The Role of Endogenous Neurogenesis in Functional Recovery and Motor Map Reorganization Induced by Rehabilitative Therapy after Stroke in Rats
Autor: | Kazumi Kimura, Yoshiki Yagita, Takashi Shiromoto, Kazuhiko Narita, Emi Maruyama-Nakamura, Naoyuki Himi, Naohiko Okabe, Osamu Miyamoto, Feng Lu |
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Rok vydání: | 2017 |
Předmět: |
Male
0301 basic medicine medicine.medical_specialty Neurogenesis Ischemia Endogeny Brain Ischemia Random Allocation 03 medical and health sciences 0302 clinical medicine Physical medicine and rehabilitation medicine Animals Stroke Neurons Neuronal Plasticity Microglia business.industry Rehabilitation Motor Cortex Stroke Rehabilitation Endothelial Cells Recovery of Function Functional recovery medicine.disease Rats Inbred F344 Cortex (botany) Disease Models Animal Treatment Outcome 030104 developmental biology medicine.anatomical_structure Astrocytes Surgery Neurology (clinical) Forelimb Cardiology and Cardiovascular Medicine business Neuroscience 030217 neurology & neurosurgery Spatial Navigation |
Zdroj: | Journal of Stroke and Cerebrovascular Diseases. 26:260-272 |
ISSN: | 1052-3057 |
DOI: | 10.1016/j.jstrokecerebrovasdis.2016.09.016 |
Popis: | Background and Objective Endogenous neurogenesis is associated with functional recovery after stroke, but the roles it plays in such recovery processes are unknown. This study aims to clarify the roles of endogenous neurogenesis in functional recovery and motor map reorganization induced by rehabilitative therapy after stroke by using a rat model of cerebral ischemia (CI). Methods Ischemia was induced via photothrombosis in the caudal forelimb area of the rat cortex. First, we examined the effect of rehabilitative therapy on functional recovery and motor map reorganization, using the skilled forelimb reaching test and intracortical microstimulation. Next, using the same approaches, we examined how motor map reorganization changed when endogenous neurogenesis after stroke was inhibited by cytosine-β- d -arabinofuranoside (Ara-C). Results Rehabilitative therapy for 4 weeks after the induction of stroke significantly improved functional recovery and expanded the rostral forelimb area (RFA). Intraventricular Ara-C administration for 4-10 days after stroke significantly suppressed endogenous neurogenesis compared to vehicle, but did not appear to influence non-neural cells (e.g., microglia, astrocytes, and vascular endothelial cells). Suppressing endogenous neurogenesis via Ara-C administration significantly inhibited (~50% less than vehicle) functional recovery and RFA expansion (~33% of vehicle) induced by rehabilitative therapy after CI. Conclusions After CI, inhibition of endogenous neurogenesis suppressed both the functional and anatomical markers of rehabilitative therapy. These results suggest that endogenous neurogenesis contributes to functional recovery after CI related to rehabilitative therapy, possibly through its promotion of motor map reorganization, although other additional roles cannot be ruled out. |
Databáze: | OpenAIRE |
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