Changes in intracellular Ca2+ levels are an important signal underlying neuron-glia cross-talk, but little is known about the possible role of voltage-gated Ca2+ channels (VGCCs) in controlling glial cell Ca2+ influx. We investigated the pharmacological and biophysical features of VGCCs in cultured rat cortical astrocytes. In whole-cell patch-clamp experiments, L-channel blockade (5 μM nifedipine) reduced Ba 2+ current amplitude by 28% of controls, and further decrease (32%) was produced by N-channel blockade (3 μM ω-conotoxin-GVIA). No significant additional changes were observed after P/Q channel blockade (3 μM ω-conotoxin-MVIIC). Residual current (36% of controls) amounted to roughly the same percentage (34%) that was abolished by R-channel blockade (100 nM SNX-482). Electrophysiological evidence of L-, N-, and R-channels was associated with RT-PCR detection of mRNA transcripts for VGCC subunits α1C (L-type), α1B (N-type), and α 1E (R-type). In cell-attached recordings, single-channel properties (L-currents: amplitude, -1.21 ± 0.02 pA at 10 mV; slope conductance, 22. 0 ± 1.1 pS; mean open time, 5.95 ± 0.24 ms; N-currents: amplitude, -1.09 ± 0.02 pA at 10 mV; slope conductance, 18.0 ± 1.1 pS; mean open time, 1.14 ± 0.02 ms; R-currents: amplitude, -0.81 ± 0.01 pA at 20 mV; slope conductance, 10.5 ± 0.3 pS; mean open time, 0.88 ± 0.02 ms) resembled those of corresponding VGCCs in neurons. These novel findings indicate that VGCC expression by cortical astrocytes may be more varied than previously thought, suggesting that these channels may indeed play substantial roles in the regulation of astrocyte Ca2+ influx, which influences neuron-glia cross-talk and numerous other calcium-mediated glial-cell functions.
- α subunit transcripts
- Ca 2.3
- High-voltage-activated Ca channels
- Rat cortical astrocytes
ASJC Scopus subject areas