Sympathetic control of tryptophan uptake and morphine analgesia in stressed rats.
Guanethidine treatment decreased morphine analgesia exhibited by restrained rats but had no effect on morphine analgesia exhibited by unrestrained rats or on baseline pain sensitivity. Guanethidine also prevented the rise in tryptophan uptake into the brain induced by the restraint stress. It is argued that the prevention of the stress-induced increase in brain tryptophan uptake is causal to guanethidine's attenuation of morphine analgesia exhibited by restrained rats, since the increase in brain tryptophan uptake has already been shown to be critical to this phenomenon. The blockade of the stress-induced increase in brain tryptophan uptake and morphine analgesia by guanethidine support the hypothesis that these effects depend upon sympathetic activity.
D000698:Analgesia; D000818:Animals; D006145:Guanethidine / Q000494:pharmacology; D006897:Hydroxyindoleacetic Acid / Q000378:metabolism; D008297:Male; D009020:Morphine / Q000494:pharmacology*; D010146:Pain / Q000503:physiopathology; D051381:Rats; D012149:Restraint, Physical; D012701:Serotonin / Q000378:metabolism; D013315:Stress, Psychological / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000502:physiology*; D014364:Tryptophan / Q000378:metabolism*
D012701:Serotonin; D006897:Hydroxyindoleacetic Acid; D009020:Morphine; D014364:Tryptophan; D006145:Guanethidine