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This Week in The Journal

Animals learn cues that signal upcoming dangers and respond by performing passive or active defensive behaviors. Tones that predict electrical shock, for example, can induce mice to freeze (a passive behavior) or to exit to a safe chamber (active avoidance). Recognition of cues that elicits passive or active responses depends on the lateral amygdala. From there, however, the circuits controlling passive and active responses diverge: whereas activation of the central amygdala leads to freezing, activation of the nucleus accumbens, a part of the basal ganglia, is required for signaled active avoidance. How the nucleus accumbens promotes active avoidance is unclear, but inhibition of neurons in the substantia nigra pars reticulata (SNr), one of the main output nuclei of the basal ganglia, might be involved. Indeed, activation of SNr can suppress signaled active avoidance, possibly by inhibiting the superior colliculus, an area that is activated during cue-triggered escape and that drives escape when stimulated. Alternatively, the SNr might inhibit signaled active avoidance through its projections to the thalamus or the pedunculopontine tegmental nucleus (PPT), a midbrain nucleus that contributes to locomotor control. Hormigo et al. used optogenetic tools to investigate the roles of SNr, PPT, superior colliculus, and thalamus in signaled active avoidance. Activation of SNr terminals in the thalamus did not affect avoidance responses, but activation of terminals in the PPT suppressed these responses. Stimulation of SNr terminals in superior colliculus sometimes suppressed avoidance, but this stimulation also led to the inhibition of PPT neurons, likely by activating SNr collaterals. Therefore, SNr likely suppresses signaled active avoidance primarily by inhibiting neurons in PPT. Consistent with this, inhibiting glutamatergic PPT neurons reduced the proportion of cue-triggered escapes and increased the escape latency, whereas exciting these neurons enhanced escape. In contrast, inhibiting GABAergic PPT neurons increased the proportion of escapes and reduced latency, whereas exciting these neurons suppressed escape. These results suggest that SNr suppresses signaled active avoidance by inhibiting glutamatergic neurons in the PPT that drive locomotor behaviors. What activates PPT neurons to promote escape in the presence of threat-associated cues remains unclear, but, given that the amygdala and ventral striatum send direct projections to the PPT, these are likely candidates.