Functional recovery and alterations in the expression and localization of protein kinase C following voluntary exercise in rat with cerebral infarction

Kenmei Mizutani, Shigeru Sonoda, Hideaki Wakita, Yoshimitsu Katoh, Kan Shimpo

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Recently, it has become widely known that rehabilitative training after stroke brings about some improvement of paralysis and disability; however, not much is known about the relationship between paralysis recovery and the participation of plasticity-related molecules. Hence, the localization and level of expression of several proteins in the cerebral cortex of rat groups with/without voluntary exercise using a running wheel after photo thrombotic infarction were examined in this study. In behavioral evaluation, the mean latency until falling from a rotating rod in the group with voluntary exercise at 6 days after infarction was significantly longer than that in the group without exercise. Immunohistochemical localization of c-Fos protein after behavioral test occurred in the area surrounding the infarction core in the exercise group. In protein expression analysis, protein kinase C (PKC), growth-associated protein 43 (GAP43) and phosphorylated at serine 41 GAP43 (p-GAP43) were significantly increased after voluntary exercise compared with those in rats without exercise. Expression of PKC immunoreactivity was observed in layer III of the perilesional cortex in rats with exercise, and the intracellular localization in the pyramidal neurons was mainly translocated to the plasma membrane. The expression and localization of these proteins may be related to the underlying mechanisms of exercise-induced paralysis recovery, that is, neuronal plasticity and remodeling of cortical connections through the phosphorylation of GAP43 by interaction with PKC. In the present study, the participation of at least some of the modulators associated with the improvement of motor deficit adjacent to the brain lesion might have been detected.

Original languageEnglish
Pages (from-to)53-59
Number of pages7
JournalNeurological Sciences
Volume35
Issue number1
DOIs
Publication statusPublished - 01-01-2014

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GAP-43 Protein
Cerebral Infarction
Protein Kinase C
Paralysis
Infarction
Neuronal Plasticity
Proto-Oncogene Proteins c-fos
Proteins
Pyramidal Cells
Running
Cerebral Cortex
Serine
Stroke
Phosphorylation
Cell Membrane
Brain

All Science Journal Classification (ASJC) codes

  • Dermatology
  • Clinical Neurology
  • Psychiatry and Mental health

Cite this

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title = "Functional recovery and alterations in the expression and localization of protein kinase C following voluntary exercise in rat with cerebral infarction",
abstract = "Recently, it has become widely known that rehabilitative training after stroke brings about some improvement of paralysis and disability; however, not much is known about the relationship between paralysis recovery and the participation of plasticity-related molecules. Hence, the localization and level of expression of several proteins in the cerebral cortex of rat groups with/without voluntary exercise using a running wheel after photo thrombotic infarction were examined in this study. In behavioral evaluation, the mean latency until falling from a rotating rod in the group with voluntary exercise at 6 days after infarction was significantly longer than that in the group without exercise. Immunohistochemical localization of c-Fos protein after behavioral test occurred in the area surrounding the infarction core in the exercise group. In protein expression analysis, protein kinase C (PKC), growth-associated protein 43 (GAP43) and phosphorylated at serine 41 GAP43 (p-GAP43) were significantly increased after voluntary exercise compared with those in rats without exercise. Expression of PKC immunoreactivity was observed in layer III of the perilesional cortex in rats with exercise, and the intracellular localization in the pyramidal neurons was mainly translocated to the plasma membrane. The expression and localization of these proteins may be related to the underlying mechanisms of exercise-induced paralysis recovery, that is, neuronal plasticity and remodeling of cortical connections through the phosphorylation of GAP43 by interaction with PKC. In the present study, the participation of at least some of the modulators associated with the improvement of motor deficit adjacent to the brain lesion might have been detected.",
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Functional recovery and alterations in the expression and localization of protein kinase C following voluntary exercise in rat with cerebral infarction. / Mizutani, Kenmei; Sonoda, Shigeru; Wakita, Hideaki; Katoh, Yoshimitsu; Shimpo, Kan.

In: Neurological Sciences, Vol. 35, No. 1, 01.01.2014, p. 53-59.

Research output: Contribution to journalArticle

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