Effect of the blockade of mu1-opioid and 5HT2A-serotonergic/alpha1-noradrenergic receptors on sweet-substance-induced analgesia.
BACKGROUND
Sweet-substance-induced analgesia has been widely studied, and the investigation of the neurotransmitters involved in this antinociceptive process is an important way for understanding the involvement of the neural system controlling this kind of antinociception.


OBJECTIVE
The aim of this study was to investigate the involvement of opioid and monoaminergic systems in sweet-substance-induced analgesia.


METHODS
The present work was carried out in an animal model with the aim of investigating whether acute (24 h) or chronic (14 days) intake of a sweet substance, such as sucrose (250 g/l), is followed by antinociception. Tail withdrawal latencies in the tail-flick test were measured before and immediately after this treatment. Immediately after the recording of baseline values, independent groups of rats were submitted to sucrose or tap-water intake and, after chronic treatment, they were pretreated with intraperitoneal administration of (1) naltrexone at 0.5, 1, 2 or 3 mg/kg; (2) naloxonazine at 5, 10, 20 or 30 mg/kg; (3) methysergide at 0.5, 1, 2 or 3 mg/kg; (4) ketanserin at 0.5, 1, 2 or 3 mg/kg; or (5) physiological saline.


RESULTS
Naltrexone and methysergide at two major doses decreased sweet-substance-induced analgesia after chronic intake of a sweet substance. These effects were corroborated by peripheral administration of naloxonazine and ketanserin.


CONCLUSIONS
These data give further evidence for: (a) the involvement of endogenous opioids and a mu1-opioid receptor in the sweet-substance-induced antinociception; (b) the involvement of monoamines and 5HT2A serotonergic/alpha1-noradrenergic receptors in the central regulation of the sweet-substance-produced analgesia.
Rebouças
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EC
Laboratório de Neuroanatomia e Neuropsicobiologia, Departamento de Farmacologia, Faculdade de Medicina de Ribeirão Preto (USP), Avenida dos Bandeirantes, 3900, Ribeirão Preto (SP), 14049-900, Brasil.
Segato
E N
EN
Kishi
R
R
Freitas
R L
RL
Savoldi
M
M
Morato
S
S
Coimbra
N C
NC
D058668:Adrenergic alpha-1 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000698:Analgesia; D000818:Animals; D004305:Dose-Response Relationship, Drug; D007650:Ketanserin / Q000494:pharmacology; D008297:Male; D008784:Methysergide / Q000494:pharmacology; D009270:Naloxone / Q000031:analogs & derivatives / Q000494:pharmacology; D009271:Naltrexone / Q000494:pharmacology; D010147:Pain Measurement / Q000187:drug effects; D017288:Pain Threshold / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D044402:Receptor, Serotonin, 5-HT2A / Q000187:drug effects*; D017450:Receptors, Opioid, mu / Q000037:antagonists & inhibitors*; D012702:Serotonin Antagonists / Q000494:pharmacology*; D013395:Sucrose / Q000494:pharmacology; D013649:Taste / Q000502:physiology*
D058668:Adrenergic alpha-1 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists; C485765:Oprm1 protein, rat; D044402:Receptor, Serotonin, 5-HT2A; D017450:Receptors, Opioid, mu; D012702:Serotonin Antagonists; D009270:Naloxone; D013395:Sucrose; D009271:Naltrexone; C034643:naloxonazine; D007650:Ketanserin; D008784:Methysergide