Peculiarities of the Expression of Inducible NO Synthase in Rat Dentate Gyrus in Depression Modeling.

Mild stress exposure contributes to the development of cognitive and emotional deficits, is considered as a model of depressive state, and is characterized by enhanced NO production. In albino mature (12-month-old) male rats, the depressive state was simulated by daily 30-min exposure to stressful stimuli (vibration, loud sound, and strobe light) over 7 days in a special chamber. On paraffin frontal sections of the brain stained with antibodies against inducible NO synthase (iNOS), the expression and distribution pattern of immunoreactive material were evaluated in various layers of the dentate gyrus under normal conditions and after depression modeling.

[COMPARATIVE MORPHOFUNCTIONAL CHARACTERISTICS OF ADULT AND OLD RAT VENTRAL HIPPOCAMPUS TO COMBINED STRESS INFLUENCE].

Animals were subjected to seven days combined stress in a special chamber (6 isolated compartments of equal area) with removable multi-modal stressors (noise, vibration, pulsating bright light) every 5 minutes on the stochastic scheme with restraint and temperature rise in the chamber during 30-minute stressing time sessions. After exposure to combined stress in the ventral hippocampus of old rats (24 months) compared with adult animals (12 months) following changes were revealed: marked dystrophic changes and increased inducible nitric oxide synthase expression in pyramidal neurons of CA3 field, signs of impaired hemodynamic disorders in the microvasculature, perivascular edema, decreased endothelial nitric oxide synthase expression in microvascular endothelial cells, as well as decreased expression of serine racemase in the neuropil of the radial layer of CA1 field.

Effect of Combined Stress on Morphological Changes and Expression of NO Synthases in Rat Ventral Hippocampus.

Adult rats were subjected to 7-day combined stress with stochastic changes of stressors of different modalities (noise, vibration, pulsating bright light) along with mobility restriction and elevated temperature in the chamber during stress exposures (daily 30-min sessions). Circulatory disorders, inhibition of endothelial NO-synthase expression in endothelial cells of the microcirculatory bed, perivascular edema, pronounced degenerative changes, and enhanced expression of inducible NO synthase in CA3 pyramidal neurons in the ventral hippocampus of stressed 12-month-old rats were observed. These findings can attest to the involvement NOdependent mechanisms and different contribution of NO synthase isoforms into the formation of hippocampal neuronal damage.