Stroke and Stem Cell Laboratory in Clinical Research Institute

Stem, South Korea

Stroke and Stem Cell Laboratory in Clinical Research Institute

Stem, South Korea
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Bae E.-K.,Stroke and Stem Cell Laboratory in Clinical Research Institute | Bae E.-K.,Seoul National University | Jung K.-H.,Stroke and Stem Cell Laboratory in Clinical Research Institute | Jung K.-H.,Seoul National University | And 13 more authors.
Journal of Clinical Neurology (Korea) | Year: 2010

Background and Purpose There is recent evidence of various types of morphological changes in the hippocampus of a rodent model of medial temporal lobe epilepsy (mTLE). However, little is known about such changes in humans. We examined the histological changes [i.e., neuronal loss, cell genesis, and granule cell dispersion (GCD)] in surgical hippocampal specimens taken from patients with mTLE. Methods Nissl staining, and nestin and Prox1 immunohistochemistry were performed on human hippocampal specimens obtained from patients with medically intractable mTLE, thus allowing the analysis of neuronal loss, cell genesis, and GCD, respectively. We also assessed the correlations between clinical parameters and the histopathologic findings. Results The degree of cell genesis in the granule cell layer was significantly correlated with the severity of GCD, history of childhood febrile seizures, and frequent generalized seizures. Cell genesis was not correlated with cell death, age at seizure onset, duration of epilepsy, or the mean frequency of all seizures. Conclusions Our results indicate that cell genesis in the dentate gyrus of patients with mTLE is associated with GCD and is influenced by the presence of febrile seizures during childhood and the frequency of episodes of generalized seizures. © 2010 Korean Neurological Association.


Lee S.-T.,Stroke and Stem cell Laboratory in Clinical Research Institute | Lee S.-T.,Neuroscience Research Institute | Chu K.,Stroke and Stem cell Laboratory in Clinical Research Institute | Chu K.,Neuroscience Research Institute | And 18 more authors.
Brain Research | Year: 2010

Stimulated vagus nerve excretes acetylcholine into the peripheral immune organs such as the spleen, reducing innate inflammation. Here, we investigated whether activation of this "cholinergic anti-inflammatory pathway" can be used to reduce cerebral inflammation in a model of hemorrhagic stroke. Experimental intracerebral hemorrhage (ICH) was induced by stereotaxic collagenase injection in rats. Muscarine, an activator of the vagus nerve, or phosphate-buffered saline (control) was injected into the lateral ventricle after induction of ICH. Intraventricular muscarine injection increased heart rate variability in the ICH model, suggesting increased vagus nerve output. Muscarine-injected ICH rats showed improved neurologic outcomes, reduced brain water content, and decreased levels of inflammatory mediators in both brain and spleen. Central muscarine injection was ineffective at reducing cerebral edema without spleen, suggesting that the effect of muscarine is mediated through the vagus nerve-spleen pathway rather than through a direct interaction with the brain. Our results suggest that the brain possesses a cholinergic anti-inflammatory pathway that counteracts the inflammatory responses after ICH, thereby limiting damage to the brain itself. © 2009 Elsevier B.V. All rights reserved.

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