Visit our Expo - Redox and Inflammation signaling 2012

Session II : Receptor signaling and G proteins Poster II, 5
Dysregulation of GABAergic Neurotransmission in Mood Disorders
Hendrik Bielau1, Tomasz Gos1, Christian Mawrin2, Kurt Trübner3, Ralf Brisch1,
Gabriela Meyer-Lotz1, Henrik Dobrowolny1, Bruno Baumann1, Hans-Gert Bernstein1,
Bernhard Bogerts1
1Department of Psychiatry, Psychotherapy und Psychosomatic Medicine and 2Institute
of Neuropathology; Otto-von-Guericke-University, Leipziger Str. 44, 39120 Magdeburg,
Germany, E-mail: Hendrik.Bielau@Medizin.Uni-Magdeburg.de
3Institute of Legal Medicine, University of Essen, Hufelandstr. 55, 45122 Essen,
Germany
Alterations of GABAergic neurotransmission are assumed to play a crucial roll in the
pathophysiology of mood disorders. GABA acts via binding to A and B receptors, whereas
the B receptor is G-protein-coupled. Glutamatdecarboxylase (GAD) is the key enzyme of
GABA synthesis. The goal of our postmortem investigation was the bihemispherical
immunohistochemical staining of GAD neurons in brain structures which are important for
mood regulation. In 20 brains of patients with mood disorders and 19 controls (C) an
immunohistochemical staining of GAD-65/67 neurons was performed in dorsolateral
prefrontal cortex, orbitofrontal cortex, anterior cingulate cortex, superior temporal gyrus,
hippocampus and medial and lateral thalamus with consecutive determination of neuronal
density. In the diagnosis group were 11 patients with bipolar disorder (BD) and 9 patients
with major depressive disorder (MDD). The data were tested statistically using ANOVA und
post-hoc Tukey tests. The evaluation revealed significant differences between the groups (C,
BD, MDD) in dorsolateral prefrontal cortex, orbitofrontal cortex, superior temporal gyrus and
hippocampus. The post-hoc tests demonstrated higher neuronal densities in unipolar patients
compared to bipolar patients and controls in dorsolateral prefrontal cortex, superior temporal
gyrus and hippocampus. In the orbitofrontal cortex a higher neuronal density was found in
bipolar and unipolar patients compared to controls. In the bipolar group dose equivalents of
antidepressants given prior to death correlated positively with the neuronal density in the
hippocampus. In conclusion, the current data on GAD-65/67 point on a dysregulation of the
GABAergic system in mood disorders. Possibly, existing deficits of GABAergic
neurotransmission will be compensated or overcompensated by antidepressants. Moreover,
preliminary data point toward a diminished density of GAD terminals.
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