RESUMO
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. The relative area of iNOS expression in the dentate gyrus of control rats was 8.2 (7.1-9.9)%, while in rats with experimental depression, this parameter was 16.7 (10.5-22.1)%, i.e. increased by 8.5% (p<0.05). In mature rats with modeled depressive state, the expression and relative area of iNOS expression in neuronal perikarya in the granular and subgranular layers of the dentate gyrus increased, which can underlie the mechanisms of damage and determine reduced neuroplasticity and suppressed neurogenesis in the dentate gyrus in rats during adulthood.
Assuntos
Giro Denteado/metabolismo , Depressão/metabolismo , Óxido Nítrico Sintase/metabolismo , Animais , Neurogênese/genética , Neurogênese/fisiologia , Plasticidade Neuronal/genética , Plasticidade Neuronal/fisiologia , RatosRESUMO
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.
Assuntos
Hipocampo , Envelhecimento , Animais , Óxido Nítrico Sintase , Óxido Nítrico Sintase Tipo II , Óxido Nítrico Sintase Tipo III , Células Piramidais , RatosRESUMO
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.