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Garth Bissette, PhD; Charles B. Nemeroff, MD, PhD
Departments of Psychiatry and Pharmacology Duke University Medical Center Durham, NC 27710

Arch Gen Psychiatry. 1988;45(6):597-598.

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In Reply.—

Charlton et al have commented on the findings of our study¹ and other studies² concerning the reduction in CSF concentrations of somatostatin in patients with major depression. They add to the literature with measurements of somatostatin in different brain regions of depressed suicides and controls and find no differences between the two groups. In their comment they state that "the reported reduction of somatostatin-I concentration in CSF in depression does not appear to be a reflection of a reduced concentration of somatostatin-I in the cortex." They further indicate that the site of origin of somatostatin in CSF is unclear. Charlton et al correctly conclude that if a reduction of the somatostatin level in CSF in depression is a true reflection of pathophysiology of central somatostatin, then a reduced turnover or impaired release may be the central mechanism, rather than neuronal degeneration, as has been observed in . . . [Full Text PDF of this Article]

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