scholarly journals Mutations in High-Voltage-Activated Calcium Channel Genes Stimulate Low-Voltage-Activated Currents in Mouse Thalamic Relay Neurons

2002 ◽  
Vol 22 (15) ◽  
pp. 6362-6371 ◽  
Author(s):  
Yi Zhang ◽  
Mayra Mori ◽  
Daniel L. Burgess ◽  
Jeffrey L. Noebels
Keyword(s):  
Calcium Channel ◽  
High Voltage ◽  
Low Voltage ◽  
Thalamic Relay ◽  
Thalamic Relay Neurons ◽  
Relay Neurons

Modulation by Extracellular pH of Low- and High-Voltage-Activated Calcium Currents of Rat Thalamic Relay Neurons

2001 ◽  
Vol 85 (3) ◽  
pp. 1051-1058 ◽  
Author(s):  
Mukesch Johannes Shah ◽  
Susanne Meis ◽  
Thomas Munsch ◽  
Hans-Christian Pape
Keyword(s):  
Steady State ◽  
High Voltage ◽  
Extracellular Ph ◽  
Calcium Currents ◽  
Extracellular Acidification ◽  
Patch Clamp Technique ◽  
Thalamic Relay ◽  
Steady State Inactivation ◽  
Thalamic Relay Neurons ◽  
Relay Neurons

The effects of changes in the extracellular pH (pHo) on low-voltage- (LVA) and high-voltage- (HVA) activated calcium currents of acutely isolated relay neurons of the ventrobasal thalamic complex (VB) were examined using the whole cell patch-clamp technique. Modest extracellular alkalinization (pH 7.3 to 7.7) reversibly enlarged LVA calcium currents by 18.6 ± 3.2% (mean ± SE, n = 6), whereas extracellular acidification (pH 7.3 to 6.9) decreased the current by 24.8 ± 3.1% ( n = 9). Normalized current amplitudes ( I/ I 7.3) fitted as a function of pHo revealed an apparent pKa of 6.9. Both, half-maximal activation voltage and steady-state inactivation were significantly shifted to more negative voltages by 2–4 mV on extracellular alkalinization and to more positive voltages by 2–3 mV on extracellular acidification, respectively. Recovery from inactivation of LVA calcium currents was not significantly affected by changes in pHo. In contrast, HVA calcium currents were less sensitive to changes in pHo. Although extracellular alkalinization increased maximal HVA current by 6.0 ± 2.0% ( n = 7) and extracellular acidification decreased it by 11.9 ± 0.02% ( n = 11), both activation and steady-state inactivation were only marginally affected by the moderate changes in pHo used in the present study. The results show that calcium currents of thalamic relay neurons exhibit different pHo sensitivity. Therefore activity-related extracellular pH transients might selectively modulate certain aspects of the electrogenic behavior of thalamic relay neurons.

Transient enhancement of low-threshold calcium current in thalamic relay neurons after corticectomy

1993 ◽  
Vol 70 (1) ◽  
pp. 20-27 ◽  
Author(s):  
J. M. Chung ◽  
J. R. Huguenard ◽  
D. A. Prince
Keyword(s):  
Calcium Currents ◽  
High Threshold ◽  
Pharmacological Properties ◽  
Current Time ◽  
Cortical Ablation ◽  
Thalamic Relay ◽  
Low Threshold ◽  
Small Change ◽  
Thalamic Relay Neurons ◽  
Relay Neurons

1. The alterations of voltage-sensitive calcium currents produced in thalamic cells by injury were investigated under voltage clamp using patch-clamp recordings in the whole-cell configuration. 2. One day after unilateral cortical ablation in immature rats (postnatal day 7), low-threshold transient calcium (T) currents in acutely isolated thalamic relay neurons (RNs) were increased by 68% compared with contralateral controls (P < 0.001). Three days after the operation, T currents in injured neurons were at 44% of control levels (P < 0.001). On the other hand, high-threshold (L) calcium currents in RNs did not change over the same interval. 3. To investigate the mechanism for the increase of T current, both kinetics and voltage dependency of activation and inactivation were examined. At a test voltage of -40 mV, the activation time constant decreased from 4.1 to 3.2 ms (P < 0.05); however, this small change was insufficient to explain the large increase in T current. Time constants for both fast and slow inactivation did not change significantly, nor did voltage dependence of activation or inactivation of thalamic T currents. 4. Methyl-phenyl-succinimide (MPS, 1 mM), a compound known to block T currents, was used to examine possible alterations in the pharmacological properties of T channels after injury. MPS was more effective in reducing T currents in normal versus injured RNs (24 and 20% reductions, respectively; P < 0.05), suggesting that pharmacological properties of T channels in the injured RNs may be different from those of the normal RNs.(ABSTRACT TRUNCATED AT 250 WORDS)

Clonazepam suppresses GABAB-mediated inhibition in thalamic relay neurons through effects in nucleus reticularis

1994 ◽  
Vol 71 (6) ◽  
pp. 2576-2581 ◽  
Author(s):  
J. R. Huguenard ◽  
D. A. Prince
Keyword(s):  
Gamma Aminobutyric Acid ◽  
Postsynaptic Inhibition ◽  
Nucleus Reticularis ◽  
Thalamic Relay ◽  
Relay Nucleus ◽  
A Site ◽  
Thalamic Relay Neurons ◽  
Gabaa Antagonist ◽  
Relay Neurons

