Abstract
The infralimbic cortex (IL) is known to facilitate the formation of extinction memory through reciprocal interactions with the amygdala, which produces fear responses such as freezing. Thus, whether presynaptic input from the amygdala and post-synaptic output of IL neurons are functionally dissociated in extinction memory formation remains unclear. Here, we demonstrated that photostimulation of IL inputs from BLA did not change freezing responses to conditioned stimuli (CS) during training, but did facilitate extinction memory, measured as a reduction in freezing responses to the CS 1 day later. On the other hand, photostimulation of somata of IL neurons induced an immediate reduction in freezing to CS, but this did not affect extinction memory tested the next day. These results provide in vivo evidence for IL-dependent facilitation of extinction memory without post-synaptic modulation of freezing circuits.
Highlights
The infralimbic cortex (IL) has been implicated in the extinction of conditioned fear responses[1,2,3]
This promoter specifies the expression of ChR2 in pyramidal neurons, except for interneurons[21,22,23,24], and has been used to successfully induce action potentials in response to laser pulses delivered to the medial prefrontal cortex[25]
Studies have shown that IL neurons modulate extinction memory through their post-synaptic impacts on the amygdala involved in fear memory processing[1, 10]
Summary
The infralimbic cortex (IL) has been implicated in the extinction of conditioned fear responses[1,2,3]. Connectome studies have shown that efferents of IL neurons innervate inhibitory neurons in the amygdala[10], explaining how electrical stimulation can reduce the freezing response to CS. Recent studies suggests that these excitatory BLA neurons are involved in fear extinction[13, 14]. A recent study showed that optogenetically induced long-term depression (LTD) of the BLA-IL synapse facilitates extinction memory to CS rather than inhibition, suggesting an inhibitory role of this synapse[19]; the role of presynaptic activity in the IL remains controversial. We optogenetically stimulated input and output circuits separately under the same experimental conditions, examined effects on freezing responses and retrieval of extinction memory in mice
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