Fluoxetine inhibits dendrite atrophy of hippocampal neurons by decreasing nitric oxide synthase expression in rat depression model
Abstract
Aim: To study the effect of fluoxetine on dendrite atrophy of hippocampal neurons in rat depression model.
Methods: CMS (chronic mild stress), mimicking human depression, was used as the animal depression model. The neurons shape and numbers of nitric oxide synthase positive cells in the hippocampal subfields were measured by Nissl staining and histochemical staining of NADPH (nicotinamide adenine dinucleotide phosphate)-diaphorase respectively.
Results: CMS deforms neurons in the hippocampal formation, and fluoxetine can renormalize the deformed neurons by inhibiting the nitric oxide synthase catalyzing the over-production of NO, which lead subsequently to the morphological abnormality in the circumscribed area of brain.
Conclusion: Fluoxetine, an antidepressant, renormalizes dendrite atrophy of hippocampal neurons by inhibiting nitric oxide synthase overexpression in rat chronic mild stress model.
Keywords:
Methods: CMS (chronic mild stress), mimicking human depression, was used as the animal depression model. The neurons shape and numbers of nitric oxide synthase positive cells in the hippocampal subfields were measured by Nissl staining and histochemical staining of NADPH (nicotinamide adenine dinucleotide phosphate)-diaphorase respectively.
Results: CMS deforms neurons in the hippocampal formation, and fluoxetine can renormalize the deformed neurons by inhibiting the nitric oxide synthase catalyzing the over-production of NO, which lead subsequently to the morphological abnormality in the circumscribed area of brain.
Conclusion: Fluoxetine, an antidepressant, renormalizes dendrite atrophy of hippocampal neurons by inhibiting nitric oxide synthase overexpression in rat chronic mild stress model.