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Markers of glutamate synaptic transmission and plasticity are increased in the anterior cingulate cortex in bipolar disorder.

Abstract：

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.

journal_name

Biol Psychiatry

journal_title

Biological psychiatry

authors

Eastwood SL,Harrison PJ

doi

10.1016/j.biopsych.2009.12.004

subject

Has Abstract

pub_date

2010-06-01 00:00:00

pages

1010-6

issue

11

eissn

0006-3223

issn

1873-2402

pii

S0006-3223(09)01428-0

journal_volume

67

pub_type

杂志文章

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