Possible involvement of a dopaminergic link in the analgesic action of morphine
Many workers have attempted to assign specific functions to catecholamines in the central nervous system, since Vogt (1954) demonstrated their presence in different areas of brain. Vedernikov and Afrikanov (1969) have reported that pretreatment with reserpine reduced the analgesic activity of morphine. Subsequently Vedernikov (1970) observed that prior administration of pyrogallol, cocaine and iproniazid also potentiated the analgesic activity of morphine. On the basis of these observations noradrenaline (NA) has been suggested as playing a significant role in the analgesic activity of morphine. The possibility of NA being a neurotransmitter at the spinothalamic pathways which transmit nociceptive impulses has also been postulated. Even though in most of these experiments there is also a change in dopamine (DA) levels in the same direction, these workers have not attached much significance to changes in DA level. Recently however, DA has also been increasingly considered to have important functions at subcortical structures such as striatum and substantia nigra. In these areas, its presence in the presynaptic nerve endings has been demonstrated by histochemical methods (Dahlström and Fuxe, 1964). The involvement of dopaminergic mechanisms in morphine analgesia has recently been suggested by some workers (Calcutt, Doggett and Spencer, 1971; Carroll and Sharp 1972). The present study was undertaken to further investigate the possible role of DA in the antinociceptive (analgesic) activity of morphine.
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