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Meeting Abstract

Brain glutamate cycle metabolites and medication interference in BD I Patients: H1-MRS Studies

MPG-Autoren
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Henning,  A
Max Planck Institute for Biological Cybernetics, Max Planck Society;
Research Group MR Spectroscopy and Ultra-High Field Methodology, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Zitation

Soeiro-de-Souza, M., Henning, A., Machado-Vieira, R., Moreno, R., Pastorello, B., Leite, C., et al. (2017). Brain glutamate cycle metabolites and medication interference in BD I Patients: H1-MRS Studies. Bipolar Orders, 19(Supplement 1), 25-25.


Zitierlink: http://hdl.handle.net/21.11116/0000-0000-C594-A
Zusammenfassung
Bipolar disorder has been consistently associated with abnormalities in the Glutamate/Glutamine cycle. Our group has investigated BD patients during depressive episode and euthymia using magnetic resonance spectroscopy (1H-MRS). We developed a technic that allow a precise individual measure of GABA, glutamine and glutamate in the anterior cingulate cortex (ACC; 2×2×4.5 cm3) using a two-dimensional JPRESS sequence. Fifty euthymic patients and 24 bipolar depression patients were studied. GABA, glutamine (Gln) and glutamate (Glu) were quantified with the ProFit program. Our findings suggest a significant effect of anticonvulsant and lithium use on the glutamatergic system. The use of anticonvulsants was associated with increased glutamine levels in euthymic patients. Moreover, in bipolar depression treated with lithium those that achieved remmition presented higher myoinositol levels at endpoint and lithium increased glutamate levels. These results indicate that the glutamatergic function in BD patients is altered and suffers great influence of mood state and medication use. Overall, the present findings support a role for myoinositol and glutamate-glutamine cycling in the response to lithium and anticonvulsants in bipolar disorder. Further long-term studies are needed to investigate the effects of mood stabilizers on ACC metabolites, in special glutamate and its direct role in mediating plasticity activation associated with antidepressant response and mood stabilization.