Abstract
Several studies have demonstrated the involvement of the central nucleus of the amygdala (CEA) in the modulation of defensive behavior and in antinociceptive regulation. In a previous study, we demonstrated the existence of a cholinergic-opioidergic interaction in the CEA, modulating the defensive response of tonic immobility in guinea pigs. In the present study, we investigated a similar interaction in the CEA, but now involved in the regulation of the nociceptive response. Microinjection of carbachol (2.7 nmol) and morphine (2.2 nmol) into the CEA promoted antinociception up to 45 min after microinjection in guinea pigs as determined by a decrease in the vocalization index in the vocalization test. This test consists of the application of a peripheral noxious stimulus (electric shock into the subcutaneous region of the thigh) that provokes the emission of a vocalization response by the animal. Furthermore, the present results demonstrated that the antinociceptive effect of carbachol (2.7 nmol; N = 10) was blocked by previous administration of atropine (0.7 nmol; N = 7) or naloxone (1.3 nmol; N = 7) into the same site. In addition, the decrease in the vocalization index induced by the microinjection of morphine (2.2 nmol; N = 9) into the CEA was prevented by pretreatment with naloxone (1.3 nmol; N = 11). All sites of injection were confirmed by histology. These results indicate the involvement of the cholinergic and opioidergic systems of the CEA in the modulation of antinociception in guinea pigs. In addition, the present study suggests that cholinergic transmission may activate the release of endorphins/enkephalins from interneurons of the CEA, resulting in antinociception.
Highlights
The central nucleus of the amygdala (CEA) is involved in diverse emotional and cognitive functions related to responses of fear and orientation [1,2], defensive behavior [3,4], and cardiovascular regulation [5]
In a previous study [15] we demonstrated that the cholinergic system of the CEA participates in the modulation of defensive behavior and in antinociception through a functional and anatomical connection with the ventrolateral periaqueductal gray matter (PAG), because pretreatment with lidocaine injected into the ventrolateral PAG blocked the decrease in the duration of the defensive behavior of tonic immobility and the reduction of the vocalization index after carbachol microinjection into the CEA
The present results demonstrated that the antinociceptive effect of carbachol (Figure 2B) was blocked by the previous administration of atropine or naloxone into the same site (Figures 1A and 2C,D)
Summary
The central nucleus of the amygdala (CEA) is involved in diverse emotional and cognitive functions related to responses of fear and orientation [1,2], defensive behavior [3,4], and cardiovascular regulation [5]. (trigemio)pontoamygdaloid pathway with relay in the parabrachial area [9] This pathway is probably involved in the affectiveemotional (fear, aggression), behavioral (vocalization, fight, freezing) and autonomic (cardiovascular and respiratory responses) reactions to noxious events [9]. Fox and Sorenson [7] have shown that lesion of the CEA promoted a reduction in antinociception induced by meeting a predator and in antinociception promoted by classical conditioning evaluated by the tailflick test. These results suggest the involvement of the CEA in the regulation of antinociception induced by aversive events
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