A tetrodotoxin-insensitive [corrected] sodium current initiates burst firing of neocortical neurons.
The ability to generate burst discharges is a widespread phenomenon in central neurons and often has been attributed to Ca2+ currents. The diversity of burst patterns seems to be at variance with a single mechanism. Selected neocortical bursting neurons were examined by intracellular recordings. Selective blockers and pulse protocols were applied to characterize the crucial components of bursting activity. In the presence of tetrodotoxin and Ca2+ channel antagonists a transient depolarization persists, which shares the activation and deinactivation properties with the burst. The sensitivity to Na+ removal and resistance to tetrodotoxin suggests a tetrodotoxin-insensitive Na+ current as the crucial component in neocortical bursting neurons. A tetrodotoxin-insensitive Na+ current has been isolated in neocortical bursting neurons. The biophysical properties of this current allow for burst firing at frequencies up to about 12 Hz. This tetrodotoxin-insensitive Na+ may generate the alpha-rhythm of the electroencephalogram by effectively synchronizing arrays of follower cells. The implications of the intrinsic currents of bursting neurons for the initiation of epileptic discharges are discussed.
Deisz
R A
RA
Max-Planck-Institute of Psychiatry, Clinical Neuropharmacology, München, Germany.
D015761:4-Aminopyridine / Q000494:pharmacology; D000513:Alpha Rhythm / Q000187:drug effects; D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects* / Q000502:physiology; D005071:Evoked Potentials / Q000187:drug effects; D006168:Guinea Pigs; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D015222:Sodium Channels / Q000187:drug effects* / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology*
D015222:Sodium Channels; D013779:Tetrodotoxin; D015761:4-Aminopyridine