Antinociception and behavioral manifestations induced by intracerebroventricular or intra-amygdaloid administration of cholinergic agonists in the rat

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Abstract
Changes in the tail-flick latency (TFL) to noxious heat stimulation and behavioral changes produced by intracerebroventricular (i.c.v.) or intra-amygdala administration of cholinergic agonists were studied in the rat. A significant increase in the TFL and behavioral changes were produced by carbachol (CCh, 2.2–8.8 nmol) injected into the dorsomedial portion (LVm) and inferior horn of the lateral ventricle (LVi), the effects being more prominent following injection into the LVi. Atropine (0.7 nmol), but not mecamylamine (5 nmol), fully inhibited the effects of CCh injected into the LVi. Bethanechol (4.4 nmol) and oxotremorine (1.1–5.5 nmol), but not dimethylphenyl-piperazinium (DMPP, 4.4 nmol), also increased the TFL following administration into the LVi. These cholinergic agonists were generally all less effective than CCh in eliciting behavioral changes. These results are indicative that muscarinic mechanisms of structures in the immediate vicinity of the LVi may be involved in cholinergic antinociception. When microinjected into the medial, central, basolateral, and posterior lateral nuclei of the amygdala complex (AC), both CCh and oxotremorine produced a significant increase in the TFL, but in no case was the effect stronger than that produced by stimulation of the medial nucleus. When microinjected into the same nuclei of the AC, CCh, but not oxotremorine, produced behavioral changes which were less frequent after stimulation of the medial nucleus. The behavioral changes, but not the antinociception, produced by CCh microinjected into the medial nucleus were inhibited by diazepam (1 mg/kg, i.p.). These results are indicative that antinociception and behavioral changes evoked by CCh injected into the AC depend on drug action on different amygdala structures. They also suggests that antinociception from the medial nucleus is not secondary to the aversive reactions evoked by CCh and depends on the activation of mechanisms different from those required for the production of behavioral changes.

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