Ni(2+)-sensitive T-type Ca(2+) channel currents are regulated in parallel with synaptic and visual response plasticity in visual cortex.

Visual cortical neurons undergo depression and potentiation of their visual responses to stimulation of the deprived and non-deprived eyes, respectively, after monocular deprivation. This modification occurs predominantly during an early postnatal period in normal development, and this critical period is postponed until adulthood in animals reared in darkness from birth. We have proposed that Ni(2+)-sensitive T-type Ca(2+) channel-dependent long-term potentiation (T-LTP) mediates the potentiation of non-deprived eye responses. In this study, to investigate the development of Ni(2+)-sensitive T-type Ca(2+) channels, presumed CaV3.2 channels, we performed whole-cell recordings from layer 2/3 pyramidal neurons in rat visual cortical slices. T-type Ca(2+) channel currents were activated by voltage steps from -100mV to -40mV under a pharmacological blockade of Na(+) and K(+) channels. We estimated presumed CaV3.2 currents from the currents obtained after subtraction of the currents in the presence of Ni(2+) (50μM) from those in control solution. The estimated currents were very small before eye opening, peaked during the critical period and then returned to a small value by adulthood. Dark rearing prevented the developmental decline in these currents until adulthood. These results suggest that the regulation of CaV3.2 currents underlies the developmental changes in T-LTP and ocular dominance plasticity.