title: A model of the electrophysiological properties of thalamocortical relay neurons.
abstract: 1. A model of the electrophysiological properties of single thalamocortical relay neurons in the rodent and cat dorsal lateral geniculate nucleus was constructed, based in part on the voltage dependence and kinetics of ionic currents detailed with voltage-clamp techniques. The model made the simplifying assumption of a single uniform compartment and incorporated a fast and transient Na+ current, INa; a persistent, depolarization-activated Na+ current, INap; a low-threshold Ca2+ current, I(T); a high-threshold Ca2+ current, IL; a Ca(2+)-activated K+ current, IC; a transient and depolarization-activated K+ current, IA; a slowly inactivating and depolarization-activated K+ current, IK2; a hyperpolarization-activated cation current, Ih; and K+ and Na+ leak currents IKleak and INaleak. 2. The effects of the various ionic currents on the electrophysiological properties of thalamocortical relay neurons were initially investigated through examining the effect of each current individually on passive membrane responses. The two leak currents, IKleak and INaleak, determined in large part the resting membrane potential and the apparent input resistance of the model neuron. Addition of IA resulted in a delay in the response of the model cell to a depolarizing current pulse, whereas addition of IK2, or IL combined with IC, resulted in a marked and prolonged decrease in the response to depolarization. Addition of Ih resulted in a depolarizing "sag" in response to hyperpolarization, whereas addition of IT resulted in a large rebound Ca2+ spike after hyperpolarization. Finally, addition of INap resulted in enhancement of depolarization. 3. The low-threshold Ca2+ spike of rodent neurons was successfully modeled with the active currents I(T), IL, IA, IC, and IK2. The low-threshold Ca2+ current I(T) generated the low-threshold Ca2+ spike. The transient K+ current IA slowed the rate of rise and reduced the peak amplitude of the low-threshold Ca2+ spike, whereas the slowly inactivating K+ current IK2 contributed greatly to the repolarization of the Ca2+ spike. Activation of IL during the peak of the Ca2+ spike led to activation of IC, which also contributed to the repolarization of the Ca2+ spike. Reduction of any one of the K+ currents resulted in an increase in the other two, thereby resulting in substantially smaller changes in the Ca2+ spike than would be expected on the basis of the amplitude of each ionic current alone.(ABSTRACT TRUNCATED AT 400 WORDS)
authors.affiliation: Section of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06510.
authors.forename: D A
authors.initials: DA
authors.lastname: McCormick
authors.forename: J R
authors.initials: JR
authors.lastname: Huguenard
mesh_terms: D000200:Action Potentials; D000818:Animals; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000502:physiology*; D002540:Cerebral Cortex / Q000502:physiology*; D004594:Electrophysiology; D005829:Geniculate Bodies / Q000502:physiology*; D007700:Kinetics; D008433:Mathematics; D008959:Models, Neurological; D009474:Neurons / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology*; D013788:Thalamus / Q000502:physiology*
chemical_list: D015220:Calcium Channels; D015221:Potassium Channels; D002118:Calcium