1H MRS Measurement of Cortical GABA and Glutamate in Primary Insomnia and Major Depressive Disorder: Relationship to Sleep Quality and Depression Severity

JOURNAL OF AFFECTIVE DISORDERS

卷:274

Article

Benson, Kathleen L.^1,2  Bottary, Ryan³  Schoerning, Laura⁴  Baer, Lee²  Gonenc, Atilla^1,2  Jensen, J. Eric^1,2  Winkelman, John W.^2,5,6 

[1] McLean Hosp, McLean Imaging Ctr, 115 Mill St, Belmont, MA 02178 USA

[2] Harvard Med Sch, Dept Psychiat, Boston, MA 02115 USA

[3] Boston Coll, Dept Psychol, Cognit & Affect Neurosci Lab, Chestnut Hill, MA 02167 USA

[4] Univ Massachusetts, Sch Med, Worcester, MA USA

[5] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA

[6] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA

关键词: GABA;    Glutamate;    Magnetic Resonance Spectroscopy;    Depression;    Insomnia;    Sleep;   

DOI  :  10.1016/j.jad.2020.05.026

来源: Elsevier

【 摘 要 】

Background: Both Major Depressive Disorder (MDD) and Primary Insomnia (PI) have been linked to de ficiencies in cortical gamma-aminobutyric acid (GABA) and glutamate (Glu) thus suggesting a shared neurobiological link be- tween these two conditions. The extent to which comorbid insomnia contributes to GABAergic or glutamatergic de ficiencies in MDD remains unclear. Methods: We used single-voxel proton magnetic resonance spectroscopy ( 1 H MRS) at 4 Tesla to examine GABA+ and Glu relative to creatine (Cr) in the dorsal anterior cingulate cortex (dACC) and in the parieto-occipital cortex (POC) of 51 non -medicated adults with MDD, 24 adults with Primary Insomnia (PI), and 25 age- and sex - matched good sleeper controls (HC). Measures of depression severity and subjective and objective sleep quality were compared with 1 H MRS metabolite measures. Results: MDD subjects exhibited a 15% decrease in Glu/Cr in the dACC compared to HC. Within the MDD group, there was a trend inverse correlation between dACC Glu/Cr and anhedonia ratings. We observed no signi ficant association between measures of sleep quality with dACC Glu/Cr in those with MDD. Limitations: The protocol and data interpretation would have been enhanced by the recruitment of MDD subjects with a broader range of a ffect severity and a more comprehensive assessment of clinical features. Conclusions: These findings support the role of cortical glutamatergic mechanisms in the pathophysiology of MDD. Insomnia severity did not further contribute to the relative de ficiency of glutamatergic measures in MDD.

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