticosterone, aldosterone, ACTH and PRA levels in adrenal demedullated rats were similar to those in the sham operated groups indicating recovery of adrenocortical function. Basal plasma VP levels were similar in sham operated controls and adrenal demedullated rats (0.93±0.13 and 1.0 ± 0.1 pg/ml, respectively) and rose to comparable levels in both groups following 48 h osmotic stimulation by water deprivation (14.4+1.3 and 20.7 + 3.4, respectively). On the other hand, while in sham operated rats, immobilization for 15 min, a non‐osmotic stress, had no effect on plasma VP levels in control or water deprived (2.0±0.9 and 15.0±2.7 pg/ml), in adrenal demedullated rats, caused dramatic increases in plasma VP from 1.0±0.1 to 126.0 + 29.9 pg/ml in controls, and from 20.7 + 3.4 to 155 + 37 pg/ml in water deprived rats. Intraperitoneal hypertonic saline injection, a combination of osmotic and painful stress, caused much higher increases in plasma VP in adrenal demedullated rats (138.0 + 22.1 compared with 34.7 + 3.7 pg/ml in sham operated rats). Water deprivation potentiated this response to 70.0 + 8.3 and 295 + 24 pg/ml in sham operated and adrenal demedullated rats, respectively. VP mRNA measured by in situ hybridization, and irVP measured by immunohistochemistry, were elevated in magnocellular neurones in the hypothalamus of adrenal demedullated rats. The demonstration of marked plasma VP responses to non‐osmotic stimuli in adrenal demedullated rats, suggests a modulatory role for the adrenal medulla in the specificity of the secretory responses of the magnocellular and parvicellular vasopressinerg

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1993.tb00514.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractForebrain vasopressin (VP) neurons of the bed nucleus of the stria terminalis (BNST) contrast with hypothalamic VP neurons in exhibiting nuclear gonadal steroid receptors which may directly effect steroid‐induced changes in VP gene expression observed in BNST cells. A transcription and Northern mRNA analysis has been performed to determine the mechanism through which gonadal steroids regulate VP gene expression in the BNST. In addition to confirming a distinctive, sexually dimorphic pattern of VP mRNA expression in the BNST as compared with the hypothalamic supraoptic nucleus (SON), our results show that the marked decrease in BNST VP mRNA levels observed two weeks after castration is not associated with a change in transcriptional activity of the VP gene. Similarly, VP gene transcription is not increased, relative to castrated animals, in the BNST of castrated rats treated with testosterone which exhibit normal or somewhat elevated levels of VP mRNA in the BNST. A post‐transcriptional mechanism therefore appears to underlie the gonadal steroid‐regulated changes in VP gene expression in the BNST. Since modulation of mRNA size (due to changes in poly (A) tail length) was also observed following castration and testosterone treatment it is apparent that the post‐transcriptional mechanism may involve regulated changes in VP mRNA poly (A) tail length.The present findings contrast with the osmotic up‐regulation of VP mRNA levels in the SON which is primarily a transcriptional response, and provide a demonstration of the potential physiological importance of post‐transcriptional mechanisms of hormonal gene

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1993.tb00515.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractThe effects of natriuretic peptides on electrical activity and cellular cGMP levels were studied in neurons of the supraoptic nucleus (SON) of rat hypothalamic slice preparations. Intracellular and extracellular recordings showed that bath application of A type natriuretic peptide (ANP) at 100 nM or B type natriuretic peptide (BNP) at 100 to 300 nM decreased the firing rate and hyperpolarized the membrane potential in phasically firing (putative vasopressin) neurons. Non‐phasically firing (putative oxytocin) neurons did not respond to these natriuretic peptides in firing rate or membrane potential. The membrane‐permeable cGMP analogue 8‐bromo cGMP at 0.5 mM and the phosphodiesterase inhibitor 3‐isobutyl‐1‐methylxanthine (IBMX) at 50 μM mimicked the inhibitory effects of ANP and BNP. The specific inhibitor of cGMP phosphodiesterase 1‐(3‐chloroanilino)‐4‐phenylphthalazine (MY5445) at 30 μM also decreased the firing rate of SON neurons. The cGMP‐dependent protein kinase inhibitor N‐(2‐(methylamino)ethyl)‐5‐isoquinoline‐sulfonamide dihydrochloride (H8) at 1 μM abolished the inhibition by natriuretic peptides. We measured cGMP and cAMP contents in discrete SON regions and compared the change of the contents before and after application of ANP and BNP. The increases in cellular cGMP accumulation were 430% for ANP and 120% for BNP, although they did not cause significant change of cAMP accumulation. The results suggest that the inhibitory effects of natriuretic peptides on putative vasopressin neurons are mediated through cGMP

