Abstract
The medial prefrontal cortex (mPFC) and its abundant connections with other brain regions play key roles in memory, cognition, decision making, social behaviors, and mood. Dysfunction in mPFC is implicated in psychiatric disorders in which these behaviors go awry. The prolonged maturation of mPFC likely enables complex behaviors to emerge, but also increases their vulnerability to disruption. Many foundational studies have characterized either mPFC synaptic or behavioral development without establishing connections between them. Here, we review this rich body of literature, aligning major events in mPFC development with the maturation of complex behaviors. We focus on emotional memory and cognitive flexibility, and highlight new work linking mPFC circuit disruption to alterations of these behaviors in disease models. We advance new hypotheses about the causal connections between mPFC synaptic development and behavioral maturation and propose research strategies to establish an integrated understanding of neural architecture and behavioral repertoires.
Highlights
We focus on cognitive flexibility and emotional learning and memory in both the aversive and appetitive domains
We propose that the maturation of the component parts of medial prefrontal cortex (mPFC) circuitry subserves the ontogeny of complex behaviors, with the behavioral functions of mPFC updating during transitions between critical windows of development
We propose that the juvenile development of mPFC’s long-range connections, those with the basolateral amygdala (BLA), is necessary for mPFC’s ability to regulate conditioned fear
Summary
Developmental Biology Neuroscience and autism spectrum disorder (ASD) (Schubert et al, 2015). Development of inhibitory neurotransmission mPFC inhibitory interneurons undergo robust developmental changes in the adolescent period and are critical for the encoding and expression of fear memories in adulthood. Given that both PV and SST interneurons within mPFC are necessary for fear expression in the adult (Courtin et al, 2014; Cummings and Clem, 2020), the dynamic changes in protein level, cell morphology, and cell density that occur in these interneuron populations through early adolescence may underlie developmental changes in fear memory retrieval These changes in interneuron populations are likely to interact with developing long-range connections from key regions including the BLA to influence fear memory retrieval. Given the unique behavioral contributions of different classes of interneurons, mapping out the unique spatiotemporal trajectory of their synaptic development within mPFC microcircuits and performing targeted manipulations of interneuron function during behavior will significantly advance our understanding of how the synaptic development of mPFC inhibitory interneurons shapes maturing behaviors
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