Background
Cortical glutamate levels are elevated in bipolar disorder, but the interpretation
of this increase is unclear because glutamate has metabolic as well as neurotransmitter
roles. We investigated this by measuring vesicular glutamate transporter 1 (VGluT1)
expression, which reflects activity at glutamate synapses. We also measured netrin-G1
and netrin-G2 messenger RNAs because these genes are involved in the formation and
plasticity of glutamatergic connections.
Methods
Using quantitative polymerase chain reaction, we quantified transcripts for VGluT1,
netrin-G1 (isoforms G1c, G1d, and G1f), and netrin-G2 in the anterior cingulate cortex
from subjects with bipolar disorder (n = 34), schizophrenia (n = 35), and healthy control subjects (n = 35).
Results
Vesicular glutamate transporter 1, netrin-G2, and netrin-G1d and G1f were increased
in bipolar disorder but not in schizophrenia. Netrin-G1c did not differ between groups.
Netrin-G1c and netrin-G1f expression showed left-right asymmetries. Vesicular glutamate
transporter 1 messenger RNA correlated with brain weight.
Conclusions
Increased VGluT1 expression is supportive of elevated glutamate neurotransmission
in the anterior cingulate cortex in bipolar disorder. The netrin-G1 and netrin-G2
findings suggest there may be an underlying difference in the plasticity of the affected
circuitry.
Key Words
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Article info
Publication history
Published online: January 18, 2010
Accepted:
December 2,
2009
Received in revised form:
October 27,
2009
Received:
September 23,
2009
Identification
Copyright
© 2010 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
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- Presynaptic Glutamatergic Dysfunction in Bipolar DisorderBiological PsychiatryVol. 67Issue 11
- PreviewIn this issue of Biological Psychiatry, Eastwood and Harrison (1) provide additional new data to support the key role that the glutamatergic system might play in the pathophysiology of bipolar disorder (BPD) and lend credence to the notion that this system might be a key target for developing novel drugs that are more effective for treating BPD than currently available therapeutic options.
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