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Ethanol reverses the direction of long-term synaptic plasticity in the dorsomedial striatum.

Artikel i vetenskaplig tidskrift
Författare Henry H Yin
Brian S Park
Louise Adermark
David M Lovinger
Publicerad i The European journal of neuroscience
Volym 25
Nummer/häfte 11
Sidor 3226-32
ISSN 0953-816X
Publiceringsår 2007
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Sidor 3226-32
Språk en
Länkar dx.doi.org/10.1111/j.1460-9568.2007...
Ämnesord Animals, Animals, Newborn, Central Nervous System Depressants, pharmacology, Corpus Striatum, cytology, Dopamine Antagonists, pharmacology, Dose-Response Relationship, Drug, Dose-Response Relationship, Radiation, Electric Stimulation, Ethanol, pharmacology, Evoked Potentials, drug effects, physiology, radiation effects, Neuronal Plasticity, drug effects, Neurons, drug effects, physiology, Patch-Clamp Techniques, methods, Piperidines, pharmacology, Pyrazoles, pharmacology, Rats, Rats, Sprague-Dawley, Sulpiride, pharmacology, Synaptic Transmission, drug effects, physiology, Time Factors
Ämneskategorier Fysiologi

Sammanfattning

The striatum is a critical structure for the control of voluntary behaviour, and striatal synaptic plasticity has been implicated in instrumental learning. As ethanol consumption can cause impairments in cognition, learning, and action selection, it is important to understand the effects of this drug on striatal function. In this study we examined the effects of ethanol on long-term synaptic plasticity in the dorsomedial striatum (DMS), a striatal subregion that plays a central role in the acquisition and selection of goal-directed actions. Ethanol was found to impair N-methyl-d-aspartic acid receptor (NMDAR)-dependent long-term potentiation (LTP) dose-dependently in the DMS, and to promote long-term depression (LTD) at the highest concentration (50 mm) used. These results suggest that ethanol, at a concentration usually associated with mild intoxication, could significantly change experience-dependent modification of corticostriatal circuits underlying the learning of goal-directed instrumental actions.

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