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An Unbiased Approach of Sampling TEM Sections in Neuroscience
Published on: April 13, 2019
Environmental enrichment delays limbic epileptogenesis and restricts pathologic synaptic plasticity
Meng Yang1, Ezgi Ozturk1, Michael R Salzberg1,2
1Department of Medicine (Royal Melbourne Hospital), Melbourne Brain Centre, The University of Melbourne, Melbourne, Victoria, Australia.
Environmental enrichment (EE) delays epilepsy development and reduces anxiety in a rat model. This suggests EE may be a strategy to combat limbic epileptogenesis and associated psychiatric conditions.
Area of Science:
- Neuroscience
- Epileptology
- Environmental Psychology
Background:
- Environmental exposures significantly influence brain disease susceptibility, including epilepsy.
- Mesial temporal lobe epilepsy (MTLE) is a prevalent epilepsy form often linked with neuropsychiatric issues.
Purpose of the Study:
- To investigate if environmental enrichment (EE) offers antiepileptogenic, psychoprotective, and neuroprotective effects in the amygdala kindling model of MTLE.
- To explore the underlying neurobiological mechanisms of EE's effects.
Main Methods:
- Male Wistar rats were housed in either enriched (EE) or standard (SH) conditions from weaning.
- Rats underwent amygdala kindling to induce seizures, followed by anxiety assessments using the elevated plus maze.
- Histologic and molecular analyses were performed to examine potential biological mediators.
Main Results:
- EE significantly delayed kindling epileptogenesis, requiring more stimulations to reach a fully kindled state compared to SH rats.
- Both EE and kindling reduced anxiety levels.
- EE significantly reduced aberrant mossy fiber sprouting and decreased the expression of TrkB and CRH genes.
Conclusions:
- Environmental enrichment demonstrates beneficial effects on limbic epileptogenesis and anxiety.
- Reduced pathological neuroplasticity and altered plasticity-related gene expression are potential mechanisms underlying EE's effects.
- Enhanced environmental stimulation emerges as a potential antiepileptogenic strategy for MTLE, possibly mitigating psychiatric comorbidities.
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