TY - JOUR
T1 - Insights into the metabolic response to traumatic brain injury as revealed by 13C NMR spectroscopy
AU - Bartnik-Olson, Brenda L.
AU - Harris, Neil G.
AU - Shijo, Katsunori
AU - Sutton, Richard L.
N1 - A significant body of work has shown that traumatic brain injury (TBI) initiates a cascade of cellular events including potassium efflux (Katayama et al., 1990; Kawamata et al., 1995), Ca++ accumulation (Fineman et al., 1993; Osteen et al., 2001), glutamate release (Katayama et al., 1990; Nilsson et al., 1990; Rose et al., 2002), and increased oxidative stress (Hall et al., 1993; Lewen and Hillered, 1998; Vagnozzi et al., 1999; Tyurin et al., 2000; Marklund et al., 2001) that contribute to reduced ATP production.
PY - 2013
Y1 - 2013
N2 - The present review highlights critical issues related to cerebral metabolism following traumatic brain injury (TBI) and the use of 13C labeled substrates and nuclear magnetic resonance (NMR) spectroscopy to study these changes. First we address some pathophysiologic factors contributing to metabolic dysfunction following TBI. We then examine how 13C NMR spectroscopy strategies have been used to investigate energy metabolism, neurotransmission, the intracellular redox state, and neuroglial compartmentation following injury. 13C NMR spectroscopy studies of brain extracts from animal models of TBI have revealed enhanced glycolytic production of lactate, evidence of pentose phosphate pathway (PPP) activation, and alterations in neuronal and astrocyte oxidative metabolism that are dependent on injury severity. Differential incorporation of label into glutamate and glutamine from 13C labeled glucose or acetate also suggest TBI-induced adaptations to the glutamate-glutamine cycle.
AB - The present review highlights critical issues related to cerebral metabolism following traumatic brain injury (TBI) and the use of 13C labeled substrates and nuclear magnetic resonance (NMR) spectroscopy to study these changes. First we address some pathophysiologic factors contributing to metabolic dysfunction following TBI. We then examine how 13C NMR spectroscopy strategies have been used to investigate energy metabolism, neurotransmission, the intracellular redox state, and neuroglial compartmentation following injury. 13C NMR spectroscopy studies of brain extracts from animal models of TBI have revealed enhanced glycolytic production of lactate, evidence of pentose phosphate pathway (PPP) activation, and alterations in neuronal and astrocyte oxidative metabolism that are dependent on injury severity. Differential incorporation of label into glutamate and glutamine from 13C labeled glucose or acetate also suggest TBI-induced adaptations to the glutamate-glutamine cycle.
KW - Acetate
KW - Glucose
KW - Glutamate-glutamine cycle
KW - Magnetic resonance spectroscopy
KW - Neuroglial compartmentation
KW - Oxidative metabolism
KW - Pentose phosphate pathway
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U2 - 10.3389/fnene.2013.00008
DO - 10.3389/fnene.2013.00008
M3 - Short survey
SN - 1662-6427
VL - 5
JO - Frontiers in Neuroenergetics
JF - Frontiers in Neuroenergetics
IS - OCT
M1 - 00008
ER -