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Neurometabolic and structural alterations in rat brain due to acute hypobaric hypoxia: in vivo 1 H MRS at 7 T
Author(s) -
Koundal Sunil,
Gandhi Sonia,
Kaur Tanzeer,
Khushu Subash
Publication year - 2014
Publication title -
nmr in biomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.278
H-Index - 114
eISSN - 1099-1492
pISSN - 0952-3480
DOI - 10.1002/nbm.3068
Subject(s) - glutamine , in vivo , glutamate receptor , creatine , endocrinology , medicine , metabolite , hypoxia (environmental) , hippocampus , choline , chemistry , biology , biochemistry , amino acid , oxygen , receptor , microbiology and biotechnology , organic chemistry
In response to hypobaric hypoxia (HH), which occurs at high altitude, the brain undergoes deleterious changes at the structural and metabolite level. In vivo T 2 weighted imaging (T2WI) and 1 H‐MRS was performed to understand the structural and metabolic changes in the hippocampus region of rat brain. Data were acquired pre‐exposure (baseline controls), immediately after exposure and subsequently at the first, fourth, seventh and 14th days post exposure at normoxia. T 2 weighted images of rat brain showed hyperintensity in the CA2/CA3 region of the hippocampus 7 d after acute HH, which persisted till 14 d, probably indicating structural changes in the hippocampus. 1 H‐MRS results showed no change in metabolite level immediately after acute HH exposure, but on the first day of normoxia the myo ‐inositol level was significantly decreased, possibly due to altered astrocyte metabolism. Metabolic alterations showing an increase in choline and decrease in glutamate on the fourth day of normoxia may be seen as a process of demyelination and loss of glutamate pool respectively. On the seventh and 14th days of normoxia, decreases in N‐acetylaspartate, creatine and glutamine + glutamate were observed, which might be due to decreased viability of glutamatergic neurons. In vivo 1 H‐MRS demonstrated early neurometabolic changes prior to probable structural changes post acute HH exposure. The extension of these studies will help in early risk assessment, developing intervention and strategies for combating HH related changes. Copyright © 2014 John Wiley & Sons, Ltd.