Changes in excitatory amino acid levels and tissue energy metabolites of neonate rat brain after hypoxia and hypoxia-ischemia

Huguet, François; Guerraoui, A.; Barrier, Laurence; Guilloteau, Denis; Tallineau, C.; Chalon, Sylvie

doi:10.1016/s0304-3940(97)00907-5

Cited by 17 publications

(8 citation statements)

References 25 publications

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“…The loss of blood flow in hypoxic ischemic injury results in an immediate energy failure that is transiently recovered as blood flow returns [43]. However, a secondary energy failure occurs, several hours after HI [5–7].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Acetyl-<smlcap>L</smlcap>-Carnitine on Neonatal Hypoxia Ischemia-Induced Brain Injury in Rats

Tang

Lü

et al. 2016

Dev Neurosci

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Perinatal hypoxia ischemia (HI) is a significant cause of brain injury in surviving infants. Although hypothermia improves outcomes in some infants, additional therapies are needed since about 40% of infants still have a poor outcome. Acetyl-L-carnitine (ALCAR), an acetylated derivative of L-carnitine, protected against early changes in brain metabolites and mitochondrial function after HI on postnatal day (PND) 7 in a rat pup model of near-term HI injury. However, its efficacy in long-term structural and functional outcomes remains unexplored. We determined the efficacy of ALCAR therapy administered to rat pups after HI at PND 7, using both longitudinal in vivo magnetic resonance imaging and behavioral tests, in male and female rats. HI led to sex-specific behavioral impairment, with males exhibiting more global functional deficits than females. Interestingly, HI reduced the volume of the contralateral hemisphere in males only, suggesting that the brain injury is more diffuse in males than in females. Treatment with ALCAR improved both morphological and functional outcomes in both male and female rats. These results suggest that ALCAR may be a potential therapy for clinical use since the treatment attenuated the moderate injury produced under the experimental conditions used and improved the functional outcome in preclinical studies.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Acetyl-<smlcap>L</smlcap>-Carnitine on Neonatal Hypoxia Ischemia-Induced Brain Injury in Rats

Tang

Lü

et al. 2016

Dev Neurosci

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“…Hypoxia and hypoxia/ischemia increased extracellular releases of excitatory amino acids, such as glutamate (GLU; Choi, 1985; Choi et al, 1987; Robertson et al, 1995; Rothman and Olney, 1986; Krajnc et al, 1996; Huguet et al, 1998; Henderson et al, 1998; Kunimatsu et al, 1999; Satoh et al, 1999; Matsushita et al, 2000), aspartate (ASP), and cysteine (Puka‐Sundvall et al, 1997), and inhibitory neurotransmitter taurine and GABA release (Hoop et al, 1999; Johns et al, 2000) in many brain areas. In view of these considerations, we supposed that hypobaric hypoxia might affect the brain function via an amino‐acid‐dependent mechanism.…”

mentioning

confidence: 99%

Intermittent hypoxia impairs performance of adult mice in the two‐way shuttle box but not in the Morris water maze

Zhang

Wang³

et al. 2006

J of Neuroscience Research

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We have previously found that neonatal intermittent hypobaric hypoxia exposure enhanced mouse spatial, but impaired associative, cognition. This study sought to investigate the effects of hypobaric hypoxia on adult mice cognition. Mice were exposed to 2, 5, 10, 15, or 25 days of intermittent hypoxia (IH; 4 hr/day) at 2 km (16.0% O2) or 5 km (10.8% O2) altitudes in a hypobaric chamber for the Morris water maze (MWM) test and exposed to IH for 2, 10, or 25 days for the shuttle-box test. Amino acid dynamics in vivo in the hippocampus and amygdala of mice exposed to 2 km hypoxia were analyzed by high-pressure liquid chromatography. The results in MWM task showed that IH-2d to -25d at 2 km or 5 km did not change the escape latencies of mice in the training test or the retention of platform in the probe test. In the shuttle-box task, however, IH-10d at 5 km significantly reduced mouse avoidances in the acquisition test on day 4, and IH-10d at 2 km reduced avoidances in the retention test; IH-25d at 5 km significantly reduced avoidances of mice throughout the acquisition days. Glutamate in the amygdala persisted in declining to 69% of baseline at 8 hr posthypoxia (P = 0.040 vs. GLU released during 30 min before hypoxia) during the posthypoxia stage. These results suggest that adult hypobaric IH impairs the hippocampal-independent, but not the hippocampal-dependent, task in mice. The different GLU releases in the hippocampus and amygdala in response to hypoxia are involved in the different behaviors.

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“…Lactate concentrations rise during hypoxia and ischemia (Lampl et al . 1990; Huguet et al . 1998) and have been used as a diagnostic indicator by clinicians for tissue hypoxia (Fullerton et al .…”

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confidence: 99%

Lactate and glucose as energy substrates during, and after, oxygen deprivation in rat hippocampal acute and cultured slices

Cater

Chandratheva

Benham

et al. 2003

Journal of Neurochemistry

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The effects of raised brain lactate levels on neuronal survival following hypoxia or ischemia is still a source of controversy among basic and clinical scientists. We have sought to address this controversy by studying the effects of glucose and lactate on neuronal survival in acute and cultured hippocampal slices. Following a 1-h hypoxic episode, neuronal survival in cultured hippocampal slices was significantly higher if glucose was present in the medium compared with lactate. However, when the energy substrate during the hypoxic period was glucose and then switched to lactate during the normoxic recovery period, the level of cell damage in the CA1 region of organotypic cultures was significantly improved from 64.3 ± 2.1 to 74.6 ± 2.1% compared with cultures receiving glucose during and after hypoxia. Extracellular field potentials recorded from the CA1 region of acute slices were abolished during oxygen deprivation for 20 min, but recovered almost fully to baseline levels with either glucose (82.6 ± 10.0%) or lactate present in the reperfusion medium (108.1 ± 8.3%). These results suggest that lactate alone cannot support neuronal survival during oxygen deprivation, but a combination of glucose followed by lactate provides for better neuroprotection than either substrate alone.

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Changes in excitatory amino acid levels and tissue energy metabolites of neonate rat brain after hypoxia and hypoxia-ischemia

Cited by 17 publications

References 25 publications

Neuroprotective Effects of Acetyl-<smlcap>L</smlcap>-Carnitine on Neonatal Hypoxia Ischemia-Induced Brain Injury in Rats

Neuroprotective Effects of Acetyl-<smlcap>L</smlcap>-Carnitine on Neonatal Hypoxia Ischemia-Induced Brain Injury in Rats

Intermittent hypoxia impairs performance of adult mice in the two‐way shuttle box but not in the Morris water maze

Lactate and glucose as energy substrates during, and after, oxygen deprivation in rat hippocampal acute and cultured slices

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