Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of two stressogenic conditions, restraint at 4 degrees C for 30 min (cold-restraint stress; CRS) or swimming at 20 degrees C for 3 min (swim stress; SS), on nociception and on convulsions triggered by different agents was assessed in mice. In saline-pretreated mice CRS and SS caused analgesia (hot-plate test, 56 degrees C), delayed the onset of convulsions induced by pentylenetetrazol (PTZ, 100 mg/kg, IP) and aggravated convulsions elicited by maximal transcorneal electroshock (150 mA pulses at 60 Hz for 0.2 s). Pretreatment with naloxone (10 mg/kg, SC, 30 min prior to testing), which did not affect the responsiveness of nonstressed mice to the hot plate or to the convulsant treatments, attenuated the development of analgesia following CRS, but not SS, and further prolonged the latency to onset of PTZ-induced convulsions in both stressed groups. Thus the extent to which CRS and SS can each delay the onset of PTZ-triggered convulsion appears to be limited by activation of a proconvulsant opioid system. In contrast, naloxone pretreatment did not modify the effects of CRS or SS on the severity of electroshock-induced seizures. In conclusion, CRS and SS can each, simultaneously, exert anticonvulsant and proconvulsant influences on responsiveness to PTZ and electroshock, respectively. Also, both forms of stress can activate an opioid system modulating the onset of PTZ-induced seizures, which is distinct from that controlling nociception. These findings, together with those of other stress, convulsions and opioid systems, which depends on the characteristics of the stressogenic condition, species, convulsant agent and parameter considered.
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PMID:Effects of cold-restraint and swim stress on convulsions induced by pentylenetetrazol and electroshock: influence of naloxone pretreatment. 180 34

The role of mu and delta opioid receptors in the spinal and supraspinal analgesic actions of morphine and [D-Pen2, L-Pen5] enkephalin were examined in the tail-flick test utilizing the mu opioid receptor deficient CXBK mouse and BALB/cBy and C57BL/6By, the progenitor strains of CXBK. The analgesic effects of i.c.v. administered morphine were equivalent in the CRS-CD1 (Swiss) standard laboratory mice and the progenitor strains of CXBK. Morphine did not, however, produce analgesia in the CXBK mice at doses greater than 10 times the ED50 dose in the progenitor strains. Similarly, the analgesic effect of i.c.v. [D-Ala2, NMePhe4, Gly-ol]enkephalin, a highly selective mu receptor peptide agonist, also was reduced greatly in the CXBK mice. These data are consistent with the deficiency in mu opioid receptors observed autoradiographically in this strain. In contrast, the highly selective delta opioid receptor peptide agonist [D-Pen2, L-Pen5]enkephalin was equipotent i.c.v. in the CXBK mice and in the progenitor strains of CXBK. In contrast to the effects produced by i.c.v. administration, the analgesic effects of intrathecally administered morphine were similar between CRS-CD1 and CXBX strains of mice. These results suggest that 1) both mu and delta opioid receptors can mediate supraspinal analgesia and 2) that the receptor(s) involved in spinally mediated analgesia is (are) quite distinct from those involved supraspinally.
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PMID:Examination of the involvement of supraspinal and spinal mu and delta opioid receptors in analgesia using the mu receptor deficient CXBK mouse. 283 33