Homeostatic Plasticity of Striatal Neurons Intrinsic Excitability following Dopamine Depletion
| Autor: | Peter Paul De Deyn, Patrick Bischop, Marcelo Chávez, Bart Marescau, David Gall, Serge N. Schiffmann, Pim Wetzelaer, Karima Azdad |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2009 |
| Předmět: |
Dendritic spine
Patch-Clamp Techniques Receptors Dopamine -- metabolism Dopamine lcsh:Medicine Striatum Biology Medium spiny neuron Neurological Disorders Models Biological Synaptic Transmission Receptors Dopamine Neostriatum -- metabolism Homeostatic plasticity medicine Premovement neuronal activity Animals Homeostasis Neurons -- metabolism Rats Wistar lcsh:Science Neurological Disorders/Movement Disorders In Situ Hybridization Neurons Multidisciplinary Neuronal Plasticity Dopamine -- metabolism -- physiology Dopaminergic lcsh:R Anatomy Sciences bio-médicales et agricoles Corpus Striatum Rats Neostriatum alpha-Methyltyrosine nervous system Excitatory postsynaptic potential lcsh:Q Human medicine Neuroscience medicine.drug alpha-Methyltyrosine -- chemistry Research Article |
| Zdroj: | PLoS ONE PLoS ONE, Vol 4, Iss 9, p e6908 (2009) PloS one, 4 (9 |
| ISSN: | 1932-6203 |
| Popis: | The striatum is the major input structure of basal ganglia and is involved in adaptive control of behaviour through the selection of relevant informations. Dopaminergic neurons that innervate striatum die in Parkinson disease, leading to inefficient adaptive behaviour. Neuronal activity of striatal medium spiny neurons (MSN) is modulated by dopamine receptors. Although dopamine signalling had received substantial attention, consequences of dopamine depletion on MSN intrinsic excitability remain unclear. Here we show, by performing perforated patch clamp recordings on brain slices, that dopamine depletion leads to an increase in MSN intrinsic excitability through the decrease of an inactivating A-type potassium current, I(A). Despite the large decrease in their excitatory synaptic inputs determined by the decreased dendritic spines density and the increase in minimal current to evoke the first EPSP, this increase in intrinsic excitability resulted in an enhanced responsiveness to their remaining synapses, allowing them to fire similarly or more efficiently following input stimulation than in control condition. Therefore, this increase in intrinsic excitability through the regulation of I(A) represents a form of homeostatic plasticity allowing neurons to compensate for perturbations in synaptic transmission and to promote stability in firing. The present observations show that this homeostatic ability to maintain firing rates within functional range also occurs in pathological conditions, allowing stabilizing neural computation within affected neuronal networks. Journal Article Research Support, Non-U.S. Gov't info:eu-repo/semantics/published |
| Databáze: | OpenAIRE |
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