Rat cortical nerve terminals contain a unique subtype of BK channels with distinct gating kinetics and regulatory mechanisms compared to conventional BKCa channels.
Answers are grounded in this paper and cite their sources.
Suggests specialized BK gating in cortical terminals; leaves open roles in excitability and translation to human neurons.
Inside-out recordings from rat cortical fused nerve terminals indicate that the most common channel observed was a large conductance K+ (BK) channel with characteristics dissimilar to conventional cell body calcium-activated BK (BKCa) channels. 2. BK channels exhibit mode switching between low (mode 1) and high (mode 2) activity, an effect not influenced by membrane voltage. Increasing internal Ca2+ concentration increased time spent in mode 2 as did application of protein kinase A, an effect not mimicked by protein kinase C or protein kinase G. 3. Mode 1 activity was voltage independent although depolarization increased mode 2 channel activity. Global average channel activity was voltage and Ca2+ dependent. 4. Alkaline phosphatase treatment induced channel activity to reside permanently in mode 2, where activity was voltage and Ca2+ dependent but unaffected by protein kinases A, G or C. 5. Internal application of tetraethylammonium blocked BK channel activity in a manner identical to that reported for BKCa channels. 6. These results indicate that nerve terminal membranes have large conductance K+ channels with significant differences in gating kinetics and regulation of activity compared with BKCa channels of other neuronal preparations. The BK channel subtype may play a unique physiological role specific to the nerve terminal.
No takes yet. Share an insight, caveat, or question.
Smith et al. (1998) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: