摘要:

AbstractThe projection fields of corticotropin‐releasing factor (CRF)‐containing perikarya in the rat central nervous system were studied using a combination of electrolytic lesions, microdissection and radioimmunoassay. The effects of bilateral electrolytic lesions of the central nucleus of the amygdala (Ce) or the paraventricular nucleus (PVN) of the hypothalamus were measured by a sensitive and specific radioimmunoassay. Following lesions of the Ce, CRF concentrations in the locus ceruleus (LC) were significantly decreased. Following lesions of the PVN, CRF concentrations in the median eminence were markedly decreased (>85%), with smaller but consistent reductions of CRF in the hippocampus as well. In contrast to the Ce lesions, PVN lesions resulted in increases in CRF concentratixhtmlons in the LC.These results further confirm the projection of CRF‐containing cells from the PVN to the median eminence, provide evidence for a PVN‐hippocampal CRF pathway, and suggest that the PVN modulates CRF neurons innervating the LC. Moreover, the existence of a CRF‐containing pathway from the Ce to the LC appears likely, and such a circuit may play a role in the behavioral and physiological responses

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1993.tb00367.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractChronic osmotic stimulation influences the hypothalamo‐adenohypophysial axis by inhibiting the synthesis of hypothalamic corticotrophin‐releasing factor (CRF‐41) and subsequently the secretion of basal and adrenalectomy‐elevated adrenocorticotrophin from the adenohypophysis. In the present study, we used a substance P antagonist to test the hypothesis that this inhibition is mediated centrally by substance P or other tachykinins. In control rats and rats given 2% saline to drink for 12 days, intracerebroventricular administration of a substance P antagonist elevated plasma adrenocorticotrophin and corticosterone levels. Using quantitativein situhybridization histochemistry, it was also demonstrated that CRF mRNA increased in the medial parvocellular division of the paraventricular nucleus of saline‐treated as well as control rats 6 h after intracerebroventricular administration of the antagonist, while vasopressin mRNA in the medial parvocellular division of the paraventricular nucleus was increased in the control animals only. These results provide evidence that central endogenous substance P has an inhibitory influence over the synthesis and release of CRF‐41 both under normal conditions and during a chronic osmot

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1993.tb00368.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractThe effects of adrenalectomy (ADX) on the amounts of immunoreactive corticotropin‐releasing factor (CRFj) and arginine vasopressin (AVPi) that are stored in the zona externa of the median eminence (ZEME) were investigated by means of quantitative immunocytochemistry. Although ADX of male Wistar rats for 1 week or 4 weeks did not affect CRFiin the ZEME as compared to sham‐operated or intact controls, AVPishowed a progressive accumulation. The ratio of AVPiover CRFiin the ZEME had already increased 1 day after ADX. However, it should be noted that the exact changes in CRFiand AVPjas measured by radioimmunoassay and/or quantitative immunocytochemistry were dependent on the substrain of rats used. The secretion rate of CRFiand AVPjwas estimated in 1 week and 4 week ADX rats, by measuring the disappearance rate of CRFiand AVPifrom the ZEME after blockade of fast axonal transport, by a low non‐toxic dose of colchicine (5 μg per rat). In contrast to intact rats, where this dose of colchicine did not affect CRFior AVPiin the ZEME, ADX rats showed a progressive depletion of the CRFiand AVPistores as measured 2.5 and 5 h later. In 1 week ADX rats, CRFiand AVPiboth disappeared at a rate of 7% to 8% of their stores per hour. In contrast, after 4 weeks of ADX the fractional disappearance rates of CRFiand AVPiwere different and were 3% and 8% of the content per hour, respectively. This indicates that in long‐term ADX rats the chance of AVP being released from the ZEME is more than twice that of CRF. Since most, if not all, of the CRF; containing nerve terminals in the ZEME of ADX rats costore AVP, we hypothesize that in long‐term ADX rats AVP may be preferentially secreted from AVP and CRF costoring nerve

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1993.tb00369.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractPrevious studies have demonstrated that acute stress or ovine corticotropin‐releasing hormone (oCRH)in vivo, or oCRHin vitro, stimulates release of β‐endorphin over β‐lipotropin from anterior pituitary corticotropes. This occurs despite the predominance of β‐lipotropin in corticotrope peptide stores.In vitrostudies with primary anterior pituitary cultures suggested that chronic exposure to oCRH results in a shift towards more β‐lipotropin secretion into the media than with short‐term exposure. The current studies explored whether increased secretory drivein vivoresults in a similar shift towards more β‐lipotropin. We used removal of glucocorticoids by adrenalectomy or metyrapone blockade of corticosterone synthesis, to stimulate endogenous secretion of CRH and vasopressin. Both treatments resulted in shifts of the ratio of β‐endorphin: β‐lipotropin in plasma of experimental animals in comparison to the sham‐treated control rats.In vitrotesting with oCRH of anterior lobe cultures from adrenalectomized or metyrapone‐treated rats demonstrated similar effects of these treatments on the ratio of β‐endorphin : β‐lipotropin. These changes occurred despite similar ratios of β‐endorphin : β‐lipotro

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1993.tb00370.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractA number of stimuli including acute footshock and electrically‐induced seizures lead to release of β‐endorphin immunoreactivity from the anterior pituitary corticotropes. Gel filtration of this β‐endorphin immunoreactivity indicates that approximately 3‐fold more β‐endorphin than β‐lipotropin is released into plasma following these acute stressors. A similar preponderance of β‐endorphin over β‐lipotropin is seen in the media of short‐term anterior lobe cell suspensions stimulated with ovine corticotropin‐releasing hormone. Previous studies indicated that footshock stress, when administered repeatedly, can increase the biosynthesis of anterior lobe proopiomelanocortin (POMC) as indicated by increased steady state adrenocorticotropin/β‐endorphin content as well as increased POMC mRNA levels and increased POMC biosynthesis and rate of processing as measured by pulse‐labeling and pulse‐chase studies. The goal of the present studies was to determine whether this increased biosynthetic drive results in an alteration in the end products secreted with repeated stress. Acute footshock in a rat which has received 14 days of chronic footshock releases proportionately more β‐lipotropin than is released in a naive rat. Chronic electrically‐induced seizures, which also increase anterior lobe POMC derived peptide stores, lead to a similar shift in the ratio of β‐lipotropin:β‐endorphin released following stress. These data suggest that chronic drive and the subsequent changes in POMC peptide stores may lead to a decrease in the proportion of β‐endorphin size immunoreactivity in the releasable pool of the anterior lobe corticotrope, thus altering the hormo

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1993.tb00371.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY