The authors of this paper do not have any commercial associations that might pose a conflict of interest in connection with this manuscript.
N-methyl-D-aspartate receptor expression in parvalbumin-containing inhibitory neurons in the prefrontal cortex in bipolar disorder
Article first published online: 24 JAN 2010
© 2010 The Authors. Journal compilation © 2010 John Wiley & Sons A/S
Volume 12, Issue 1, pages 95–101, February 2010
How to Cite
Bitanihirwe, B. K., Lim, M. P. and Woo, T.-U. W. (2010), N-methyl-D-aspartate receptor expression in parvalbumin-containing inhibitory neurons in the prefrontal cortex in bipolar disorder. Bipolar Disorders, 12: 95–101. doi: 10.1111/j.1399-5618.2009.00785.x
- Issue published online: 24 JAN 2010
- Article first published online: 24 JAN 2010
- Received 23 February 2009, revised and accepted for publication 15 September 2009
- gene expression;
- in situ hybridization;
Bitanihirwe BKY, Lim MP, Woo T-UW. N-methyl-D-aspartate receptor expression in parvalbumin-containing inhibitory neurons in the prefrontal cortex in bipolar disorder. Bipolar Disord 2010: 12: 95–101. © 2010 The Authors. Journal compilation © 2010 John Wiley & Sons A/S.
Objectives: Inhibitory neural circuits and the glutamatergic regulation of these circuits in the cerebral cortex appear to be disturbed in bipolar disorder. In this study, we addressed the hypothesis that, in the prefrontal cortex (PFC), disturbances of glutamatergic regulation of the class of inhibitory neurons that contain the calcium buffer parvalbumin (PV) via N-methyl-D-aspartate (NMDA) receptor may contribute to the pathophysiology of bipolar disorder.
Methods: We used double in situ hybridization with a sulfur-35-labeled riboprobe for the NR2A subunit of the NMDA receptor and a digoxigenin-labeled riboprobe for PV in a cohort of 18 subjects with bipolar disorder and 18 demographically matched normal control subjects.
Results: We observed no differences in the relative density and laminar distribution of the PV-expressing neurons between subjects with bipolar disorder and matched normal control subjects. Furthermore, the density of the PV neurons that co-expressed NR2A messenger RNA (mRNA) or the cellular expression of NR2A mRNA in the PV neurons that exhibited a detectable level of this transcript was unaltered in subjects with bipolar disorder.
Conclusions: These findings suggest that, in the PFC, glutamatergic regulation of PV-containing inhibitory neurons via NR2A-containing NMDA receptors does not appear to be altered in bipolar disorder. However, the possibility that other subsets of γ-aminobutyric acid (GABA) neurons or other glutamate receptor subtypes are affected cannot be excluded.