Behavioral sensitization induced by dorsal periaqueductal gray electrical stimulation is counteracted by NK1 receptor antagonism in the ventral hippocampus and central nucleus of the amygdala

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Abstract

A single threatening experience may change the behavior of an animal in a long-lasting way and elicit generalized behavioral responses to a novel threatening situation that is unrelated to the original aversive experience. Electrical stimulation (ES) of the dorsal periaqueductal gray (dPAG) produces a range of defensive reactions, characterized by freezing, escape, and post-stimulation freezing (PSF). The latter reflects the processing of ascending aversive information to prosencephalic structures, including the central nucleus of the amygdala (CeA), which allows the animal to evaluate the consequences of the aversive situation. This process is modulated by substance P (SP) and its preferred receptor, neurokinin 1 (NK1). The ventral hippocampus (VH) has been associated with the processing of aversive information and expression of emotional reactions with negative valence, but the participation of the VH in the expression of these defensive responses has not been investigated. The VH is rich in NK1 receptor expression and has a high density of SP-containing fibers. The present study examined the role of NK1 receptors in the VH in the expression of defensive responses and behavioral sensitization that were induced by dPAG-ES. Rats were implanted with an electrode in the dPAG for ES, and a cannula was implanted in the VH or CeA for injections of vehicle (phosphate-buffered saline) or the NK1 receptor antagonist spantide (100 pmol/0.2 μL. Spantide reduced the duration of PSF that was evoked by dPAG-ES, without changing the aversive freezing or escape thresholds. One and 7 days later, exploratory behavior was evaluated in independent groups of rats in the elevated plus maze (EPM). dPAG-ES in rats that received vehicle caused higher aversion to the open arms of the EPM compared with rats that did not receive dPAG stimulation at both time intervals. Injections of spantide in the VH or CeA prevented the proaversive effects of dPAG-ES in the EPM only 1 day later. These findings suggest that NK1 receptors are activated in both the VH and CeA during the processing of aversive information that derives from dPAG-ES. As previously shown for the CeA, SP/NK1 receptors in the VH are recruited during PSF that is evoked by dPAG-ES, suggesting that a 24-h time window is susceptible to interventions with NK1 antagonists that block the passage of aversive information from the dPAG to higher brain areas.

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