Propofol causes neuronal degeneration in neonatal mice and long-term neurocognitive consequences in adult mice
Purpose: To investigate the effect of propofol on brain development in neonatal mice and long-term neurocognitive impact in adult mice. Method: The offspring of female C57Bl/6 and male CD-1 mice were administered propofol at concentrations of 2.5 and 5.0 mg/kg (treatment group) or normal saline (con...
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Published in | Tropical journal of pharmaceutical research Vol. 15; no. 9; p. 1889 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, Nigeria
01.09.2016
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Subjects | |
Online Access | Get full text |
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Summary: | Purpose: To investigate the effect of propofol on brain development in
neonatal mice and long-term neurocognitive impact in adult mice.
Method: The offspring of female C57Bl/6 and male CD-1 mice were
administered propofol at concentrations of 2.5 and 5.0 mg/kg (treatment
group) or normal saline (control) on postnatal day 7. Thereafter,
histological and immunohistochemical examinations were performed on the
mice brain. Apoptotic assay, neuronal nuclei antigen
immunohistochemistry (to assess neuron density), and behavioral and
neurocognitive tests were conducted on the adult mice. Results:
Propofol induced cellular degeneration and apoptosis in the brains of
neonatal mice. It also modulated physiological parameters (pH, PO2,
glucose and lactate), among which decreased blood glucose might be
associated with cellular degeneration in the brain. Propofol also
caused long-term neuronal deficits in adults, which showed impaired
neurocognitive functions. Upon reaching adulthood, propofol-treated
mice showed slow learning response and poor memory compared to
controls. Conclusion: Propofol causes neurodegeneration in neonatal
mice and has long-term neurocognitive consequences in adults,
indicating that the use of propofol anesthetics in neonates requires
careful consideration. |
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ISSN: | 1596-5996 1596-9827 |
DOI: | 10.4314/tjpr.v15i9.11 |