Journal
JOURNAL OF NEUROSCIENCE
Volume 39, Issue 43, Pages 8584-8599Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1249-19.2019
Keywords
BDNF/TrkB pathway; COX-2; neonatal ventral hippocampus lesion; oxidative/nitrosative stress; prefrontal cortex; risperidone
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Funding
- Spanish Ministry of Economy, Industry and Competitiveness (MINECO-EU-FEDER) [SAF2016-75500-R]
- PRODEP [CA-BUAP-120]
- CONACYT [252808]
- CONACYT
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Reduction of the dendritic arbor length and the lack of dendritic spines in the pyramidal cells of the prefrontal cortex (PFC) are prevalent pathological features in schizophrenia (SZ). Neonatal ventral hippocampus lesion (NVHL) in male rats reproduces these neuronal characteristics and here we describe how this is a consequence of BDNF/TrkB pathway disruption. Moreover, COX-2 proinflammatory state, as well as Nrf-2 antioxidant impairment, triggers oxidative/nitrosative stress, which also contributes to dendritic spine impairments in the PFC. Interestingly, oxidative/nitrosative stress was also detected in the periphery of NVHL animals. Furthermore, risperidone treatment had a neurotrophic effect on the PFC and antioxidant effects on the brain and periphery of NVHL animals; these cellular effects were related to behavioral improvement. Our data highlight the link between brain development and immune response, as well as several other factors to understand mechanisms related to the pathophysiology of SZ.
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