The correlation between swim-stress induced antinociception and [3H] leu-enkephalin binding to brain homogenates in mice.
Mice which had been made to swim for 3 minutes showed a tail flick latency which was significantly longer than that of unswum controls. The [3H] leu-enkephalin [LE] binding to brain homogenates from swum mice was significantly reduced when compared with that form unswum controls. Scatchard analysis revealed that the reduction in binding occurred at the LE low affinity site. However, when homogenates were allowed a preincubation period of 20 min at 37 degree C, the difference in LE binding between swum and unswum mice was no longer apparent. These data are interpreted to suggest that the reduced LE binding may be due to the occupation of a proportion of the opiate receptor population by an endogenous ligand. A correlation between the duration of the swim induced antinociceptive response and the changes in LE binding is described which although non-significant, is consistent with the interpretation for the involvement of endogenous opiates in the observed increases in tail flick latency.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D004723:Endorphins / Q000378:metabolism*; D004743:Enkephalin, Leucine; D004745:Enkephalins / Q000378:metabolism*; D005260:Female; D007700:Kinetics; D009115:Muridae; D009619:Nociceptors / Q000378:metabolism*; D011957:Receptors, Opioid / Q000378:metabolism*; D013312:Stress, Physiological / Q000378:metabolism*; D013550:Swimming
D004723:Endorphins; D004745:Enkephalins; D011957:Receptors, Opioid; D004743:Enkephalin, Leucine