cGMP-dependent protein kinase type I promotes CREB/CRE-mediated gene expression in neurons of the lateral amygdala.

The process transforming newly learned information into stable long-term memory is called memory consolidation and, like the underlying long-term synaptic plasticity, critically depends on de novo RNA and protein synthesis. We have shown recently that the cGMP-dependent protein kinase Type I (cGKI) plays an important role for the consolidation of amygdala-dependent fear memory and long-term potentiation (LTP) in the lateral amygdala. Signalling downstream of cGKI at the level of transcriptional regulation remained unclear.

Signaling through cGMP-dependent protein kinase I in the amygdala is critical for auditory-cued fear memory and long-term potentiation.

Long-term potentiation (LTP) of inputs relaying sensory information from cortical and thalamic neurons to principal neurons in the lateral amygdala (LA) is thought to serve as a cellular mechanism for associative fear learning. Nitric oxide (NO), a messenger molecule widely implicated in synaptic plasticity and behavior, has been shown to enhance LTP in the LA as well as consolidation of associative fear memory. Additional evidence suggests that NO-induced enhancement of LTP and amygdala-dependent learning requires signaling through soluble guanylyl cyclase (sGC) and cGMP-dependent protein kinase (cGK).