Sodium current in rat and cat thalamocortical neurons: role of a non-inactivating component in tonic and burst firing.
The properties of the Na+ current present in thalamocortical neurons of the dorsal lateral geniculate nucleus were investigated in dissociated neonate rat and cat neurons and in neurons from slices of neonate and adult rats using patch and sharp electrode recordings. The steady-state activation and inactivation of the transient Na+ current (INa) was well fitted with a Boltzmann curve (voltage of half-maximal activation and inactivation, V1/2, -29.84 mV and -70.04 mV, respectively). Steady-state activation and inactivation curves showed a small region of overlap, indicating the occurrence of a INa window current. INa decay could be fitted with a single exponential function, consistent with the presence of only one channel type. Voltage ramp and step protocols showed the presence of a noninactivating component of the Na+ current (INaP) that activated at potentials more negative (V1/2 = -56.93 mV) than those of INa. The maximal amplitude of INaP was approximately 2.5% of INa, thus significantly greater than the calculated contribution (0.2%) of the INa window component. Comparison of results from dissociated neurons and neurons in slices suggested a dendritic as well as a somatic localization of INaP. Inclusion of papain in the patch electrode removed the fast inactivation of INa and induced a current with voltage-dependence (V1/2 = -56.92) and activation parameters similar to those of INaP. Current-clamp recordings with sharp electrodes showed that INaP contributed to depolarizations evoked from potentials of approximately -60 mV and unexpectedly to the amplitude and latency of low-threshold Ca2+ potentials, suggesting that this noninactivating component of the Na+ channel population plays an important role in the integrative properties of thalamocortical neurons during both tonic and burst-firing patterns.
Parri
H R
HR
Physiology Unit, School of Molecular and Medical Biosciences, University of Wales Cardiff, Cardiff CF1 3US, United Kingdom.
Crunelli
V
V
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn; D002415:Cats; D002540:Cerebral Cortex / Q000166:cytology*; D005829:Geniculate Bodies / Q000166:cytology*; D015640:Ion Channel Gating / Q000187:drug effects / Q000502:physiology; D007700:Kinetics; D008297:Male; D008839:Microelectrodes; D009474:Neurons / Q000737:chemistry* / Q000187:drug effects / Q000502:physiology; D018408:Patch-Clamp Techniques; D010507:Periodicity; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000378:metabolism*; D015222:Sodium Channels / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology; D013788:Thalamus / Q000166:cytology*; D014795:Visual Pathways / Q000166:cytology / Q000502:physiology
D015222:Sodium Channels; D013779:Tetrodotoxin; D012964:Sodium