Differential Regulation of Type I and Type VIII Ca2+-Stimulated Adenylyl Cyclases by Gi-Coupled Receptors in Vivo

Some forms of synaptic plasticity rely on coupling intracellular Ca2+ to cAMP increases. Neural-specific type I adenylyl cyclase (I-AC), stimulated by Ca2+, is inhibited by Gi-coupled receptors like somatostatin and dopamine D2L, primarily through Giα subunits, whereas type VIII adenylyl cyclase (VIII-AC) remains unaffected by such inhibition, suggesting distinct regulatory roles in synaptic plasticity mechanisms. 

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