Age-related changes in neuronal glucose uptake in response to glutamate and beta-amyloid - PubMed (original) (raw)
Comparative Study
. 2003 May 15;72(4):527-36.
doi: 10.1002/jnr.10602.
Affiliations
- PMID: 12704814
- DOI: 10.1002/jnr.10602
Comparative Study
Age-related changes in neuronal glucose uptake in response to glutamate and beta-amyloid
Jigisha R Patel et al. J Neurosci Res. 2003.
Abstract
Energy supplies that may decline with age are crucial for cells to maintain ionic homeostasis and prevent neuron death. We examined baseline glucose transporter expression and rate of glucose uptake in cultured hippocampal neurons from embryonic, middle-age (12-month-old), and old (24-month-old) rats and exposed the neurons to glutamate, beta-amyloid, and mitochondrial inhibitors. Without stress, the rate of glucose uptake was similar in middle-age and old neurons, and the rate of glucose uptake in embryonic neurons was threefold greater than that in middle-age and old neurons. Glucose uptake increased in the presence of mitochondrial inhibitors (FCCP and oligomycin) for embryonic and middle-age neurons. The old neurons failed to increase glucose uptake. In the presence of glutamate, FCCP, and oligomycin, embryonic neurons showed a decrease in glucose uptake and the middle-age and old neurons showed no change in glucose uptake. Middle-age neurons took up significantly more glucose than old neurons when under mitochondrial and glutamate stress. In the presence of beta-amyloid, only embryonic neurons increased glucose uptake; middle-age and old neurons did not. Fluorescence imaging of immunoreactive glut3 in response to beta-amyloid demonstrated a 16-49% increase in glut3 immunoreactivity at the plasma membrane for the three ages. The results suggest that old neurons were not able to upregulate glucose uptake to ensure cell survival. Neuron aging does not indicate a defect in normal glut3 function; rather, our results suggest that mechanisms regulating glucose uptake under stress fail to react in time to ensure cell survival.
Copyright 2003 Wiley-Liss, Inc.
Similar articles
- Amyloid beta-peptide decreases neuronal glucose uptake despite causing increase in GLUT3 mRNA transcription and GLUT3 translocation to the plasma membrane.
Prapong T, Buss J, Hsu WH, Heine P, West Greenlee H, Uemura E. Prapong T, et al. Exp Neurol. 2002 Apr;174(2):253-8. doi: 10.1006/exnr.2001.7861. Exp Neurol. 2002. PMID: 11922666 - Age-related calcium changes, oxyradical damage, caspase activation and nuclear condensation in hippocampal neurons in response to glutamate and beta-amyloid.
Brewer GJ, Lim A, Capps NG, Torricelli JR. Brewer GJ, et al. Exp Gerontol. 2005 May;40(5):426-37. doi: 10.1016/j.exger.2005.03.007. Exp Gerontol. 2005. PMID: 15919595 - Amyloid beta-peptide inhibits neuronal glucose uptake by preventing exocytosis.
Uemura E, Greenlee HW. Uemura E, et al. Exp Neurol. 2001 Aug;170(2):270-6. doi: 10.1006/exnr.2001.7719. Exp Neurol. 2001. PMID: 11476592 - Neurological changes induced by stress in streptozotocin diabetic rats.
Reagan LP, Magariños AM, McEwen BS. Reagan LP, et al. Ann N Y Acad Sci. 1999;893:126-37. doi: 10.1111/j.1749-6632.1999.tb07822.x. Ann N Y Acad Sci. 1999. PMID: 10672234 Review. - Role of neuron-glia interaction in the regulation of brain glucose utilization.
Pellerin L, Bonvento G, Chatton JY, Pierre K, Magistretti PJ. Pellerin L, et al. Diabetes Nutr Metab. 2002 Oct;15(5):268-73; discussion 273. Diabetes Nutr Metab. 2002. PMID: 12625467 Review. No abstract available.
Cited by
- Global Metabolic Shifts in Age and Alzheimer's Disease Mouse Brains Pivot at NAD+/NADH Redox Sites.
Dong Y, Brewer GJ. Dong Y, et al. J Alzheimers Dis. 2019;71(1):119-140. doi: 10.3233/JAD-190408. J Alzheimers Dis. 2019. PMID: 31356210 Free PMC article. - Age-related deficiencies in complex I endogenous substrate availability and reserve capacity of complex IV in cortical neuron electron transport.
Jones TT, Brewer GJ. Jones TT, et al. Biochim Biophys Acta. 2010 Feb;1797(2):167-76. doi: 10.1016/j.bbabio.2009.09.009. Epub 2009 Sep 30. Biochim Biophys Acta. 2010. PMID: 19799853 Free PMC article. - Age-related differences in NFkappaB translocation and Bcl-2/Bax ratio caused by TNFalpha and Abeta42 promote survival in middle-age neurons and death in old neurons.
Patel JR, Brewer GJ. Patel JR, et al. Exp Neurol. 2008 Sep;213(1):93-100. doi: 10.1016/j.expneurol.2008.05.007. Epub 2008 May 22. Exp Neurol. 2008. PMID: 18625500 Free PMC article. - Reversible epigenetic histone modifications and Bdnf expression in neurons with aging and from a mouse model of Alzheimer's disease.
Walker MP, LaFerla FM, Oddo SS, Brewer GJ. Walker MP, et al. Age (Dordr). 2013 Jun;35(3):519-31. doi: 10.1007/s11357-011-9375-5. Epub 2012 Jan 12. Age (Dordr). 2013. PMID: 22237558 Free PMC article. - Response to 'comment on recent modeling studies of astrocyte-neuron metabolic interactions': much ado about nothing.
Mangia S, DiNuzzo M, Giove F, Carruthers A, Simpson IA, Vannucci SJ. Mangia S, et al. J Cereb Blood Flow Metab. 2011 Jun;31(6):1346-53. doi: 10.1038/jcbfm.2011.29. Epub 2011 Mar 23. J Cereb Blood Flow Metab. 2011. PMID: 21427731 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical