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Reduced density of glutamine synthetase immunoreactive astrocytes in different cortical areas in major depression but not in bipolar I disorder.

Bernstein HG, Meyer-Lotz G, Dobrowolny H, Bannier J, Steiner J, Walter M, Bogerts B - Front Cell Neurosci (2015)

Bottom Line: Counting of GS expressing astrocytes (ACs) and OLs in eight cortical and two subcortical brain regions of subjects with mood disorder (N = 14), BD (N = 15), and controls (N = 16) revealed that in major depression the densities of ACs were significantly reduced in some cortical but not subcortical gray matter areas, whereas no changes were found for OLs.In BD no alterations of GS-immunoreactive glia were found.From our findings we conclude that (1) GS expressing ACs are prominently involved in glutamate-related disturbances in major depression, but not in BD and (2) GS expressing OLs, though being present in significant numbers in prefrontal cortical areas, play a minor (if any) role in mood disorder pathology.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychiatry, University of Magdeburg Magdeburg, Germany.

ABSTRACT
There is increasing evidence for disturbances within the glutamate system in patients with affective disorders, which involve disruptions of the glutamate-glutamine-cycle. The mainly astroglia-located enzyme glutamine synthetase (GS) catalyzes the ATP-dependent condensation of ammonia and glutamate to form glutamine, thus playing a central role in glutamate and glutamine homoeostasis. However, GS is also expressed in numerous oligodendrocytes (OLs), another class of glial cells implicated in mood disorder pathology. To learn more about the role of glia-associated GS in mental illnesses, we decided to find out if numerical densities of glial cells immunostained for the enzyme protein differ between subjects with major depressive disorder, bipolar disorder (BD), and psychically healthy control cases. Counting of GS expressing astrocytes (ACs) and OLs in eight cortical and two subcortical brain regions of subjects with mood disorder (N = 14), BD (N = 15), and controls (N = 16) revealed that in major depression the densities of ACs were significantly reduced in some cortical but not subcortical gray matter areas, whereas no changes were found for OLs. In BD no alterations of GS-immunoreactive glia were found. From our findings we conclude that (1) GS expressing ACs are prominently involved in glutamate-related disturbances in major depression, but not in BD and (2) GS expressing OLs, though being present in significant numbers in prefrontal cortical areas, play a minor (if any) role in mood disorder pathology. The latter assumption is supported by findings of others showing that - at least in the mouse brain cortex - GS immunoreactive oligodendroglial cells are unable to contribute to the glutamate-glutamine-cycle due to the complete lack of amino acid transporters (Takasaki et al., 2010).

No MeSH data available.


Related in: MedlinePlus

Numerical densities of GS-expressing glial cells in the AiC of suicide completers with MDD, non-suicide completers with MDD, suicide completers with BD, non-suicide completers with BD, and controls. No significant alterations were found.
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Figure 7: Numerical densities of GS-expressing glial cells in the AiC of suicide completers with MDD, non-suicide completers with MDD, suicide completers with BD, non-suicide completers with BD, and controls. No significant alterations were found.

Mentions: Since there are reports showing that GS expression is altered in brains of suicide victims with and without mood disorder (Kim et al., 2007; Sequeira et al., 2009; Bernstein et al., 2013) we next analyzed the influence of the confounding factor “death by suicide” on the densities of GS immunoreactive ACs in the brain regions under study. For this purpose we divided MDD and BD cases into subgroups of suicide victims (MDD: N = 11; BD: N = 7) and depressed subjects who died of natural causes (MDD: N = 3; BD: N = 8). With regard to MDD cases in none of the brain regions there appeared significant differences in the densities of GS-expressing cells between depressed subjects dying by suicide and non-suicidal individuals with MDD. The same holds true for subjects with BD: Suicidal and non-suicidal BD cases did not significantly differ with regard to glial cell densities in any of the regions studied, as exemplified for the AiC in Figure 7. It should be emphasized, however, that the subgroup of non-suicidal subjects with MDD is too small (N = 3) to come to far-reaching conclusions from these data.


