Facilitation of fear extinction by novelty depends on dopamine acting on D1-subtype dopamine receptors in hippocampus.

Extinction is the learned inhibition of retrieval. Recently it was shown that a brief exposure to a novel environment enhances the extinction of contextual fear in rats, an effect explainable by a synaptic tagging-and-capture process. Here we examine whether this also happens with the extinction of another fear-motivated task, inhibitory avoidance (IA), and whether it depends on dopamine acting on D1 or D5 receptors. Rats were trained first in IA and then in extinction of this task. The retention of extinction was measured 24 h later. A 5-min exposure to a novel environment 30 min before extinction training enhanced its retention. Right after exposure to the novelty, animals were given bilateral intrahippocampal infusions of vehicle (VEH), of the protein synthesis inhibitor anisomycin, of the D1/D5 dopaminergic antagonist SCH23390, of the PKA inhibitor Rp-cAMP or of the PKC inhibitor Gö6976, and of the PKA stimulator Sp-cAMP or of the PKC stimulator PMA. The novelty increased hippocampal dopamine levels and facilitated the extinction, which was inhibited by intrahippocampal protein synthesis inhibitor anisomysin, D1/D5 dopaminerdic antagonist SCH23390, or PKA inhibitor Rp-cAMP and unaffected by PKC inhibitor Gö6976; additionally, the hippocampal infusion of PKA stimulator Sp-cAMP reverts the effect of D1/D5 dopaminergic antagonist SCH 23390, but the infusion of PKC stimulator PMA does not. The results attest to the generality of the novelty effect on fear extinction, suggest that it relies on synaptic tagging and capture, and show that it depends on hippocampal dopamine D1 but not D5 receptors.

Chronic exposure to low mercury chloride concentration induces object recognition and aversive memories deficits in rats.

This work examines the effects of chronic exposure to low inorganic mercury (mercury chloride, HgCl(2)) concentration on the recognition and aversive memories. Forty male Wistar rats were divided into 4 groups treated during 30 or 60 days with saline (control) or HgCl(2) doses. After treated the animals were tested considering object recognition and inhibitory avoidance behavioral memory paradigms. Elevated plus maze, open field and tail flick tests were used to assess anxiety, locomotor and exploratory activity and pain thresholds. Only exposure for 60 days to HgCl(2) induced in memory deficits quantified in the object recognition task. In the inhibitory avoidance all the animals exposed to mercury (for 30 or 60 days) presented worst performance than control animals. Our results suggest that chronic exposure to low mercury chloride concentrations impairs memory formation.