Cerebrospinal fluid concentrations of glutamate and GABA during perinatal cerebral hypoxia-ischemia and seizures

doi:10.1016/0006-8993(95)01437-3

Brain Research

Volume 709, Issue 2, 19 February 1996, Pages 326-330

https://doi.org/10.1016/0006-8993(95)01437-3 Get rights and content

Abstract

Cerebrospinal fluid (CSF) concentrations of glutamate and γ-aminobutyric acid (GABA), as estimates of levels in the extracellular compartment of brain, were determined in 7-day postnatal rats at the terminus of hypoxia-ischemia and during status epilepticus, induced with bicuculline, at 2 and 24 h of recovery. Hypoxia-ischemia was associated with increased CSF glutamate, which was not increased further during status epilepticus. In contrast, CSF GABA was increased by hypoxia-ischemia as well as by status epilepticus during recovery. CSF glutamate/GABA ratios in rat pups subjected to status epilepticus with or without prior hypoxia-ischemia were lower than control animals during recovery. The lack of any significant increase in glutamate or in the glutamate/GABA ratio during status epilepticus would preclude any neuronal injury from occurring in those immature rats sustaining seizures alone or any accentuation of brain damage in those animals subjected to prior cerebral hypoxia-ischemia.

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Moreover, amino acid neurotransmitters are closely linked to the vulnerability of the immature brain to neuronal injury [12–14]. Data from studies performed in immature rats indicate that these animals may be especially susceptible to elevated concentrations of aspartate (Asp), glutamate (Glu), glutamine (Gln) and γ-aminobutyric acid (GABA) [15–18]. Therefore, the investigation of these amino acids and others is important to understand the evolution of developmental brain damage.
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With models designed to look at the implication of neonatal seizures consequent to a hypoxic-ischemic insult, again controversy exists. Cataltepe et al. [19-21] observed no increase in cell death or glutamate release as a result of bicuculline-induced seizures after hypoxia-ischemia in the 7-day old rat. In this model, however, brain injury was profound simply as a result of the hypoxia-ischemia, and hence further exacerbation of injury would have been difficult to determine.
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^☆: Supported by Grant #P01 HD30704 from the National Institute of Child Health and Human Development.

²: Present address: Epilepsy Service, Massachusetts General Hospital, Harvard Medical School, Boston, MA.

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Short communicationCerebrospinal fluid concentrations of glutamate and GABA during perinatal cerebral hypoxia-ischemia and seizures☆

Abstract

Dev. Brain Res.

Neurosci. Lett.

Anal. Biochem.

Brain Res.

Brain Res.

Brain Res.

J. Biol. Chem.

J. Biol. Chem.

Exp. Neurol.

Effect of hypoxia-ischemia on bicuculline induced seizures in immature rats: behavioral and electrocortical phenomena

Epilepsia

Short communication
Cerebrospinal fluid concentrations of glutamate and GABA during perinatal cerebral hypoxia-ischemia and seizures☆