Possible relationship between neuropeptide Y (NPY) and major depression – evidence from human and animal studies

Abstract

Neuropeptide Y (NPY) – like immunoreactivity – (LI) was measured in cerebrospinal fluid (CSF) from patients with major depressive disorder and from healthy volunteers without physical or mental illness. NPY-LI was significantly lower (p<0.001) in the CSF of depressives than in that of the healthy controls. Possible correlates to the findings in human CSF were studied in rats. Using the same assay for NPY-LI, the concentrations were measured in brain regions of rats following treatment with antidepressants (imipramine and zimeldine) or bulbectomy, a proposed animal model for depression. In the cerebral cortex, both antidepressants increased the Concentrations of NPY-LI, whereas bulbectomy had the opposite effect. The hypothalamic concentrations of the peptide were increased by imipramine only, whereas other brain regions were unaffected by either treatment. The effects of intracerebroventricular administration of NPY on open field and home cage behaviour were investigated in the rat. In the open field, NPY reduced activity in a dose-related manner. Behavioural adaptation or gross neurological functions were not influenced. NPY greatly suppressed home cage activity, an effect lasting throughout the recording period of 22 h. Thus, NPY abolished the normal circadian variation in activity and seemed to exert sedative effects when given centrally to rats.

Key Words:

• Animal models
• Antidepressants
• Bulbectomy
• Depression
• Neuropeptide Y (NPY)