Honors Theses

Date of Award


Document Type

Undergraduate Thesis



First Advisor

Carol Britson

Relational Format



Background: Several lines of evidence suggest dysfunction of the γ-aminobutyric acid (GABA)ergic system in major depressive disorder. Neuroimaging studies report reduced levels of GABA in the dorsolateral prefrontal and occipital cortex of depressed patients. Our previous postmortem study re-vealed a reduction in the density and size of calbindin-immunoreactive (CB-IR) GABAergic neurons in the prefrontal cortex in major depressive disorder. The goal of this study was to test whether the changes in CB-IR neurons can also be detected in the occipital cortex, where neuroimaging studies report a prominent GABA decrease. Methods: A three-dimensional cell counting probe was used to assess the cell-packing density and size of CB-IR neurons in layer II of the occipital cortex in 10 major depressive disorder subjects and 10 psychiatrically healthy control subjects. Results: The density of CB-IR neurons was significantly decreased by 28% in major depressive dis-order subjects compared with the control group. The size of CB-IR neurons was unchanged in major depressive disorder subjects when compared with control subjects. Conclusions: The reduction in the density of CB-IR GABAergic neurons in the occipital cortex in depression is similar to that observed previously in the prefrontal cortex. Deficits in cortical GA-BAergic interneurons may contribute to the low GABA levels detected in neuroimaging studies in major depressive disorder patients. Future Directions: Experiments are proposed to determine whether or not decreases in calbindin-immunoreactivity are due to decreases in calbindin expression. Further experiments will be designed to investigate potential involvement of calbindin interactors in MDD.

Included in

Biology Commons



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