Lesions of the periaqueductal gray disrupt input to the rostral ventromedial medulla following microinjections of morphine into the medial or basolateral nuclei of the amygdala

doi:10.1016/j.brainres.2004.02.048

Brain Research

Volume 1009, Issues 1–2, 29 May 2004, Pages 223-227

https://doi.org/10.1016/j.brainres.2004.02.048 Get rights and content

Abstract

Microinjections of morphine into the basolateral (BLa) and medial (MEa) nuclei of the amygdala differentially affect rostral ventromedial medulla (RVM) neuronal activity and nocifensive behaviors. PAG lesions attenuated or blocked the effects of both BLa and MEa morphine on RVM cell activity, and interfered with the behavioral antinociception produced by BLa infusions. These results demonstrate that the influences from both the BLa and MEa to the RVM are relayed via the PAG.

Section snippets

Histology

RVM recording sites were marked with an electrolytic lesion, and Pontamine Sky Blue dye injected through the micropipettes. The rat was then killed with an overdose of methohexital and perfused intracardially with physiological saline followed by 10% formalin. Recording, lesion, and infusion sites were all histologically verified. Lesions typically encompassed both the ventral and dorsal regions of the PAG and included at least the lateral edges of the dorsal raphe nucleus. In eight rats, the

Basolateral nucleus

In sham-lesioned animals, infusions of morphine into the BLa produced a significant, naloxone-reversible increase in TF latency (Fig. 1), with a significant attenuation of the reflex-related OFF-cell pause (Table 1, p<0.01). Spontaneous discharge of OFF-cells was increased and that of ON-cells decreased (Fig. 1). The TF-related ON-cell burst was also attenuated (41.2±16.6% of baseline, p<0.01). Each of these effects was blocked in PAG-lesioned animals. Thus, TF latencies were not elevated

Medial nucleus

In sham-lesioned animals, infusions of morphine into the MEa had no effect on TF latency (Fig. 2) or the TF-related OFF-cell pause (Table 1), but resulted in a significant, naloxone-reversible increase in spontaneous activity of OFF-cells, with a decrease in the spontaneous activity of ON-cells (Fig. 2). The ON-cell burst was also significantly reduced, to 54.2±12.5% of baseline (p<0.01). These controls thus replicate our previous finding that infusions of morphine into the MEa fail to alter TF

Acknowledgements

This research was supported by grants from NIDA (DA05608) and the Medical Research Foundation of Oregon. SM was supported by an INVEST fellowship from NIDA.

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Short communicationLesions of the periaqueductal gray disrupt input to the rostral ventromedial medulla following microinjections of morphine into the medial or basolateral nuclei of the amygdala

Abstract

Section snippets

Histology

Basolateral nucleus

Medial nucleus

Acknowledgements

Brain Res.

Neuroscience

Brain Res.

Neuroscience

Neuroscience

Brain Res.

Pain

Brain Res.

Brain Res. Bull.

Brain Res.

Brain Res.

A perceptual–defensive–recuperative model of fear and pain

Behav. Brain Sci.

Short communication
Lesions of the periaqueductal gray disrupt input to the rostral ventromedial medulla following microinjections of morphine into the medial or basolateral nuclei of the amygdala