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

  1 Department of Neurobiology, State University of New York, Stony Brook, 11794-5230; and   2 Center 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...

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Published in:Journal of neurophysiology 1999-05, Vol.81 (5), p.2360-2373
Main Authors: Zhan, X. J, Cox, C. L, Rinzel, J, Sherman, S. Murray
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description   1 Department of Neurobiology, State University of New York, Stony Brook, 11794-5230; and   2 Center 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 Ca 2+ 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 Ca 2+ 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 Ca 2+ current ( I T ) underlying the Ca 2+ spike, depolarizing current injections typically produced a purely ohmic response when subthreshold and a full-blown Ca 2+ spike of nearly invariant amplitude when suprathreshold. The transition between the ohmic response and activated Ca 2+ spikes was abrupt and reflected a difference in depolarizing inputs of
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J ; Cox, C. L ; Rinzel, J ; Sherman, S. Murray</creator><creatorcontrib>Zhan, X. J ; Cox, C. L ; Rinzel, J ; Sherman, S. Murray</creatorcontrib><description>  1 Department of Neurobiology, State University of New York, Stony Brook, 11794-5230; and   2 Center 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 Ca 2+ 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 Ca 2+ 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 Ca 2+ current ( I T ) underlying the Ca 2+ spike, depolarizing current injections typically produced a purely ohmic response when subthreshold and a full-blown Ca 2+ spike of nearly invariant amplitude when suprathreshold. The transition between the ohmic response and activated Ca 2+ spikes was abrupt and reflected a difference in depolarizing inputs of &lt;1 mV. However, activation of a full-blown Ca 2+ spike was preceded by a slower period of depolarization that was graded with the amplitude of current injection, and the full-blown Ca 2+ spike activated when this slower depolarization reached a sufficient membrane potential, a quasithreshold. As a result, the latency of the evoked Ca 2+ spike became less with stronger activating inputs because a stronger input produced a stronger depolarization that reached the critical membrane potential earlier. Although Ca 2+ 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 I T deinactivation. Our simulations could reproduce all of the main experimental observations. They further suggest that the voltage-dependent K + conductance underlying I A , which is known to delay firing in many cells, does not seem to contribute to the variable latency seen in activation of Ca 2+ spikes. Instead the simulations indicate that the activation of I T starts initially with a slow and graded depolarization until enough of the underling transient (or T) Ca 2+ channels are recruited to produce a fast, "autocatalytic" depolarization seen as the Ca 2+ spike. This can produce variable latency dependent on the strength of the initial activation of T channels. 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All thalamic relay cells display a voltage-dependent low-threshold Ca 2+ 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 Ca 2+ 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 Ca 2+ current ( I T ) underlying the Ca 2+ spike, depolarizing current injections typically produced a purely ohmic response when subthreshold and a full-blown Ca 2+ spike of nearly invariant amplitude when suprathreshold. The transition between the ohmic response and activated Ca 2+ spikes was abrupt and reflected a difference in depolarizing inputs of &lt;1 mV. However, activation of a full-blown Ca 2+ spike was preceded by a slower period of depolarization that was graded with the amplitude of current injection, and the full-blown Ca 2+ spike activated when this slower depolarization reached a sufficient membrane potential, a quasithreshold. As a result, the latency of the evoked Ca 2+ spike became less with stronger activating inputs because a stronger input produced a stronger depolarization that reached the critical membrane potential earlier. Although Ca 2+ 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 I T deinactivation. Our simulations could reproduce all of the main experimental observations. They further suggest that the voltage-dependent K + conductance underlying I A , which is known to delay firing in many cells, does not seem to contribute to the variable latency seen in activation of Ca 2+ spikes. Instead the simulations indicate that the activation of I T starts initially with a slow and graded depolarization until enough of the underling transient (or T) Ca 2+ channels are recruited to produce a fast, "autocatalytic" depolarization seen as the Ca 2+ spike. This can produce variable latency dependent on the strength of the initial activation of T channels. 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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 Ca 2+ 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 Ca 2+ 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 Ca 2+ current ( I T ) underlying the Ca 2+ spike, depolarizing current injections typically produced a purely ohmic response when subthreshold and a full-blown Ca 2+ spike of nearly invariant amplitude when suprathreshold. The transition between the ohmic response and activated Ca 2+ spikes was abrupt and reflected a difference in depolarizing inputs of &lt;1 mV. However, activation of a full-blown Ca 2+ spike was preceded by a slower period of depolarization that was graded with the amplitude of current injection, and the full-blown Ca 2+ spike activated when this slower depolarization reached a sufficient membrane potential, a quasithreshold. As a result, the latency of the evoked Ca 2+ spike became less with stronger activating inputs because a stronger input produced a stronger depolarization that reached the critical membrane potential earlier. Although Ca 2+ 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 I T deinactivation. Our simulations could reproduce all of the main experimental observations. They further suggest that the voltage-dependent K + conductance underlying I A , which is known to delay firing in many cells, does not seem to contribute to the variable latency seen in activation of Ca 2+ spikes. Instead the simulations indicate that the activation of I T starts initially with a slow and graded depolarization until enough of the underling transient (or T) Ca 2+ channels are recruited to produce a fast, "autocatalytic" depolarization seen as the Ca 2+ spike. This can produce variable latency dependent on the strength of the initial activation of T channels. The nearly all-or-none nature of Ca 2+ spike activation suggests that when a burst of action potentials normally is evoked as a result of a Ca 2+ spike and transmitted to cortex, this signal is largely invariant with the amplitude of the input activating the relay cell.</abstract><cop>United States</cop><pub>Am Phys Soc</pub><pmid>10322072</pmid><doi>10.1152/jn.1999.81.5.2360</doi><tpages>14</tpages></addata></record>
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source American Physiological Society:Jisc Collections:American Physiological Society Journals ‘Read Publish & Join’ Agreement:2023-2024 (Reading list); American Physiological Society Free
subjects Action Potentials - physiology
Animals
Calcium - physiology
Cats
Computer Simulation
Differential Threshold - physiology
Female
Geniculate Bodies - cytology
Geniculate Bodies - physiology
Male
Models, Neurological
Neurons - physiology
Patch-Clamp Techniques
Reaction Time - physiology
Thalamus - cytology
Thalamus - physiology
title Current Clamp and Modeling Studies of Low-Threshold Calcium Spikes in Cells of the Cat's Lateral Geniculate Nucleus
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