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After extinction, fear memories are not erased rather they are inhibited. This inhibition of fear is limited to the extinction context, and fear memory returns or “renews” outside of the extinction context. It has been suggested that a hippocampal – prefrontal – amygdala circuit is involved in the contextual regulation of extinguished fear memories. In this talk I will present recent experiments using anatomical disconnections and functional retrograde tracing that map the neural circuit for fear renewal in rats. These data reveal that projections from both the ventral hippocampus and prelimbic cortex to the basolateral amygdala are necessary for the renewal of fear after extinction.
Substantial evidence indicates that extinguished fear can be recovered after a change in experimental context (i.e., the renewal effect). The aim of this study was to characterize the neural circuitry underlying the retrieval of extinguished fear memories using c-Fos immunohistochemistry. Firstly, rats received auditory fear conditioning. Subsequently, they were extinguished by presenting CS-alone trials in either the same context as conditioning or in a second context. Then, all rats were tested for their fear of the auditory CS in the second context and sacrifi ced 90 min after testing. The presentation of the extinguished CS outside of the extinction context resulted in renewal of the freezing response relative to animals tested to the CS in the extinction context. In addition, the renewal of fear was associated with c-Fos expression in the prelimbic division of the medial prefrontal cortex, the lateral and basolateral nuclei of the amygdala, and the medial division of the central nucleus of the amygdala. In contrast, the presentation of the CS in the extinction context induced c-Fos expression in the infralimbic cortex, the intercalated nuclei of the amygdala and the dentate gyrus. Hippocampal areas CA1 and CA3 exhibited c-Fos expression when the CS was presented in either context. These data suggest that the context-specifi city of extinction may be mediated by prefrontal modulation of amygdala activity, and that the hippocampus may have a fundamental role in contextual memory retrieval.
It is well known that emotions participate in regulation of social behaviors and that the emotional states displayed by a conspecifi c can seriously affect the behavior of other animals. In its simplest forms empathy can be characterized as the capacity to be affected by and/or share the emotional state of another. However, to date, relatively little is known about the mechanisms by which the animals that are not in a direct danger can share emotions. In the present study we used the model of between-subject transfer of fear to characterize the social interaction during which fear is transmitted, as well as the effects of socially transmitted fear on behavior of its recipients. We found that: (1) during social interaction with a recently fear conditioned partner, observers and demonstrators exhibit social exploratory behaviors rather than aggressive behaviors; (2) learning in a shockmotivated shuttle avoidance task is facilitated in rats that under-went the social interaction with a partner that had been either fear conditioned or trained in two-way avoidance; (3) a brief social interaction with a recently fear conditioned partner immediately before fear conditioning improves conditioned freezing measured on the next day; this effect can be also seen in rats that are unfamiliar to each other. Collectively, the obtained data suggest that a brief social interaction with a cage-mate that had undergone an aversive learning experience promotes aversive learning in an otherwise naïve animal.
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