Mechanism of 4-aminopyridine block of the transient outward K-current in identified Helix neuron.
The block of the transient outward K-current, I(K(A)) by 4-aminopyridine (4-AP) and blood-depressing substances (BDS) was investigated in identified Helix pomatia neurons (LPa3) using the two microelectrode voltage-clamp technique. The present study shows that 4-AP inhibits I(K(A)) in snail neurons in a voltage- and concentration-dependent manner. The 4-AP block of I(K(A)) involves the block of both open and closed states of the channel, however binding to open channels is preferred. It is suggested that 4-AP have two binding sites on the identified Helix neuron. One site causes an open channel block, which affects the N-type inactivation, and binding to the second site induces closed channel block, which affects C-type inactivation. In control solution the inactivating phase of the current is biexponential, suggesting simultaneous presence of two types of inactivation. The counterplay of these mechanisms results in the crossover of the current traces recorded from control and 4-AP blocked channels. It is assumed that use-dependence does not occur through blocker 'trapping', but rather by a different mechanism. BDS had no effect on Helix I(K(A)), suggesting that transient potassium channels in LPa3 neuron are not Kv3.4 type channels.[1]References
- Mechanism of 4-aminopyridine block of the transient outward K-current in identified Helix neuron. Kiss, T., László, Z., Szabadics, J. Brain Res. (2002) [Pubmed]
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