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)

These studies were designed to further test the hypothesis that corticotropin-releasing hormone (CRH) is released from axons innervating the noradrenergic neurons of the locus coeruleus (LC) and serves to activate these neurons during stress responses. Specifically, the effects of exogenous CRH on the electrophysiological activity of LC neurons in unanesthetized rats were characterized. Intracerebroventricular (I.C.V.) injection of CRH (0.3-3.0 micrograms) caused a dose-dependent increase in LC spontaneous discharge rates that became statistically significant 6-9 min after injection and was still evident 30-40 min later. A 1.0 and 3.0 micrograms amount of CRH caused peak increases of 86 +/- 32% and 184 +/- 29% (SEM), respectively. In contrast, neither the lowest dose of CRH (0.3 microgram) nor a high dose of Ala 14CRH (3.0 micrograms), an inactive analog of CRH, altered LC spontaneous activity. The effects of CRH administration on sensory-evoked activity of LC neurons were also determined. As previously reported (Foote et al., 1980; Aston-Jones and Bloom, 1981b), the repeated presentation of auditory tone stimuli resulted in a brief enhancement of LC discharge, which was usually followed by a period of relatively decreased activity. Administration of 1.0 or 3.0 micrograms CRH enhanced basal discharge during sensory testing, but discharge rates during the excitatory component of the sensory response were not altered. Quantitative analyses revealed that these doses of CRH produced a statistically significant decrease in the ratio of sensory-evoked to basal discharge rates. Additional analyses of the temporal distribution of discharge activity for individual recording sites during sensory testing demonstrated that 1.0 and 3.0 micrograms CRH altered relative response magnitudes to a statistically significant extent in 7 of 10 and 5 of 7 cases, respectively, while 0.3 microgram CRH and 3.0 micrograms Ala 14CRH were without effect. The present results are consistent with previous studies of CRH effects on LC activity in anesthetized rats (Valentino et al., 1983; Valentino and Foote, 1987). However, in unanesthetized animals, CRH is more potent in increasing tonic activity and does not decrease the absolute magnitude of sensory-evoked activity. The present results support the hypothesis that CRH released from fibers innervating the LC may affect the tonic activity of these cells and the relationship between tonic discharge and phasic, sensory-evoked activity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Corticotropin-releasing hormone increases tonic but not sensory-evoked activity of noradrenergic locus coeruleus neurons in unanesthetized rats. 325 21

The interaction of the peptide hormone adrenocorticotropin with solvent-free planar lipid bilayers (BLM) and liposomes was studied by measurements of elasticity modulus perpendicular to the plane of the membrane (E perpendicular, measured by electrostriction), surface potential difference (delta phi m), electrical capacitance, capacitance relaxation following a voltage jump (yielding relaxation times for molecular dipoles or dipolar domains), and fluorescence polarization. Addition of the 6-fold positively charged peptide to one side of the membrane leads to a more positive membrane surface potential, an increase of BLM capacitance, a decrease of elasticity modulus, and faster relaxation time constants. This also caused a decrease of DPH fluorescence anisotropy of the liposome suspension modified by fluorescent dye DPH. Mixed BLM of palmitoyl-oleoyl-phosphatidylcholine (POPC)+soybean phosphatidylcholine (SBPC) (10:1 w/w), which carry a negative surface charge, exhibit considerably larger changes than electroneutral POPC membranes. Our results confirm that ACTH1-24 binds to BLM and interacts with the hydrophobic part of the bilayer.
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PMID:Interaction of adrenocorticotropin-(1-24)-tetracosapeptide with lipid bilayers. 907 6