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Calcium influx through N‐ and P/Q‐type channels activate apamin‐sensitive calcium‐dependent potassium channels generating the late afterhyperpolarization in lamprey spinal neurons
Author(s) -
Manira A. El
Publication year - 1998
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1998.00194.x
Subject(s) - afterhyperpolarization , apamin , chemistry , sk channel , calcium channel , voltage dependent calcium channel , calcium activated potassium channel , t type calcium channel , calcium , potassium channel , neuroscience , p type calcium channel , channel blocker , biophysics , ion channel , biology , biochemistry , receptor , organic chemistry
Lamprey spinal neurons exhibit a fast afterhyperpolarization and a late afterhyperpolarization (AHP) which is due to the activation of apamin‐sensitive SK Ca 2+ ‐dependent K + channels (K Ca ) activated by calcium influx through voltage‐dependent channels during the action potential (Hill et al . 1992, Neuroreport , 3, 943–945). In this study we have investigated which calcium channel subtypes are responsible for the activation of the K Ca channels underlying the AHP. The effects of applying specific calcium channel blockers and agonists were analysed with regard to their effects on the AHP. Blockade of N‐type calcium channels by ω‐conotoxin GVIA resulted in a significant decrease in the amplitude of the AHP by 76.2 ± 14.9% (mean ± SD). Application of the P/Q‐type calcium channel blocker ω‐agatoxin IVA reduced the amplitude of the AHP by 20.3 ± 10.4%. The amplitude of the AHP was unchanged during application of the L‐type calcium channel antagonist nimodipine or the agonist (±)‐BAY K 8644, as was the compound afterhyperpolarization after a train of 10 spikes at 100 Hz. The effects of calcium channel blockers were also tested on the spike frequency adaptation during a train of action potentials induced by a 100–200 ms depolarizing pulse. The N‐ and P/Q‐type calcium channel antagonists decreased the spike frequency adaptation, whereas blockade of L‐type channels had no effect. Thus in lamprey spinal cord motor‐ and interneurons, apamin‐sensitive K Ca channels underlying the AHP are activated primarily by calcium entering through N‐type channels, and to a lesser extent through P/Q‐type channels.