Electrophysiological and molecular evidence of L-(Cav1), N- (Cav2.2), and R- (Cav2.3) type Ca2+ channels in rat cortical astrocytes

✍ Scribed by Marcello D'Ascenzo; Mauro Vairano; Catia Andreassi; Pierluigi Navarra; Gian Battista Azzena; Claudio Grassi

• Publisher: John Wiley and Sons
• Year: 2004
• Tongue: English
• Weight: 393 KB
• Volume: 45
• Category: Article
• ISSN: 0894-1491
• DOI: 10.1002/glia.10336

✦ Synopsis

Abstract

Changes in intracellular Ca^2+^ levels are an important signal underlying neuron‐glia cross‐talk, but little is known about the possible role of voltage‐gated Ca^2+^ channels (VGCCs) in controlling glial cell Ca^2+^ 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 α~1C~ (L‐type), α~1B~ (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 Ca^2+^ influx, which influences neuron‐glia cross‐talk and numerous other calcium‐mediated glial‐cell functions. © 2003 Wiley‐Liss, Inc.