title: Differences between unipolar and bipolar I depression in the quantitative analysis of glutamic acid decarboxylase-immunoreactive neuropil.
abstract: Alterations in GABAergic neurotransmission are assumed to play a crucial role in the pathophysiology of mood disorders. Glutamic acid decarboxylase (GAD) is the key enzyme in GABA synthesis. This study aimed to differentiate between unipolar and bipolar I depression using quantitative evaluation of GAD-immunoreactive (GAD-ir) neuropil in several brain regions known to be involved in the pathophysiology of mood disorders. Immunohistochemical staining of GAD 65/67 was performed in the orbitofrontal, anterior cingulate and dorsolateral prefrontal cortex (DLPFC), the entorhinal cortex, the hippocampal formation and the medial dorsal and lateral dorsal (LD) thalamic nuclei, with a quantitative densitometric analysis of GAD-ir neuropil. The study was performed on paraffin-embedded brains from 9 unipolar and 12 bipolar I depressed patients (8 and 6 suicidal patients, respectively) and 18 matched controls. In unipolar patients, compared with controls, only the increased relative density of GAD-ir neuropil in the right LD was different from the previous results in depressed suicides from the same cohort (Gos et al. in J Affect Disord 113:45-55, 2009). On the other hand, the left DLPFC was the only area where a significant decrease was observed, specific for bipolar I depression. Significant differences between both diagnostic groups were found in these regions. By revealing abnormalities in the relative density of GAD-ir neuropil in brain structures, our study suggests a diathesis of the GABAergic system in mood disorders, which may differentiate the pathophysiology of unipolar from that of bipolar I depression.
authors.affiliation: Institute of Forensic Medicine, Medical University of Gdańsk, Gdańsk, Poland. gost@gumed.edu.pl
authors.forename: Tomasz
authors.initials: T
authors.lastname: Gos
authors.forename: Johann
authors.initials: J
authors.lastname: Steiner
authors.forename: Hendrik
authors.initials: H
authors.lastname: Bielau
authors.forename: Henrik
authors.initials: H
authors.lastname: Dobrowolny
authors.forename: Karoline
authors.initials: K
authors.lastname: Günther
authors.forename: Christian
authors.initials: C
authors.lastname: Mawrin
authors.forename: Maciej
authors.initials: M
authors.lastname: Krzyżanowski
authors.forename: Roman
authors.initials: R
authors.lastname: Hauser
authors.forename: Ralf
authors.initials: R
authors.lastname: Brisch
authors.forename: Hans-Gert
authors.initials: HG
authors.lastname: Bernstein
authors.forename: Zbigniew
authors.initials: Z
authors.lastname: Jankowski
authors.forename: Katharina
authors.initials: K
authors.lastname: Braun
authors.forename: Bernhard
authors.initials: B
authors.lastname: Bogerts
mesh_terms: D000328:Adult; D000368:Aged; D001714:Bipolar Disorder / Q000188:drug therapy / Q000473:pathology*; D001921:Brain / Q000187:drug effects / Q000201:enzymology / Q000473:pathology*; D016022:Case-Control Studies; D003866:Depressive Disorder / Q000188:drug therapy / Q000473:pathology*; D005260:Female; D005968:Glutamate Decarboxylase / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D019581:Neuropil / Q000201:enzymology* / Q000473:pathology; D011619:Psychotropic Drugs / Q000494:pharmacology / Q000627:therapeutic use; D018709:Statistics, Nonparametric
chemical_list: D011619:Psychotropic Drugs; D005968:Glutamate Decarboxylase; C402565:glutamate decarboxylase 1; C401141:glutamate decarboxylase 2