Abstract
Adolescents, both humans and rodents, exhibit a marked impairment in extinction of learned fear relative to both younger (i.e., juveniles) and older (i.e., adults) groups. This impairment could be due to the medial or lateral prefrontal cortex (PFC) not being efficiently recruited during extinction. For example, unlike juveniles and adults, adolescent rats do not express extinction-induced increases in phosphorylated mitogen activated protein kinase (pMAPK), a marker of synaptic plasticity, in the medial PFC. The NMDA receptor partial agonist D-cycloserine (DCS), which enhances exposure therapy in humans with anxiety disorders, overcomes the extinction retention deficit in adolescent rats. The present experiments investigated the effects of DCS on the PFC and amygdala by measuring pMAPK-immunoreactive (IR) neurons.
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