Analgesia brain pathways

The above discrepancies seem to be due mainly to the stringencies of the end-points in each test. However, one can also doubt the applicability of these tests for cannabinoids. These tests were developed for opiates and may not necessarily parallel and be fully relevant to THC activity in man. Indeed, recent work on electrodes implanted into several distinct brain areas of the rat led to the conclusion that the apparent analgesia produced by the cannabinoids is more related to their disruption of discharge in response to some synthetic impact rather than to a depression of pain pathways [130]. The question whether cannabinoids cause analgesia by interference with pain reception or with pain perception is still unresolved. 

In addition to its central stimulation of I1-IBS and Q2-adrenoceptors (20,21), clonidine (as well as other Q2-adrenergic agonists), when administered epidurally, produces analgesia by stimulation of spinal a2-adrenoceptors, inhibiting sympathetically mediated pain pathways that are activated by nociceptive stimuli, thus preventing transmission of pain signals to the brain (9). Activation of a2-adrenoceptors also apparently stimulates acetylcholine release and inhibits... 

Electrolytic lesions to the nucleus raph dorsalis cause a marked decrease in forebrain 5-HT levels which results in an antagonism of morphine analgesia [272,273], but not of methadone or pethidine analgesia [274]. This led the authors to suggest that morphine may be atypical (amongst opiate analgesics) in its reliance upon intact 5-HT pathways. There have been other reports that methadone [146] and pethidine [258,259] behave differently from morphine, as they do not increase rat brain 5-HT turnover following their acute administra-... 

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