How do G proteins directly control neuronal Ca2+ channel function?

Ca2+ entry into neuronal cells is modulated by the activation of numerous G-protein-coupled receptors (GPCRs). Much effort has been invested in studying direct G-protein-mediated inhibition of voltage-dependent CaV2 Ca2+ channels. This inhibition occurs through a series of convergent modifications in the biophysical properties of the channels.

Paradoxical potentiation of neuronal T-type Ca2+ current by ATP at resting membrane potential.

Despite the marked influence on neuronal physiology of the low-voltage activated T-type Ca(2+) currents, little is known about the intracellular pathways and neurotransmitters involved in their regulations. Here, we report that in thalamocortical neurons a phosphorylation mechanism induces an increase both in the current amplitude (1.5 +/- 0.

Slow inactivation of the Ca(V)3.1 isotype of T-type calcium channels.

T-type calcium channels (the Ca(V)3 channel family) are involved in defining the resting membrane potential and in neuronal activities such as oscillations and rebound depolarization. Their physiological roles depend upon the channel activation and inactivation kinetics. A fast inactivation that stops the ionic flux of calcium in tens of milliseconds has already been described in both native and heterologously expressed channels.