Dopamine-deprived striatal GABAergic interneurons burst and generate repetitive gigantic IPSCs in medium spiny neurons

Striatal GABAergic microcircuits modulate cortical responses and movement execution in part by controlling the activity of medium spiny neurons (MSNs). How this is altered by chronic dopamine depletion, such as in Parkinson's disease, is not presently understood. We now report that, in dopamine...

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Vydané v:The Journal of neuroscience Ročník 29; číslo 24; s. 7776
Hlavní autori: Dehorter, Nathalie, Guigoni, Celine, Lopez, Catherine, Hirsch, June, Eusebio, Alexandre, Ben-Ari, Yehezkel, Hammond, Constance
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 17.06.2009
Predmet:
6-Cyano-7-nitroquinoxaline-2,3-dione - pharmacology
Action Potentials - drug effects
Action Potentials - physiology
Adrenergic Agents - pharmacology
Animals
Biological Clocks - drug effects
Biophysics
Corpus Striatum - cytology
Dopamine - deficiency
Dose-Response Relationship, Drug
Electric Stimulation
Excitatory Amino Acid Antagonists - pharmacology
GABA Agents - pharmacology
gamma-Aminobutyric Acid - metabolism
In Vitro Techniques
Inhibitory Postsynaptic Potentials - drug effects
Inhibitory Postsynaptic Potentials - physiology
Interneurons - classification
Interneurons - drug effects
Interneurons - metabolism
Lysine - analogs & derivatives
Lysine - metabolism
Mice
Nicotine - pharmacology
Nicotinic Agonists - pharmacology
Oxidopamine - pharmacology
Patch-Clamp Techniques - methods
Spectrum Analysis
Tyrosine 3-Monooxygenase - metabolism
Valine - analogs & derivatives
Valine - pharmacology
ISSN:1529-2401, 1529-2401
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Shrnutí:Striatal GABAergic microcircuits modulate cortical responses and movement execution in part by controlling the activity of medium spiny neurons (MSNs). How this is altered by chronic dopamine depletion, such as in Parkinson's disease, is not presently understood. We now report that, in dopamine-depleted slices of the striatum, MSNs generate giant spontaneous postsynaptic GABAergic currents (single or in bursts at 60 Hz) interspersed with silent episodes, rather than the continuous, low-frequency GABAergic drive (5 Hz) observed in control MSNs. This shift was observed in one-half of the MSN population, including both "D(1)-negative" and "D(1)-positive" MSNs. Single GABA and NMDA channel recordings revealed that the resting membrane potential and reversal potential of GABA were similar in control and dopamine-depleted MSNs, and depolarizing, but not excitatory, actions of GABA were observed. Glutamatergic and cholinergic antagonists did not block the GABAergic oscillations, suggesting that they were generated by GABAergic neurons. In support of this, cell-attached recordings revealed that a subpopulation of intrastriatal GABAergic interneurons generated bursts of spikes in dopamine-deprived conditions. This subpopulation included low-threshold spike interneurons but not fast-spiking interneurons, cholinergic interneurons, or MSNs. Therefore, a population of local GABAergic interneurons shifts from tonic to oscillatory mode when dopamine deprived and gives rise to spontaneous repetitive giant GABAergic currents in one-half the MSNs. We suggest that this may in turn alter integration of cortical signals by MSNs.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
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content type line 23
ISSN:1529-2401
1529-2401
DOI:10.1523/JNEUROSCI.1527-09.2009