μ-Opioid-receptor-mediated inhibidon of the N-type calcium-channel current

Transient changes in sodium concentration in response to electrical activity were detected in Purkinje cells by using the fluorescent indicator SBFI (Minta & Tsien (J. biol. Chem. 264, 19 449 (1989)). Fast sodium action potentials caused large increases in internal sodium concentration, [Na]$_{\text{i}}$, in the soma and axon, and were generally undetectable in the dendrites. No changes were detected in the dendrites corresponding to calcium action potentials. The spatial distribution of these transients corresponds to that expected if the increase in [Na]$_{\text{i}}$ were the result of Na$^{+}$ entry through voltage-dependent Na channels generating sodium spikes in the axon hillock and soma. The [Na]$_{\text{i}}$ transients rapidly recovered ($\tau $ < 1 s) in the axon hillock, probably by Na$^{+}$ diffusion into the soma. Climbing fibre activation produced distinct [Na]$_{\text{i}}$ transients in the dendrites in addition to somatic and axonal signals. As regenerative potentials did not produce transients in this region, these signals may be caused by Na$^{+}$ entry through ligand-gated channels. These results confirm and extend the description of channel distribution and electrical signalling in Purkinje cells.