Figure 7.

A model of fear memory consolidation. Fear memory consolidation is hypothesized to involve both pre- and postsynaptic modifications at thalamo-LA synapses. These modifications are first triggered by NMDAR-mediated alterations in protein kinase signaling pathways in LA neurons that ultimately promote postsynaptic functional and/or structural changes that contribute to the formation of the memory (Step 1). Second, NMDAR-driven synaptic plasticity in LA neurons is hypothesized to lead to the activation of nNOS in LA neurons and the release of nitric oxide (NO; Step 2), which can in turn engage ERK-dependent signaling and transcription in MGm/PIN neurons (Step 3). ERK-driven gene expression in MGm/PIN neurons (Step 4) is, in turn, hypothesized to promote presynaptic functional and/or structural changes at thalamo-LA synapses (Step 5). Together with the postsynaptic modifications driven by ERK signaling in the LA, these presynaptic modifications act to strengthen the connectivity of thalamo-LA synapses, which is reflected neurophysiologically in an enhanced response to the CS in the LA after training (Step 6).