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

Soeiro-de-Souza, M; Henning, A; Machado-Vieira, R; Moreno, RA; Pastorello, BF; Leite, C; Vallada, H; Otaduy, MC

doi:10.1111/bdi.09_12477

Item

ITEM ACTIONSEXPORT

Add to Basket

Local TagsRelease HistoryDetailsSummary

Released

Meeting Abstract

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

MPS-Authors

/persons/resource/persons84402

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;

External Resource

Link
(Any fulltext)

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

Fulltext (public)

There are no public fulltexts stored in PuRe

Supplementary Material (public)

There is no public supplementary material available

Citation

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.

Cite as: https://hdl.handle.net/21.11116/0000-0000-C594-A

Abstract

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.