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The glucocorticoid hypothesis of depression therefore had been modified, as the behavioural abnormalities of mood are perhaps as likely due to low rather than high glucocorticoid signalling, a hypothesis supported by the affective phenotype of mice lacking GR selectively in the forebrain [24].
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Taken together, our findings support the glial hypothesis of mood abnormalities [ 28] and concur with the literature on a putative role of glutamate dysregulation in suicidal behaviour.
The variable presence and magnitude of such abnormalities in mood disorders likely reflects the heterogeneity encompassed within the MDD and BD syndromes with respect to pathophysiology and etiology.
Abnormalities of dopamine innervation may produce mood fluctuations via effects on PCC, an area strongly linked to mood and anxiety and with known rCBF responsiveness to levodopa or D2-like dopamine receptor agonists.
As such, it is difficult to disentangle which abnormalities represent causes and which are consequences of mood episodes (Bellivier et al. 2015).
During recent years, also glial abnormalities have been implicated in the pathophysiology of mood disorders.
Yuksel C, Ongur D. Magnetic resonance spectroscopy studies of glutamate-related abnormalities in mood disorders.
This abnormality may be related to the mechanisms of action of mood stabilizers and the previous findings on the abnormal psychoimmunology of patients with bipolar disorder.
An emerging literature suggests motor abnormalities accompany mood and psychotic symptoms of BD, although the relationship between motor and mood disorders has rarely been studied explicitly [3].
Rios AC, Maurya PK, Pedrini M, Zeni-Graiff M, Asevedo E, Mansur RB, et al. Microbiota abnormalities and the therapeutic potential of probiotics in the treatment of mood disorders.
However, it is unclear if rhythm abnormalities contribute to depressive symptoms or they are a consequence of mood symptoms.
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