Protective Function of Nicotinamide Against Ketamine-induced Apoptotic Neurodegeneration in the Infant Rat Brain
- Authors
- Ullah, Najeeb; Ullah, Ikram; Lee, Hae Young; Naseer, Muhammad Imran; Seok, Park Moon; Ahmed, Jawad; Kim, Myeong Ok
- Issue Date
- May-2012
- Publisher
- HUMANA PRESS INC
- Keywords
- Apoptosis; Ketamine; Neurodegeneration; Nicotinamide; Neuroprotection; NMDA
- Citation
- JOURNAL OF MOLECULAR NEUROSCIENCE, v.47, no.1, pp.67 - 75
- Indexed
- SCIE
SCOPUS
- Journal Title
- JOURNAL OF MOLECULAR NEUROSCIENCE
- Volume
- 47
- Number
- 1
- Start Page
- 67
- End Page
- 75
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/22202
- DOI
- 10.1007/s12031-011-9685-1
- ISSN
- 0895-8696
- Abstract
- During development, anesthetics activate neuroapoptosis and produce damage in the central nervous system that leads to several types of neurological disorders. A single dose of ketamine (40 mg/kg) during synaptogenesis in a 7-day-old rat brain activated the apoptotic cascade and caused extensive neuronal cell death in the forebrain. In this study, we investigated the protective effect of nicotinamide against ketamine-induced apoptotic neurodegeneration. After 4 h, neuronal cell death induced by ketamine was associated with the induction of Bax, release of cytochrome c into the cytosol, and activation of caspase-3. One single dose of 1 mg/g nicotinamide was administered to a developing rat and was found to inhibit ketamine-induced neuroapoptosis by downregulating Bax, inhibiting cytochrome c release from mitochondria into cytosol, and inhibiting the expression of activated caspase-3. TUNEL and immunohistochemical analyses showed that ketamine-induced cell death occurred through apoptosis and that it was inhibited by nicotinamide. Fluoro-Jade-B staining demonstrated an increased number of dead cells in the cortex and thalamus after ketamine treatment; treatment with nicotinamide reduced the number of dead cells in these brain regions. Our findings suggest that nicotinamide attenuated ketamine-induced neuronal cell loss in the developing rat brain and is a promising therapeutic and neuroprotective agent for the treatment of neurodevelopmental disorders.
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