Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was conducted to determine whether the cerebrospinal fluid pressure (CSFP) obtained by the lumbar puncture technique is capable of evaluating the pathological state of the cervical spinal canal stenosis (CSCS). A method was developed in which the CSFP was measured with a small piezoelectric semiconductor in combination with the lumbar puncture technique. The data thus obtained were quantitatively analysed using a personal computer. Using this method, we studied patients with cervical myelopathy due to vertebral canal stenosis. The CSFP wave form obtained by compression of the cervical region was converted into a regression curve using the computer. In order to estimate the vertebral canal stenosis ratio (spinal cord/dural tube) of patients with CSCS by CSFP, multiple regression analysis was performed to obtain a multiple regression with respective parameters as expository variables. Descending curve coefficients (CND, CFD and CED) were found to be useful as parameters estimating the state of CSCS by means of CSFP analysis. On the basis of these parameters, CND, the coefficient of a descending curve obtained at the neutral cervical position, and CED, the coefficient of a descending curve obtained at the extended position, patients with CSCS were able to distinguish from normal subjects. The multiple regression equation (Y = 73.2-3890 CNA-4740 CND + 3620 CFD-10470 CEA-802 CED-0.119 NPP) was statistically significant at P = 0.01, therefore, useful in estimating the vertebral canal stenosis ratio. On the contrary, the values calculated from the multiple regression equation were not well correlated with either the JOA (Japanese Orthopedic Association) scores evaluated in accordance with the JOA Criteria or with the spinal compression ratio (anterior-to-posterior diameter/right-to-left diameter).
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PMID:[An evaluation of cervical spinal canal stenosis--a correlation with cerebrospinal fluid pressure using a semiconductor and its coefficients]. 223 Apr 28

Chlornaltrexamine (beta-CNA, 0.5 micrograms) alone or beta-CNA plus either mu-agonist, D-Ala2-NMePhe4-Gly-ol-enkephalin (DAMGO, 500 ng) or delta-agonist, D-Pen2-D-Pen5-enkephalin (DPDPE, 10 micrograms) was injected intrathecally (i.t.) to protect mu- or delta-opioid receptors, respectively, for 24 h in male ICR mice. The antinociception was assessed by the tail-flick and hot-plate test. DPDPE or DAMGO injected i.t. increased inhibition of the tail-flick and hot-plate response in a dose-dependent manner. The dose-response curve for tail-flick and hot-plate response induced by DPDPE or DAMGO in i.t. saline-treated group significantly shifted to the right in i.t. beta-CNA alone treated group but returned to the control level in the group treated with i.t. beta-CNA coadministered with DPDPE or DAMGO, respectively. The effects of protection of mu- and delta-opioid receptor in the spinal cord on inhibition of the tail-flick and hot-plate response induced by beta-endorphin and morphine administered intracerebroventricularly (i.c.v.) were then studied. Intrathecal pretreatment with beta-CNA or beta-CNA coadministered with DAMGO attenuated inhibition of the tail-flick response induced by beta-endorphin administered i.c.v. However, i.t. treatment with beta-CNA coadministered with DPDPE did not affect inhibition of the tail-flick response induced by beta-endorphin administered i.c.v. Intrathecal pretreatment with beta-CNA or beta-CNA coadministered with either DPDPE or DAMGO did not alter inhibition of the hot-plate response induced by beta-endorphin administered i.c.v.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of protection by D-Pen2-D-Pen5-enkephalin or D-Ala2-NMePhe4-Gly-ol-enkephalin against beta-chlornaltrexamine in the spinal cord on the antinociception induced by beta-endorphin administered intracerebroventricularly in the mouse. 799 Oct 69

Nicotine is known to have multiple effects on neuroendocrine, autonomic, and behavioral responses. Its neuroendocrine effect on the stress-responsive hormone, ACTH, depends on central pathways that act on corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus of the hypothalamus (PVN). Other CRH neurons throughout the brain also are involved in coordinating aspects of the stress response, but very little is known about the effect of nicotine on CRH neurons in extrahypothalamic regions that are involved in the autonomic and behavioral responses to stress. The current study sought to determine the extent of nicotinic activation of extrahypothalamic CRH neurons, since these neurons may be involved in mediating the central effects of nicotine. Freely moving rats were pretreated with a low dose of colchicine, infused with nicotine (0.045 mg/kg/30 s or 0.135 mg/kg/90 s, i.v.), and cardiac perfused 1 h later. Double-label immunocytochemistry identified the activated (positive for cFos protein) CRH neurons in limbic structures (bed nucleus of the stria terminalis [BNST] and central nucleus of the amygdala [CNA]), the dorsal raphe (DR), and Barrington's nucleus (BN); comparisons were made to the PVN. In all of these areas, nicotine activated CRH neurons in a dose-dependent manner, showing differential sensitivity and efficacy with respect to region. CNA CRH neurons were most responsive and were maximally stimulated by the low dose of nicotine (62% of CRH neurons were cFos+, compared to 10-27% of the CRH population in other regions, including the PVN). Although the BNST also was activated by the low dose, only the non-CRH+ neurons were involved; in contrast, 41% of the BNST CRH neurons responded to the higher dose. Nicotinic activation of DR neurons was dose-dependent, with 22% of the CRH neurons activated by the high dose. Few BN neurons were activated by the low dose of nicotine, but 26% of the CRH population responded to the higher dose. These results indicate that the effect(s) of nicotine on the brain may be mediated, in part, by the selective activation of specific extrahypothalamic regions containing CRH neurons that also are involved in autonomic and behavioral responses to stress. The large fraction of CRH neurons responding to the low dose of nicotine in the CNA suggests that this limbic region may be particularly important in mediating these CNS effects of nicotine.
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PMID:Nicotinic activation of CRH neurons in extrahypothalamic regions of the rat brain. 954 51

While the present understanding of pituitary-adrenal function predicts attenuation of responses to a repeated stressor, experimental observations often show occurrence of potentiation rather than inhibition. The role of the CNS in this phenomenon was investigated in rats sustaining either a single (S-HEM) or a double episode (R-HEM) of hemorrhage. For S-HEM, blood was withdrawn over 3min and retransfused at 10min; for R-HEM, the stimulus was repeated at 90 min. S-HEM elicited 26- and 9-fold increases in circulating adrenocorticotropin (ACTH) and corticosterone, respectively. After R-HEM the plasma ACTH response was potentiated by 82%. Sixty min after S-HEM, Fos-like immunoreactivity (Fos-IR) was increased in medullary (solitary nucleus, NTS and ventrolateral medulla, VLM), pontine (locus coeruleus, LC and parabrachial nucleus, PBN), limbic (central amygdala, CNA and bed nucleus, BNST), and hypothalamic (supraoptic nucleus, SON and paraventricular nucleus, PVN) regions activated by hemodynamic stimuli. However after R-HEM, the Fos-IR response was significantly potentiated only in the VLM and PVN, while only a moderate increase was evident in the NTS. In other brain regions (LC, PBN, CNA, BNST, HPC and SON), Fos-IR either did not change or the increases were less than those observed after S-HEM. It is suggested that this plasticity in the pattern of neuronal activation following repetition of a stimulus may account for the maintenance of pituitary-adrenal secretory responses and its potentiation after R-HEM.
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PMID:Patterns of Fos-Immunoreactivity in the CNS Induced by Repeated Hemorrhage in Conscious Rats: Correlations with Pituitary-Adrenal Axis Activity. 978 63