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Chronic dopamine depletion augments the functional expression of K-ATP channels in the rat subthalamic nucleus

Highlights► NMDA evokes K-ATP currents in rat subthalamic nucleus (STN) neurons. ► STN neurons were recorded in slices from rats treated with 6-OHDA. ► NMDA evoked more outward current in STN neurons from dopamine-depleted rats. ► NMDA inhibited firing rate in slices from 6-OHDA-treated but not norm... Full description

Journal Title: Neuroscience Letters 07 December 2012, Vol.531(2), pp.104-108
Main Author: Shen, Ke-Zhong
Other Authors: Johnson, Steven W
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0304-3940 ; E-ISSN: 1872-7972 ; DOI: 10.1016/j.neulet.2012.10.030
Link: https://www.sciencedirect.com/science/article/pii/S0304394012013985
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recordid: elsevier_sdoi_10_1016_j_neulet_2012_10_030
title: Chronic dopamine depletion augments the functional expression of K-ATP channels in the rat subthalamic nucleus
format: Article
creator:
  • Shen, Ke-Zhong
  • Johnson, Steven W
subjects:
  • ATP-Sensitive K+ Channel
  • Subthalamic Nucleus
  • N-Methyl-D-Aspartate
  • Sulfonylurea
  • Tolbutamide
  • Brain Slice
  • Medicine
  • Anatomy & Physiology
ispartof: Neuroscience Letters, 07 December 2012, Vol.531(2), pp.104-108
description: Highlights► NMDA evokes K-ATP currents in rat subthalamic nucleus (STN) neurons. ► STN neurons were recorded in slices from rats treated with 6-OHDA. ► NMDA evoked more outward current in STN neurons from dopamine-depleted rats. ► NMDA inhibited firing rate in slices from 6-OHDA-treated but not normal rats. ► We conclude that dopamine deficiency up-regulates functional K-ATP expression. Symptoms of Parkinson's disease caused by dopamine depletion are associated with burst firing in the subthalamic nucleus (STN). Moreover, regularization or suppression of STN neuronal activity is thought to improve symptoms of Parkinson's disease. We reported recently that N-methyl-d-aspartate (NMDA) receptor stimulation of rat STN neurons evokes ATP-sensitive K+ (K-ATP) current via a Ca2+- and nitric oxide-dependent mechanism. The present studies were done to determine whether or not K-ATP channel function in STN neurons is altered in a model of chronic dopamine depletion. Brain slices were prepared from rats with unilateral dopamine depletion caused by intracerebral 6-hydroxydopamine (6-OHDA) injections. Whole-cell patch-clamp recordings showed that NMDA evoked more outward current at −70mV and greater positive slope conductance in STN neurons located ipsilateral to 6-OHDA treatment compared to neurons located contralateral. Moreover, extracellular, loose-patch recordings showed that NMDA increased spontaneous firing rate in STN neurons in slices from normal rats, whereas NMDA produced a tolbutamide-sensitive inhibition of firing rate in STN neurons located ipsilateral to 6-OHDA treatment. These results show that K-ATP channel function in STN neurons is up-regulated by chronic dopamine deficiency. We suggest that K-ATP channel activation in the STN might benefit symptoms of Parkinson's disease.
language: eng
source:
identifier: ISSN: 0304-3940 ; E-ISSN: 1872-7972 ; DOI: 10.1016/j.neulet.2012.10.030
fulltext: fulltext
issn:
  • 0304-3940
  • 03043940
  • 1872-7972
  • 18727972
url: Link


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titleChronic dopamine depletion augments the functional expression of K-ATP channels in the rat subthalamic nucleus
creatorShen, Ke-Zhong ; Johnson, Steven W
ispartofNeuroscience Letters, 07 December 2012, Vol.531(2), pp.104-108
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subjectATP-Sensitive K+ Channel ; Subthalamic Nucleus ; N-Methyl-D-Aspartate ; Sulfonylurea ; Tolbutamide ; Brain Slice ; Medicine ; Anatomy & Physiology
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descriptionHighlights► NMDA evokes K-ATP currents in rat subthalamic nucleus (STN) neurons. ► STN neurons were recorded in slices from rats treated with 6-OHDA. ► NMDA evoked more outward current in STN neurons from dopamine-depleted rats. ► NMDA inhibited firing rate in slices from 6-OHDA-treated but not normal rats. ► We conclude that dopamine deficiency up-regulates functional K-ATP expression. Symptoms of Parkinson's disease caused by dopamine depletion are associated with burst firing in the subthalamic nucleus (STN). Moreover, regularization or suppression of STN neuronal activity is thought to improve symptoms of Parkinson's disease. We reported recently that N-methyl-d-aspartate (NMDA) receptor stimulation of rat STN neurons evokes ATP-sensitive K+ (K-ATP) current via a Ca2+- and nitric oxide-dependent mechanism. The present studies were done to determine whether or not K-ATP channel function in STN neurons is altered in a model of chronic dopamine depletion. Brain slices were prepared from rats with unilateral dopamine depletion caused by intracerebral 6-hydroxydopamine (6-OHDA) injections. Whole-cell patch-clamp recordings showed that NMDA evoked more outward current at −70mV and greater positive slope conductance in STN neurons located ipsilateral to 6-OHDA treatment compared to neurons located contralateral. Moreover, extracellular, loose-patch recordings showed that NMDA increased spontaneous firing rate in STN neurons in slices from normal rats, whereas NMDA produced a tolbutamide-sensitive inhibition of firing rate in STN neurons located ipsilateral to 6-OHDA treatment. These results show that K-ATP channel function in STN neurons is up-regulated by chronic dopamine deficiency. We suggest that K-ATP channel activation in the STN might benefit symptoms of Parkinson's disease.
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