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Structurally dissimilar antimanic agents modulate synaptic plasticity by regulating AMPA glutamate receptor subunit
Jing Du1, Neil A Gray, Cynthia Falke
1Laboratory of Molecular Pathophysiology, National Institutes of Mental Health, National Institutes of Health, Bethesda, Maryland 20892-4405, USA.
Annals of the New York Academy of Sciences
|December 20, 2003
Summary
Mood stabilizers like lithium and valproate reduce AMPA receptor subunit GluR1 in the hippocampus. This suggests targeting glutamatergic synaptic plasticity may offer new treatments for mood disorders.
Area of Science:
- Neuroscience
- Psychiatry
- Pharmacology
Background:
- The glutamatergic system is a potential therapeutic target for mood disorders.
- Synapse-specific glutamate receptor expression is crucial for synaptic plasticity.
Purpose of the Study:
- To investigate the effects of mood stabilizers on AMPA receptor expression.
- To explore the role of synaptic plasticity in mood disorder treatment.
Main Methods:
- Chronic treatment of rats with lithium or valproate.
- Isolation of hippocampal synaptosomes and determination of GluR1 levels.
- Biotinylation assays and double-immunostaining in cultured hippocampal neurons.
Main Results:
- Both lithium and valproate significantly reduced AMPA receptor subunit GluR1 expression in hippocampal synaptosomes.
- Surface and synaptic GluR1 levels were affected by mood stabilizer treatment.
Conclusions:
- AMPA receptor subunit GluR1 is a common target for lithium and valproate.
- Regulation of glutamatergic synaptic plasticity may be key in treating mood disorders.
- Targeting synaptic GluR1 could lead to novel therapies for mood disorders.