Reduced density of glutamine synthetase immunoreactive astrocytes in different cortical areas in major depression but not in bipolar I disorder.

Bernstein HG, Meyer-Lotz G, Dobrowolny H, Bannier J, Steiner J, Walter M, Bogerts B - Front Cell Neurosci (2015)

Numerical densities of GS-expressing glial cells in the AiC of suicide completers with MDD, non-suicide completers with MDD, suicide completers with BD, non-suicide completers with BD, and controls. No significant alterations were found.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4530620&req=5

Figure 7: Numerical densities of GS-expressing glial cells in the AiC of suicide completers with MDD, non-suicide completers with MDD, suicide completers with BD, non-suicide completers with BD, and controls. No significant alterations were found.
Mentions: Since there are reports showing that GS expression is altered in brains of suicide victims with and without mood disorder (Kim et al., 2007; Sequeira et al., 2009; Bernstein et al., 2013) we next analyzed the influence of the confounding factor “death by suicide” on the densities of GS immunoreactive ACs in the brain regions under study. For this purpose we divided MDD and BD cases into subgroups of suicide victims (MDD: N = 11; BD: N = 7) and depressed subjects who died of natural causes (MDD: N = 3; BD: N = 8). With regard to MDD cases in none of the brain regions there appeared significant differences in the densities of GS-expressing cells between depressed subjects dying by suicide and non-suicidal individuals with MDD. The same holds true for subjects with BD: Suicidal and non-suicidal BD cases did not significantly differ with regard to glial cell densities in any of the regions studied, as exemplified for the AiC in Figure 7. It should be emphasized, however, that the subgroup of non-suicidal subjects with MDD is too small (N = 3) to come to far-reaching conclusions from these data.

Bottom Line: Counting of GS expressing astrocytes (ACs) and OLs in eight cortical and two subcortical brain regions of subjects with mood disorder (N = 14), BD (N = 15), and controls (N = 16) revealed that in major depression the densities of ACs were significantly reduced in some cortical but not subcortical gray matter areas, whereas no changes were found for OLs.In BD no alterations of GS-immunoreactive glia were found.From our findings we conclude that (1) GS expressing ACs are prominently involved in glutamate-related disturbances in major depression, but not in BD and (2) GS expressing OLs, though being present in significant numbers in prefrontal cortical areas, play a minor (if any) role in mood disorder pathology.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychiatry, University of Magdeburg Magdeburg, Germany.

ABSTRACT
There is increasing evidence for disturbances within the glutamate system in patients with affective disorders, which involve disruptions of the glutamate-glutamine-cycle. The mainly astroglia-located enzyme glutamine synthetase (GS) catalyzes the ATP-dependent condensation of ammonia and glutamate to form glutamine, thus playing a central role in glutamate and glutamine homoeostasis. However, GS is also expressed in numerous oligodendrocytes (OLs), another class of glial cells implicated in mood disorder pathology. To learn more about the role of glia-associated GS in mental illnesses, we decided to find out if numerical densities of glial cells immunostained for the enzyme protein differ between subjects with major depressive disorder, bipolar disorder (BD), and psychically healthy control cases. Counting of GS expressing astrocytes (ACs) and OLs in eight cortical and two subcortical brain regions of subjects with mood disorder (N = 14), BD (N = 15), and controls (N = 16) revealed that in major depression the densities of ACs were significantly reduced in some cortical but not subcortical gray matter areas, whereas no changes were found for OLs. In BD no alterations of GS-immunoreactive glia were found. From our findings we conclude that (1) GS expressing ACs are prominently involved in glutamate-related disturbances in major depression, but not in BD and (2) GS expressing OLs, though being present in significant numbers in prefrontal cortical areas, play a minor (if any) role in mood disorder pathology. The latter assumption is supported by findings of others showing that - at least in the mouse brain cortex - GS immunoreactive oligodendroglial cells are unable to contribute to the glutamate-glutamine-cycle due to the complete lack of amino acid transporters (Takasaki et al., 2010).

No MeSH data available.


Related in: MedlinePlus