Document Detail

Interhemispheric regulation of the medial prefrontal cortical glutamate stress response in rats.
MedLine Citation:
PMID:  20519537     Owner:  NLM     Status:  MEDLINE    
While stressors are known to increase medial prefrontal cortex (PFC) glutamate (GLU) levels, the mechanism(s) subserving this response remain to be elucidated. We used microdialysis and local drug applications to investigate, in male Long-Evans rats, whether the PFC GLU stress response might reflect increased interhemispheric communication by callosal projection neurons. We report here that tail-pinch stress (20 min) elicited comparable increases in GLU in the left and right PFC that were sodium and calcium dependent and insensitive to local glial cystine-GLU exchanger blockade. Unilateral ibotenate-induced PFC lesions abolished the GLU stress response in the opposite hemisphere, as did contralateral mGlu(2/3) receptor activation. Local dopamine (DA) D(1) receptor blockade in the left PFC potently enhanced the right PFC GLU stress response, whereas the same treatment applied to the right PFC had a much weaker effect on the left PFC GLU response. Finally, the PFC GLU stress response was attenuated and potentiated, respectively, following alpha(1)-adrenoreceptor blockade and GABA(B) receptor activation in the opposite hemisphere. These findings indicate that the PFC GLU stress response reflects, at least in part, activation of callosal neurons located in the opposite hemisphere and that stress-induced activation of these neurons is regulated by GLU-, DA-, norepinephrine-, and GABA-sensitive mechanisms. In the case of DA, this control is asymmetrical, with a marked regulatory bias of the left PFC DA input over the right PFC GLU stress response. Together, these findings suggest that callosal neurons and their afferentation play an important role in the hemispheric specialization of PFC-mediated responses to stressors.
Derek Lupinsky; Luc Moquin; Alain Gratton
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  30     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-06-03     Completed Date:  2010-06-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  7624-33     Citation Subset:  IM    
Douglas Hospital Research Centre, Department of Psychiatry, McGill University, Montr?al, Qu?bec, Canada.
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MeSH Terms
Adrenergic alpha-Antagonists / pharmacology
Amino Acids / pharmacology
Analysis of Variance
Baclofen / pharmacology
Benzazepines / pharmacology
Bicyclo Compounds, Heterocyclic / pharmacology
Chromatography, High Pressure Liquid / methods
Disease Models, Animal
Dopamine Antagonists / pharmacology
Excitatory Amino Acid Agonists / toxicity
Functional Laterality / physiology*
GABA Agonists / pharmacology
Glutamic Acid / metabolism*
Ibotenic Acid / toxicity
Microdialysis / methods
Neural Pathways / drug effects,  injuries
Oxathiins / pharmacology
Prefrontal Cortex / drug effects,  injuries,  metabolism*
Rats, Sprague-Dawley
Sodium Channel Blockers / administration & dosage
Stress, Psychological / pathology*
Tail / innervation
Tetrodotoxin / administration & dosage
Grant Support
//Canadian Institutes of Health Research
Reg. No./Substance:
0/Adrenergic alpha-Antagonists; 0/Amino Acids; 0/Benzazepines; 0/Bicyclo Compounds, Heterocyclic; 0/Dopamine Antagonists; 0/Excitatory Amino Acid Agonists; 0/GABA Agonists; 0/LY 379268; 0/Oxathiins; 0/SCH 23390; 0/Sodium Channel Blockers; 1134-47-0/Baclofen; 2552-55-8/Ibotenic Acid; 4368-28-9/Tetrodotoxin; 56-86-0/Glutamic Acid; 92642-94-9/benoxathian

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