1. Experiments were carried out using patch-clamp techniques in rat thalamic slices, maintained in vitro, to examine the effects of the benzodiazepine compound, clonazepam (CZP), on intrathalamic inhibition. Bath-applied CZP reduced the gamma-aminobutyric acid-B (GABAB) component of inhibitory postsynaptic potentials and currents (IPSPs and IPSCs, respectively) evoked in rat thalamic somatosensory relay neurons by stimulation of nucleus reticularis thalami (nRt), without consistently affecting the GABAA IPSP. Secondary IPSPs, which occur as a result of intrathalamic oscillations, were dramatically reduced. 2. Voltage-clamp experiments combined with local or bath perfusion of the GABAA antagonist bicuculline methiodide (BMI), demonstrated that nRt is a site of GABAA-mediated postsynaptic inhibition that affects inhibitory output onto relay neurons. BMI enhanced both GABAA and GABAB postsynaptic inhibition in relay neurons when applied to nRt. Focal applications in the ventrobasal relay nucleus near the recording electrode blocked the GABAA-mediated IPSP but had no effects on GABAB inhibitory potentials. 3. Results suggest that CZP acts to facilitate recurrent inhibition in nRt and decrease its inhibitory output onto relay neurons. Intra-nRt GABAA-mediated inhibition thus has an important role in controlling thalamic excitability and in the anti-absence actions of CZP.

Membrane Channel Interactions Underlying Rat Subthalamic Projection Neuron Rhythmic and Bursting Activity

2006 ◽  
Vol 95 (4) ◽  
pp. 2352-2365 ◽  
Author(s):  
Andrew Gillies ◽  
David Willshaw
Keyword(s):  
Calcium Channel ◽  
High Voltage ◽  
Low Voltage ◽  
Low Frequency ◽  
Projection Neuron ◽  
Morphological Data ◽  
Primary Role ◽  
Small Current ◽  
Wide Range

A computational model of the rat subthalamic nucleus projection neuron is constructed using electrophysiological and morphological data and a restricted set of channel specifications. The model cell exhibits a wide range of electrophysiological behaviors characteristic of rat subthalamic neurons. It reveals that a key set of three channels play a primary role in distinguishing behaviors: a high-voltage-activated calcium channel (Cav1.2.-1.3), a low-voltage-activated calcium channel (Cav3.-), and a small current calcium-activated potassium channel (KCa2.1–2.3). Short and long posthyperpolarization rebound responses, low-frequency rhythmic bursting (<1 Hz), higher-frequency rhythmic bursting (4–7 Hz), and slow action and depolarizing potentials are behaviors all mediated by the interaction of these channels. This interaction can generate a robust calcium-dependent extended depolarization in the dendrites (a depolarizing plateau). The diversity observed in the rat subthalamic physiology (such as short or long rebounds, or the presence of low-frequency rhythmic busting) can arise from alterations in both the density and distributions of these channel types and, consequently, their ability to generate this depolarizing plateau. A number of important predictions arise from the model. For example, blocking or disrupting the low-voltage-activated Cav3.- calcium current should mute the emergence of rebound responses and rhythmic bursting. Conversely, increasing this channel current via large hyperpolarizing potentials in combination with partial blockade of the high-voltage-activated calcium channels should lead to the more experimentally elusive in vitro high-frequency bursting.

Substantia Nigra Output to Prefrontal Cortex Via Thalamus in Monkeys. II. Activity of Thalamic Relay Neurons in Delayed Conditional Go/No-Go Discrimination Task

2009 ◽  
Vol 102 (5) ◽  
pp. 2946-2954 ◽  
Author(s):  
Ikuo Tanibuchi ◽  
Hiroyuki Kitano ◽  
Kohnosuke Jinnai
Keyword(s):  
Substantia Nigra ◽  
Discrimination Task ◽  
Present Report ◽  
Delay Period ◽  
Visual Signals ◽  
Inhibitory Input ◽  
Related Activity ◽  
Thalamic Relay ◽  
Thalamic Relay Neurons ◽  
Relay Neurons

The present report investigated the involvement of primate nigro-thalamo-cortical projections in discrimination of visual signals with behavioral meaning. We tested the extracellular unit activity of mediodorsal (MD) and ventral anterior (VA) thalamic neurons monosynaptically receiving inhibitory input from the substantia nigra pars reticulata (SNr) and projecting to the frontal cortex in Japanese monkeys performing a delayed conditional go/no-go discrimination task. In the task two colored stimuli (S1, S2) intervened by delay period required the monkeys lifting a lever (go) or not (no-go); the same and different colored pairs of S1 and S2 meant go and no-go signals, respectively. Prominent task-relevant responses were sustained activity with color preference to S1 during delay period and S2-related activity with different firing rates between go and no-go trials. In particular, a high proportion of such go/no-go differential S2-related activity was found in thalamic relay neurons, receiving input from the caudolateral SNr and projecting to the prefrontal area (PSv) ventral to the principal sulcus, in the rostrolateral MD. The findings suggest that the caudolateral SNr–rostrolateral MD–PSv pathways may be possible conduits of signals coding the behavioral meaning of the visual stimuli and thus may be responsible for generating similar neuronal activity in the PSv.

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