Nucleus accumbens carbachol disrupts olfactory and contextual fear-potentiated startle and attenuates baseline startle reactivity

Although the nucleus accumbens (NAc) typically is not considered a primary component of the circuitry underlying either the acquisition or retrieval of conditioned fear, evidence suggests that this region may play some role in modulating fear-related behaviors. The goal of the present study was to explore a potential role for NAc cholinergic receptors in the expression of fear-potentiated startle (FPS) and baseline startle reactivity. Intra-NAc infusion of the broad-acting cholinergic receptor agonist, carbachol, suppressed FPS elicited by re-exposure to both a discrete odor previously paired with footshock and the conditioning context. Although carbachol elevated spontaneous motor activity, activity bouts did not account for startle suppression in carbachol-treated Ss. In addition, intra-NAc carbachol suppressed baseline startle over a range of acoustic pulse intensities in the absence of explicit fear conditioning. Collectively, these findings suggest that NAc cholinergic receptors play a role in the modulation of baseline startle reactivity, rather than in the retrieval of learned fear, and that this role is independent of overt motor activity.

Research highlights▶ Conditioned olfactory fear-potentiated startle was observed following either one or six odor-shock pairings, but not following odor-alone or unpaired odor and shock. ▶ Nucleus accumbens infusion of the nonselective cholinergic agonist, carbachol, disrupted the expression of both conditioned olfactory and contextual fear potentiated startle. ▶ Nucleus accumbens infusion of carbachol disrupted baseline startle in unconditioned Ss. ▶ The effects of nucleus accumbens carbachol on the expression of fear-potentiated startle are likely due to a performance deficit rather than a retrieval deficit.