Psychopharmacological evidences for the involvement of muscarinic and nicotinic cholinergic receptors on sweet substance-induced analgesia in Rattus norvegicus

Effect of the blockade of ?1-opioid and 5HT2A-serotonergic/?1-noradrenergic receptors on sweet-substance-induced analgesia

“…The present results suggest that chronic intake of sweet substances, such as sucrose, induces clearly significant analgesic effects, and these findings are in accordance with previous studies (Bergmann et al 1985;Segato et al 1997;Irusta et al 2001). In the present work, the temporal curve of the analgesic effect of intake of sucrose solutions showed the presence of sweet-substance-induced antinociception after chronic treatment with 250 g/l sucrose solution.…”

“…In fact, a recent report showed evidence that chronic exposure to a stressful situation exerts influence on feeding behavior, decreasing the ingestion of sweet food, and also the monoaminergic neurotransmission in the hypothalamus (Gamaro et al 2003). Animals were given tap water or a concentrated (250 g/l) sucrose solution as the only source of liquid instead of a preference paradigm in order to easily compare the previous data from this laboratory and others (Segato et al 1997;Irusta et al 2001, Anseloni et al 2002.…”

“…There is evidence that the consumption of sweet palatable substances produces analgesia in animals (Holder 1988;Blass and Shide 1994;Segato et al 1997;Irusta et al 2001;Anseloni et al 2002) and in humans (Blass and Hoffmeyer 1991;Abad et al 1996;Mercer and Holder 1996). In fact, concentrated sucrose solutions seem to reduce crying and other pain-related behavior in healthy normal babies, and sucrose may be a safe and useful analgesic for minor surgical interventions in full-term infants (Haouari et al 1995;Abad et al 1996;Skogsdal et al 1997).…”

“…Although we must consider the evidence that the consumption of sucrose solutions or the sweet-food intake can change the nociceptive sensitivity by the activation of opioid mechanism (Davis et al 1956;Kanarek et al 2001), we cannot dismiss the possibility of the involvement of other neurotransmitters, such as serotonin (5-HT) and other chemical mediators, in this process. In fact, in addition to the involvement of the opioid system (Blass and Fitzgerald 1988;Segato et al 1997), cholinergic mechanisms mediated by the nicotinic receptor may exert an important role in the manifestation of the sweet-substance-induced analgesia (Irusta et al 2001). A recent report suggests that the intake of palatable food and fluids acts within the dorsomedial and dorsolateral columns of the periaqueductal gray matter, a mesencephalic structure rich in 5-HT-containing terminals and endogenous opioid-containing perikaria (Steinbusch 1981;Eichenberger et al 2002;Osaki et al 2003), to moderate the behavioral action of opioid drugs (Kanarek et al 2001).…”

Sweet Solution Analgesia

“…Besides, endogenous opioid system, other neurotransmiters and receptors are probably involved. One study revealed a major involvement of nicotinic cholinergic receptors in the sweet substanceinduced analgesia as atropine (cholinergic antagonist) diminished sucrose-induced analgesia [76]. Other studies have shown the involvement of noradrenaline, serotonin and their receptors in the central modulation sweet substance-induced analgesia [71,77,78].…”