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Lesion of the ventromedial nucleus of the thalamus blocks acute cocaine‐induced changes in striatal glutamate
Author(s) -
McKee Brenda L.,
Keyghobadi Modjgan,
Tozier De La Poterie Adrienne P.,
Meshul Charles K.
Publication year - 2010
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.20749
Subject(s) - microdialysis , glutamate receptor , thalamus , striatum , extracellular , neuroscience , lesion , chemistry , nucleus , psychology , dopamine , biochemistry , psychiatry , receptor
A single injection of cocaine increases extracellular glutamate in the rat dorsolateral striatum 1 day after the acute cocaine was administered (McKee and Meshul, 2005). However, the nuclei that facilitate this increase in striatal glutamate remain unknown. We hypothesized that the cocaine‐induced increase in striatal glutamate was produced by activation of the ventromedial (VM) nucleus of the thalamus via the thalamo‐corticostriatal or thalamostriatal pathways. First, rats received an electrolytic lesion of the VM. One day after a single cocaine or vehicle injection, extracellular glutamate was measured in the dorsolateral striatum using in vivo microdialysis. The motor thalamus lesion blocked the cocaine‐induced increase in striatal glutamate and reduced extracellular glutamate to the level of the vehicle‐treated group. This study shows a critical role for the VM nucleus of the thalamus in mediating the effects of cocaine on extracellular glutamate levels in the rat dorsolateral striatum. Synapse 64:445–448, 2010. © 2010 Wiley‐Liss, Inc.