Figure 1
Schematic representation of the postsynaptic mechanisms involved in signal transduction related to induction of LTP/LTD. Intracellular calcium ions (Ca2+) bind to calmodulin (CaM), which further affects the activation of protein phosphatase 2B (PP2B) a.k.a. calcineurin (CaN), CaM-dependent kinase II (CaMKII), adenylyl cyclase (AC, the catalyst of the reaction producing cyclic adenosine monophosphate (cAMP)), and phosphodiesterase type 1B (PDE1B). Dopamine (DA) increases cAMP concentration via AC activation. Together with PDE1B, also PDE type 4 (PDE4) degrades cAMP. cAMP-dependent protein kinase (PKA) phosphorylates α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor (AMPAR) and protein phosphatase 1 (PP1) inhibitor 1 (I1). In addition, protein phosphatase 2A (PP2A) and cyclin-dependent kinase 5 (Cdk5) affect PP1 regulatory subunit a.k.a. DA- and cAMP-regulated neuronal phosphoprotein of 32 kDa (D32).