Journal
APOPTOSIS
Volume 11, Issue 9, Pages 1603-1615Publisher
SPRINGER
DOI: 10.1007/s10495-006-8762-3
Keywords
Akt; caspase; ceramide; neurotoxicity; neurotrophins; p75(NTR); synaptogenesis; beta estradiol
Categories
Funding
- NIA NIH HHS [AG 11355] Funding Source: Medline
- NICHD NIH HHS [HD 44517] Funding Source: Medline
- NIDA NIH HHS [K08-DA00406] Funding Source: Medline
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [R01HD044517] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P01AG011355] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [K08DA000406] Funding Source: NIH RePORTER
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Brain-derived neurotrophic factor (BDNF) is important in supporting neuronal development. BDNF imbalance due to excessive neuronal inhibition can result in the apoptotic degeneration of developing neurons. Since general anesthetics cause profound depression of neuronal activity and are known to induce widespread degeneration in the developing brain, we studied their potential to activate BDNF-mediated developmental neuroapoptosis. When P7 rats (at the peak of brain development) were exposed to a commonly-used and highly pro-apoptotic anesthesia protocol (midazolam, isoflurane, nitrous oxide) for a period of 2, 4 or 6 h, we found that anesthesia modulates the key steps in BDNF-activated apoptotic cascade in two of the most vulnerable brain regions-cerebral cortex and thalamus in time-dependent fashion by activating both Trk-dependent (in thalamus) and Trk-independent p75(NTR) dependent (in cerebral cortex) neurotrophic pathways. beta-estradiol, a sex hormone that upregulates the protein levels of the activated Akt, protects against anesthesia-induced neuroapoptosis.
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