Interplay of Amygdala and Cingulate Plasticity in Emotional Fear

Figure 3

A cellular model for ACC plasticity. (a) Diagram of an ACC slice showing the placement of whole-cell patch recording and stimulation electrode. (b) LTP is induced by 80 pulses at 2 Hz with postsynaptic holding at +30 mV. (c) Activations of postsynaptic glutamate NMDA receptors or L-VDCCs lead to an increase in postsynaptic Ca²⁺ in dendritic spines. Ca²⁺ binds to CaM and leads to activation of calcium-stimulated ACs, mainly AC1 and other Ca²⁺/CaM-dependent protein kinases (PKC, CaMKII, and CaMKIV). Subsequently, GluA1-containing AMPA receptor will undergo the upregulation. Activation of CaMKIV, a kinase predominantly expressed in the nuclei, will trigger CREB signaling pathways. In addition, activation of AC1 leads to activation of PKA, and subsequently CREB as well. MAPK/ERK could translocate from the cytosol to the nucleus and then regulate the CREB activity. Postsynaptic PKMζ is critical for maintaining synaptic potentiation in the ACC.