Dynamics of low-threshold spike activation in relay neurons of the cat lateral geniculate nucleus.
The low-threshold spike (LTS), generated by the transient Ca(2+) current I(T), plays a pivotal role in thalamic relay cell responsiveness and thus in the nature of the thalamic relay. By injecting depolarizing current ramps at various rates to manipulate the slope of membrane depolarization (dV/dt), we found that an LTS occurred only if dV/dt exceeded a minimum value of approximately 5-12 mV/sec. We injected current ramps of variable dV/dt into relay cells that were sufficiently hyperpolarized to de-inactivate I(T) completely. Higher values of dV/dt activated an LTS. However, lower values of dV/dt eventually led to tonic firing without ever activating an LTS; apparently, the inactivation of I(T) proceeded before I(T) could be recruited. Because the maximum rate of rise of the LTS decreased with slower activating ramps of injected current, we conclude that slower ramps allow increasing inactivation of I(T) before the threshold for its activation gating is reached, and when the injected ramps have a sufficiently low dV/dt, the inactivation is severe enough to prevent activation of an LTS. In the presence of Cs(+), we found that even the lowest dV/dt that we applied led to LTS activation, apparently because Cs(+) reduced the K(+) "leak" conductance and increased neuronal input resistance. Nonetheless, under normal conditions, our data suggest that there is neither significant window current (related to the overlap of the inactivation and activation curves for I(T)), rhythmogenic properties, nor bistability properties for these neurons. Our theoretical results using a minimal model of LTS excitability in these neurons are consistent with the experimental observations and support our conclusions. We suggest that inputs activating very slow EPSPs (i.e., via metabotropic receptors) may be able to inactivate I(T) without generating sizable I(T) and a spurious burst of action potentials to cortex.
Gutierrez
C
C
Department of Neurobiology, State University of New York, Stony Brook, New York 11794-5230, USA.
Cox
C L
CL
Rinzel
J
J
Sherman
S M
SM
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D020013:Calcium Signaling / Q000502:physiology; D002415:Cats; D002586:Cesium / Q000494:pharmacology; D003198:Computer Simulation; D004558:Electric Stimulation / Q000379:methods; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D005829:Geniculate Bodies / Q000166:cytology / Q000502:physiology*; D066298:In Vitro Techniques; D008239:Lysine / Q000031:analogs & derivatives; D008959:Models, Neurological; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D011188:Potassium / Q000378:metabolism; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology; D012684:Sensory Thresholds / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology; D013788:Thalamus / Q000166:cytology / Q000502:physiology
D002586:Cesium; D013779:Tetrodotoxin; C013411:biocytin; D008239:Lysine; D011188:Potassium