GABAergic antagonism of the central nucleus of the amygdala attenuates reductions in rapid eye movement sleep after inescapable footshock stress.

STUDY OBJECTIVES

Rapid eye movement sleep (REM) appears to be especially susceptible to the effects of stress; inescapable footshock stress (IS) can produce reductions in REM that can occur without recovery sleep. The amygdala has well-established roles in stress and emotion; the central nucleus of the amygdala (CNA) projects to REM regulatory regions in the brainstem and has been found to play a key role in the regulation of REM. The objective of this study was to determine whether the reduction in REM induced by IS could be regulated by CNA and brainstem regions.

DESIGN

The GABAergic agonist muscimol (MUS) and GABAergic antagonist bicuculline (BIC) were microinjected into CNA before IS, and sleep was recorded for 20 h. In a second experiment using the same manipulations, sleep was recorded for 2 h, after which the rats were killed to evaluate Fos expression (a marker of neuronal activity) in the locus coeruleus (LC), a brainstem REM regulatory region.

SETTING

NA.

PATIENTS OR PARTICIPANTS

The subjects were male, outbred Wistar rats.

INTERVENTIONS

The rats were surgically implanted with standard electrodes or with telemetry transmitters for determining arousal state.

MEASUREMENTS AND RESULTS

IS preceded by control or MUS microinjections selectively reduced REM and increased Fos expression in LC. By comparison, microinjection of BIC into CNA prior to IS attenuated both the reduction in REM and Fos expression in LC to levels seen in non-shocked controls.

CONCLUSIONS

The results suggest that the effects of IS on REM may involve local GABAergic inhibition in CNA and activation of LC.