Elsevier

Biological Psychiatry

Volume 60, Issue 8, 15 October 2006, Pages 892-895
Biological Psychiatry

Brief report
Increased Arginine Vasopressin mRNA Expression in the Human Hypothalamus in Depression: A Preliminary Report

https://doi.org/10.1016/j.biopsych.2005.12.010Get rights and content

Background

Elevated arginine vasopressin (AVP) plasma levels have been observed in major depression, particularly in relation to the melancholic subtype. Two hypothalamic structures produce plasma vasopressin: the supraoptic nucleus (SON) and the paraventricular nucleus (PVN). The aim of this study was to establish which structure is responsible for the increased vasopressin plasma levels in depression.

Methods

Using in situ hybridization, we determined the amount of vasopressin messenger ribonucleic acid (mRNA) in the PVN and SON in postmortem brain tissue of nine depressed subjects (six with the melancholic subtype) and eight control subjects.

Results

In the SON, a 60% increase of vasopressin mRNA expression was found in depressed compared with control subjects. In the melancholic subgroup, AVP mRNA expression was significantly increased in both the SON and the PVN compared with control subjects.

Conclusions

We found increased AVP gene expression in the SON in depressed subjects. This might partly explain the observed increased vasopressin levels in depression.

Section snippets

Subjects

Hypothalami of nine depressed subjects and eight control subjects matched for age and gender (Table 1) were obtained from the Netherlands Brain Bank, in accordance with the formal protocols for use of human brain material and clinical information for research purposes. The MD patients were diagnosed during their lifetime, and the diagnosis was confirmed by a board-certified psychiatrist (WJGH) retrospectively using the medical record, according to DSM-IV criteria, paying special attention to

Results

The arginine vasopressin mRNA signal in the SON of depressed subjects was 60% higher than in control subjects (Z = −2.3, p = .021; Figure 1). In the PVN, the signal in the depressed group was 15% higher than in control subjects, but this difference was not significant (Z = −1.3, p = .21; Figure 2). Leaving out two patients who suffered from a cerebrovascular accident, leaving out the patient and control subject who used prednisone, and leaving out the DDNOS patient had no effect on the outcome.

Discussion

This is the first report in which AVP mRNA has been quantified in the SON and the PVN in depressed and control subjects. We found a significant (60%) increase in the amount of AVP mRNA signal in the SON of depressed subjects (Figure 1). We also expected to find an increase in AVP expression in the PVN, which would have been in line with our earlier finding of an increased number of AVP-immunoreactive neurons in the PVN in depression (Purba et al 1996), but the rise we observed in the PVN was

References (25)

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