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1993.tb00516.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractVasopressin and its fragment peptides such as [pGlu4, Cyt6]AVP(4–9)(AVP(4–9)) represent putative neuromodulators within central nervous homeostatic, memory and behavioural circuits. To localize their central receptor systems, the previously characterized monoclonal anti‐idiotypic antibody mAb 237 was employed in immunocytological investigations of rat brain tissue sections. This antibody was raised to the monoclonal idiotypic anti‐AVP antibody mAb 113 which preferentially binds to the acyclic C‐terminal portion of the AVP molecule and is therefore also capable of binding the naturally occurring AVP(4–9)fragment. Immunoreactive magnocellular neurones were detected in the AVP‐synthesizing supraoptic but not paraventricular nuclei. Dense staining was observed within circumventricular organs lacking a blood‐brain barrier (BBB). These structures include the subfornical organ, the organum vasculosum laminae terminalis, the internal layer of the median eminence, the body of the pineal gland, the choroid plexus and the area postrema, where immunoreactivity was found on capillaries, neurones and fibres. Further staining was found in the nucleus of the solitari tract and the arcuate nucleus, endowed with a leaky BBB. Distinct cell patches in the ependymal lining of the third ventricle as well as dendritic processes of juxtaependymal neurones were labelled by the anti‐idiotypic antibody mAb 237. The observed staining pattern did not parallel that obtained in autoradiographic studies performed using either radiolabelled AVP or a V1‐receptor antagonist, but that found with the [35S]‐labelled AVP(4–9)fragment. Using [35S]‐labelled AVP(4–9)fragment, specific high density binding sites could be localized autoradiographically in structures within and outside the BBB, in complete agreement with the anti‐idiotypic immunoreactivity.Since the anti‐idiotypic methodology is based on transfer of complementary structures, and the epitope recognized by the corresponding idiotypic antibody resembles the sequence of AVP(4–9), the anti‐idiotypic antibodies might recognize the

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1993.tb00517.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractA novel precursor neuropeptide termed 7B2 is present within specific brain areas, including the hypothalamic magnocellular neurosecretory neurons, and appears to be processed to smaller fragments. In order to determine whether specific C‐terminal fragments of 7B2 might exert local effects on neurosecretory cells, we used intracellular current‐clamp recordings in supraoptic neurons maintained in superfused hypothalamic explants to evaluate membrane potential and resistance changes in 25 supraoptic nucleus neurons during bolus applications of 7B2174–186and two other C‐terminal peptide fragments 7B2156–173and 7B2141–150. In 15 supraoptic neurons, only the 7B2174–186fragment induced a gradual 2–8 mV membrane depolarization that lasted for 4 to 30 min and was accompanied by 15 + 8% reduction in input resistance. Immunocytochemical identification of the recorded cells revealed that both vasopressin (VP)‐ and oxytocin (OT)‐containing neurons were depolarized by 7B2174–186. These data suggest that 7B2174–186is a biologically active fragment of 7B2 and may regulate the excitability of magnocellular sup

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1993.tb00518.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractPopulation spikes, evoked in the CA1 hippocampal area by stimulation of the Schaffer collaterals at various intensities, were recorded over a period of 70 min in slices from 7‐day adrenalectomized (ADX) or sham‐operated rats. Slices from sham‐operated rats with intermediate plasma corticosterone levels (between 0.5 and 5μg corticosterone/100 ml plasma) at the start of the experiment displayed very stable synaptic responses. However, the responses recorded in slices from rats with lower or higher corticosterone levels gradually declined, with repeated stimulation. Similarly, a significant decline of the population spike over time was observed in slices from ADX rats, particularly with low stimulus intensities; characteristics of the compound EPSP were much more stable. The decline of the population spike amplitude was alleviated when: 1) single rather than repeated stimulation was applied; 2) the experiments were performed in the presence of 20 mM glucose; or, 3) moderately high (10−8or 10−7M) concentrations of corticosterone were administeredin vitro; low (10−9M) or high (10−6M) corticosterone concentrationsin vitrodid not improve the stability of the synaptic response in slices from ADX rats. These data suggest that intermediate levels of corticosterone are necessary to maintain the stability of the Schaffer collateral input to CA1 neurons. With very low or high corticosterone levels, CA1 neurons apparently fail to respond to synaptic stimulation, over time. The possible mechanisms underlying this bell‐shaped dose response curve for corticostero

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1993.tb00519.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY