• Publications
  • Influence
Glutamate as a neurotransmitter in the brain: review of physiology and pathology.
  • B. Meldrum
  • Medicine, Biology
    The Journal of nutrition
  • 1 April 2000
Endogenous glutamate, by activating NMDA, AMPA or mGluR1 receptors, may contribute to the brain damage occurring acutely after status epilepticus, cerebral ischemia or traumatic brain injury, and may also contribute to chronic neurodegeneration in such disorders as amyotrophic lateral sclerosis and Huntington's chorea.
Excitatory amino acid neurotoxicity and neurodegenerative disease.
In vivo and in vitro studies of the cytotoxicity of amino acids are reviewed and the contribution of such toxicity to acute and chronic neurodegenerative disorders is summarized.
Molecular targets for antiepileptic drug development
SummaryThis review considers how recent advances in the physiology of ion channels and other potential molecular targets, in conjunction with new information on the genetics of idiopathic epilepsies,
Cerebral blood flow and metabolic rate early and late in prolonged epileptic seizures induced in rats by bicuculline.
This high metabolic rate during sustained seizure activity will increase the susceptibility of the brain to 'ischaemic' damage during prolonged seizures in man in which an additional metabolic stress may be imposed by cerebral hypoxia, arterial hypotension, hyperpyrexia or hypoglycaemia.
Blockade of N-methyl-D-aspartate receptors may protect against ischemic damage in the brain.
In rats ischemia of the forebrain induced by a 30-minute occlusion of the carotid artery, followed by 120 minutes of arterial reperfusion, produced ischemic lesions of selectively vulnerable
Factors influencing the frequency of fluorescence transients as markers of peri-infarct depolarizations in focal cerebral ischemia.
The results suggest that the relationship of frequency of peri-infarct depolarizations with plasma glucose requires further examination, to confirm the finding and to determine a safe lower limit for a target range for control of plasma glucose if insulin is used in the management of patients with cerebral ischemia.
Na+ channels as targets for neuroprotective drugs.
Evidence indicating that Na+ channel modulators are neuroprotective is reviewed and recent ideas for the molecular sites of action of voltage-dependentNa+ channel blockers are described.
Update on the Mechanism of Action of Antiepileptic Drugs
  • B. Meldrum
  • Chemistry, Medicine
  • 1 December 1996
Novel antiepileptic drugs (AEDs) are thought to act on voltage‐sensitive ion channels, on inhibitory neurotransmission or on excitatory neurotransmission, possibly involving potentiation of GABA‐mediated inhibition and possibly also inactivation of sodium channels.
Concept of activity-induced cell death in epilepsy: historical and contemporary perspectives.
  • B. Meldrum
  • Biology, Medicine
    Progress in brain research
  • 2002
Changes in enzyme, transporter, ion-channel or receptor function or in network properties may lead to altered vulnerability to the effects of seizures, and this type of modification and the cumulative effect of oxidative damage to proteins and lipids may explain the long-term consequences of repetitive brief seizures.