Galanin (GAL) is suggested to be a neuropeptide involved in pain
transmission. In this study we tried to determine, whether the
increase of GAL concentration in brain cells affects impulse
transmission between the motor centers localized in the vicinity
of the third and fourth cerebral ventricles. The experiments were
carried out on rats under chloralose anesthesia. The study
objectives were realized using the method allowing to record the
amplitude of evoked tongue jerks (ETJ) in response to noxious
tooth pulp stimulation during the perfusion of the cerebral
ventricles with solutions containing tested compounds. Perfusion
of the cerebral ventricles with GAL concentration-dependently
inhibited the ETJ amplitude. The antinociceptive effect of GAL
was blocked by a galanin receptor antagonist, galantide (GLT)
and by opioid antagonists: non-selective naloxone (Nal) and μselective β-funaltrexamine (β-FNA). In contrast, a δ-opioid
receptor antagonist, naltrindole (NTI) or the κ-opioid receptor
antagonist, nor-binaltrophimine (nor-BNI) did not inhibit the
effect of GAL. The antinociceptive effect of GAL was more
pronounced when GAL was perfused in combination with other
neuropeptides/neurohormones, such as endomorphin-2 (EM-2),
vasopressin (AVP) and oxytocin (OT). The present results
demonstrate that in the orofacial area analgesic activity is
modulated by GAL, OT and AVP and that EM-2-induced
antinociception involves GAL.
κ-Opioid receptor mediates the antinociceptive effect of nitrous oxide in mice
