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J Neurophysiol 81: 2360-2373, 1999;
0022-3077/99 $5.00
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The Journal of Neurophysiology Vol. 81 No. 5 May 1999, pp. 2360-2373
Copyright ©1999 by the American Physiological Society

Current Clamp and Modeling Studies of Low-Threshold Calcium Spikes in Cells of the Cat's Lateral Geniculate Nucleus

X. J. Zhan,1 C. L. Cox,1 J. Rinzel,2 and S. Murray Sherman1

 1Department of Neurobiology, State University of New York, Stony Brook, 11794-5230; and  2Center for Neural Science and Courant Institute of Mathematical Sciences, New York University, New York, New York 10003

Zhan, X. J., C. L. Cox, J. Rinzel, and S. Murray Sherman. Current Clamp and Modeling Studies of Low-Threshold Calcium Spikes in Cells of the Cat's Lateral Geniculate Nucleus. J. Neurophysiol. 81: 2360-2373, 1999.Current clamp and modeling studies of low-threshold calcium spikes in cells of the cat's lateral geniculate nucleus. All thalamic relay cells display a voltage-dependent low-threshold Ca2+ spike that plays an important role in relay of information to cortex. We investigated activation properties of this spike in relay cells of the cat's lateral geniculate nucleus using the combined approach of current-clamp intracellular recording from thalamic slices and simulations with a reduced model based on voltage-clamp data. Our experimental data from 42 relay cells showed that the actual Ca2+ spike activates in a nearly all-or-none manner and in this regard is similar to the conventional Na+/K+ action potential except that its voltage dependency is more hyperpolarized and its kinetics are slower. When the cell's membrane potential was hyperpolarized sufficiently to deinactivate much of the low-threshold Ca2+ current (IT) underlying the Ca2+ spike, depolarizing current injections typically produced a purely ohmic response when subthreshold and a full-blown Ca2+ spike of nearly invariant amplitude when suprathreshold. The transition between the ohmic response and activated Ca2+ spikes was abrupt and reflected a difference in depolarizing inputs of <1 mV. However, activation of a full-blown Ca2+ spike was preceded by a slower period of depolarization that was graded with the amplitude of current injection, and the full-blown Ca2+ spike activated when this slower depolarization reached a sufficient membrane potential, a quasithreshold. As a result, the latency of the evoked Ca2+ spike became less with stronger activating inputs because a stronger input produced a stronger depolarization that reached the critical membrane potential earlier. Although Ca2+ spikes were activated in a nearly all-or-none manner from a given holding potential, their actual amplitudes were related to these holding potentials, which, in turn, determined the level of IT deinactivation. Our simulations could reproduce all of the main experimental observations. They further suggest that the voltage-dependent K+ conductance underlying IA, which is known to delay firing in many cells, does not seem to contribute to the variable latency seen in activation of Ca2+ spikes. Instead the simulations indicate that the activation of IT starts initially with a slow and graded depolarization until enough of the underling transient (or T) Ca2+ channels are recruited to produce a fast, "autocatalytic" depolarization seen as the Ca2+ spike. This can produce variable latency dependent on the strength of the initial activation of T channels. The nearly all-or-none nature of Ca2+ spike activation suggests that when a burst of action potentials normally is evoked as a result of a Ca2+ spike and transmitted to cortex, this signal is largely invariant with the amplitude of the input activating the relay cell.




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