Anti-KCNA1 (C-terminal) polyclonal antibody

Pyramidal neurons from layers II/III of somatosensory and motor cortex express multiple Kv1 alpha-subunits and a current sensitive to block by alpha-dendrotoxin ( alpha-DTX). We examined functional roles of native Kv1 channels in these cells using current-clamp recordings in brain slices and current- and voltage-clamp recordings in dissociated cells. alpha-DTX caused a significant negative shift in voltage threshold for action potentials ( APs) and reduced rheobase. Correspondingly, a ramp-voltage protocol revealed that the alpha-DTX-sensitive current activated at subthreshold voltages. AP width at threshold increased with successive APs during repetitive firing. The steady-state threshold width for a given firing rate was similar in control and alpha-DTX, despite an initially broader AP in alpha-DTX. AP voltage threshold increased similarly during a train of spikes under control conditions and in the presence of alpha-DTX. alpha-DTX had no effect on input resistance or resting membrane potential and modest effects on the amplitude or width of a single AP. Accordingly, experiments using AP waveforms ( APWs) as voltage protocols revealed that alpha-DTX-sensitive current peaked late during the AP repolarization phase. Application of alpha-DTX increased the rate of firing to intracellular current injection and increased gain ( multiplicative effects), but did not alter spike-frequency adaptation. Consistent with these findings, voltage-clamp experiments revealed that the proportion of outward current sensitive to alpha-DTX was highest during the interval between two APWs, reflecting slow deactivation kinetics at -50 mV. Finally, alpha-DTX did not alter the selectivity of pyramidal neurons for DC versus time-varying stimuli.

Introduction. Epilepsy is one of the major neurological disorders characterized by spontaneous and recurrent seizures. Traditionally temporal lobe epilepsy (TLE) was considered as a multifactorial syndrome due to environmental factors. Advances in molecular biology have facilitated the detection of many genetic alterations that may have a pathogenic effect in ELT Recently, many authors show evidence about the existence of genetic components as the source of some types of ELT Development. This review aims to provide an overview of mutations and polymorphisms associated with temporal lobe epilepsy, which have been described in scientific literature and its contribution to the pathophysiology of epileptogenesis. We have reviewed the following genes; LGI1, PDYN (prodynorphin), interleucine 1beta, PRPN (prion protein), ApoE (apolipoprotein E), GABBR1, SCN1A, SCN1B, KCNA1, KCND2. Conclusion. The ELT is a complex disease and its development could depend on either genetics factors or other factors. Functional studies are necessary in order to correlate its molecular basis and their development. [REV NEUROL 2009; 49: 541-6]