Markers of Glutamate Synaptic Transmission and Plasticity Are Increased in the Anterior Cingulate Cortex in Bipolar Disorder

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 glutam...

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Published in	Biological psychiatry (1969) Vol. 67; no. 11; pp. 1010 - 1016
Main Authors	Eastwood, Sharon L., Harrison, Paul J.
Format	Journal Article
Language	English
Published	New York, NY Elsevier Inc 01.06.2010 Elsevier
Subjects	Adult Adult and adolescent clinical studies Aged Analysis of Variance Biological and medical sciences Bipolar Disorder - genetics Bipolar Disorder - metabolism Bipolar disorders Female Functional Laterality - physiology Gene expression Genotype Glutamic Acid - genetics Glutamic Acid - metabolism Glycoproteins - genetics Glycoproteins - metabolism GPI-Linked Proteins Gyrus Cinguli - metabolism Humans In Situ Hybridization laminets Male Medical sciences Middle Aged Mood disorders mRNA Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Netrins Neuronal Plasticity - physiology Neurons - metabolism Presynaptic Terminals - metabolism Psychiatry Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychoses Reverse Transcriptase Polymerase Chain Reaction Schizophrenia Schizophrenia - genetics Schizophrenia - metabolism Synaptic Transmission - physiology Vesicular Glutamate Transport Protein 1 - genetics Vesicular Glutamate Transport Protein 1 - metabolism vesicular glutamate transporter laminets mRNA schizophrenia Gene expression vesicular glutamate transporter netrins Mood disorder Central nervous system Schizophrenia Bipolar disorder Genetic determinism Encephalon Psychosis Cingulate cortex Synaptic transmission Synaptic plasticity Genetics VGLUT glutamate transporter Glutamatergic transmission
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Abstract	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. 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). 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. 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.
AbstractList	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.BACKGROUNDCortical 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.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).METHODSUsing 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).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.RESULTSVesicular 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.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.CONCLUSIONSIncreased 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. 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. 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. 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). 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. 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. 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. 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). 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. 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.
Author	Eastwood, Sharon L. Harrison, Paul J.
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Keywords	laminets mRNA schizophrenia Gene expression vesicular glutamate transporter netrins Mood disorder Central nervous system Schizophrenia Bipolar disorder Genetic determinism Encephalon Psychosis Cingulate cortex Synaptic transmission Synaptic plasticity Genetics VGLUT glutamate transporter Glutamatergic transmission
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Snippet	Cortical glutamate levels are elevated in bipolar disorder, but the interpretation of this increase is unclear because glutamate has metabolic as well as... Background Cortical glutamate levels are elevated in bipolar disorder, but the interpretation of this increase is unclear because glutamate has metabolic as...
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SubjectTerms	Adult Adult and adolescent clinical studies Aged Analysis of Variance Biological and medical sciences Bipolar Disorder - genetics Bipolar Disorder - metabolism Bipolar disorders Female Functional Laterality - physiology Gene expression Genotype Glutamic Acid - genetics Glutamic Acid - metabolism Glycoproteins - genetics Glycoproteins - metabolism GPI-Linked Proteins Gyrus Cinguli - metabolism Humans In Situ Hybridization laminets Male Medical sciences Middle Aged Mood disorders mRNA Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Netrins Neuronal Plasticity - physiology Neurons - metabolism Presynaptic Terminals - metabolism Psychiatry Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychoses Reverse Transcriptase Polymerase Chain Reaction Schizophrenia Schizophrenia - genetics Schizophrenia - metabolism Synaptic Transmission - physiology Vesicular Glutamate Transport Protein 1 - genetics Vesicular Glutamate Transport Protein 1 - metabolism vesicular glutamate transporter
Title	Markers of Glutamate Synaptic Transmission and Plasticity Are Increased in the Anterior Cingulate Cortex in Bipolar Disorder
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