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)

1. The actions of the neuropeptide nociceptin on the calcium channel currents (IBa) of acutely dissociated rat periaqueductal grey (PAG) neurons were examined using whole-cell patch clamp techniques. These effects were compared with those of opioid receptor agonists and the GABAB receptor agonist baclofen. 2. Neurons from young adult rats (23 to 56 days old) expressed predominantly omega-conotoxin GVIA (N-type)- and omega-agatoxin IVA (P/Q-type)-sensitive IBa, together with smaller amounts of nimodipine-sensitive current and current resistant to all three blockers. There was proportionately more N-type IBa in neurons from female rats and proportionately more resistant current in neurons from male rats. 3. Nociceptin (EC50, 5 nM) and baclofen (EC50, 0.8 microM) inhibited IBa in all PAG neurons, while the opioid agonist methionine enkephalin (met-enkephalin; 300 nM-10 microM) inhibited IBa in 40 % of neurons. The effects of met-enkephalin were reversed by the mu-opioid antagonist CTAP, and mimicked by the mu-opioid agonist DAMGO (300 nM-3 microM). The delta-opioid agonists DPDPE and deltorphin II, and the kappa-opioid agonist U69593, did not affect IBa in any neuron. The actions of nociceptin were not mimicked or blocked by the opioid antagonist naloxone or the nociceptin analogue [desPhe1]-nociceptin. 4. The effects of nociceptin and baclofen on IBa were blocked by pretreatment of the neurons with pertussis toxin (500 ng ml-1, 8 h). 5. Nociceptin predominantly inhibited the N-type (EC50, 2 nM; maximum inhibition, 50 %) and P/Q-type (EC50, 7 nM; maximum inhibition, 33 %) IBa while having little effect on the L-type and R-type IBa. 6. These results are consistent with the previously described actions of nociceptin, baclofen and micro-opioids in PAG slices, whereby they couple to increases in an inwardly rectifying K+ conductance. These agonists thus have the potential to modulate the function of PAG neurons via a number of different cellular effectors.
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PMID:Modulation of Ca2+ channel currents of acutely dissociated rat periaqueductal grey neurons. 954 80

In the corticotroph-like murine pituitary tumor cell line, AtT-20, adrenocorticotropic hormone release is triggered by corticotropin-releasing hormone and is attenuated by the synthetic adrenal steroid dexamethasone. The precise mechanisms by which dexamethasone inhibits secretion are under investigation. We examined whether dexamethasone can modulate release via regulation of calcium homeostasis. More specifically, we have evaluated the effects of dexamethasone on calcium current, intracellular calcium concentration, and adrenocorticotropic hormone release. Using perforated patch-clamp and calcium imaging with fura PE3/AM, we found that dexamethasone decreases calcium current and intracellular calcium levels. The inhibition of current by dexamethasone is not, however, altered by the calcium channel antagonists nifedipine (L-type) or omega-agatoxin IVA (P/Q-type), despite the presence of these calcium channel subtypes in AtT-20 cells and the exclusive coupling of adrenocorticotropic hormone release to the L-type channel in these cells. We also evaluated the temporal relationship between dexamethasone-mediated inhibition of secretion and calcium influx. Whereas a prolonged (2 h) incubation with dexamethasone inhibits corticotropin-induced release by approximately 40%, a rapid (10 min) incubation (a time interval sufficient for dexamethasone-mediated inhibition of calcium transients) does not inhibit release. These data suggest, therefore, that dexamethasone does, indeed, modulate calcium homeostasis in AtT-20 cells, but that this effect is not responsible for its inhibition of secretion.
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PMID:Dexamethasone-mediated inhibition of calcium transients and ACTH release in a pituitary cell line (AtT-20). 1043 77

Comparisons of two assessment measures for ADHD: the ADHD Behavior Checklist and the Integrated Visual and Auditory Continuous Performance Test (IVA CPT) were examined using undergraduates (n=44) randomly assigned to a control or a simulated malingerer condition and undergraduates with a valid diagnosis of ADHD (n=16). It was predicted that malingerers would successfully fake ADHD on the rating scale but not on the CPT for which they would overcompensate, scoring lower than all other groups. Analyses indicated that the ADHD Behavior Rating Scale was successfully faked for childhood and current symptoms. IVA CPT could not be faked on 81% of its scales. The CPT's impairment index results revealed: sensitivity 94%, specificity 91%, PPP 88%, NPP 95%. Results provide support for the inclusion of a CPT in assessment of adult ADHD.
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PMID:Detection of malingering in assessment of adult ADHD. 1459 53