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Animal Models of Depression - Chronic Despair Model (CDM)
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Reduced GAD(65/67) immunoreactivity in the hypothalamic paraventricular nucleus in depression: a postmortem study
Shang-Feng Gao1, Anne Klomp, Juan-Li Wu
1Department of Neurobiology, Key Laboratory of Medical Neurobiology of Ministry of Health of China, Zhejiang University School of Medicine, Hangzhou, Zhejiang, PR China.
Journal of Affective Disorders
|January 15, 2013
Summary
Reduced GABAergic input to the brain's PVN may drive CRH neuron overactivity in depression, particularly major depressive disorder (MDD). This suggests GABAergic agonists could be beneficial treatments for depression.
Area of Science:
- Neuroscience
- Neurobiology
- Psychiatry
Background:
- Gamma-aminobutyric acid (GABA) is a key inhibitory neurotransmitter regulating the hypothalamo-pituitary-adrenal (HPA) axis.
- HPA axis hyperactivity is implicated in the pathophysiology of depression.
Purpose of the Study:
- To investigate GABAergic input within the hypothalamic paraventricular nucleus (PVN) in patients with depression.
- To examine the correlation between GABAergic input and corticotropin-releasing hormone (CRH) neuron activity in depression.
Main Methods:
- Quantification of glutamic acid decarboxylase (GAD65/67) immunoreactivity in the postmortem PVN of major depressive (MDD), bipolar depressive (BD), and control subjects.
- Comparison of GAD65/67-immunoreactivity density with previously determined CRH-expressing neuron counts.
Main Results:
- A significant 43% reduction in GAD65/67-immunoreactivity density was observed in the PVN of MDD patients compared to controls (P=0.028).
- A non-significant 20% decrease in GAD65/67-immunoreactivity density was found in BD patients.
- A significant negative correlation (Rho=-0.527, P=0.032) was found between GAD65/67-immunoreactivity density and CRH-immunoreactivity neuron number in the depression group.
Conclusions:
- Diminished GABAergic input to the PVN may contribute to CRH neuron activation in depression, especially MDD.
- These findings support the rationale for using GABAergic agonists as a therapeutic strategy for depression.
