Post-mortem high affinity glutamate uptake in human brain
References (27)
- et al.
Evidence of glutamate as the neurotransmitter of corticothalamic and corticorubral pathways
Brain Res.
(1981) - et al.
Clinical, neuropathological and pharmacological aspects of Huntington's disease: correlates with a new animal model
Prog. Neuropsychopharmac.
(1977) - et al.
Alterations of brain neurotransmitter receptor binding in Huntington's chorea
Brain Res.
(1976) - et al.
Biochemical evidence for glutamate as neurotransmitter in cortico-striatal and corticothalamic fibres in rat brain
Neuroscience
(1981) - et al.
Postmortem isolation of synaptosomes from human brain
Brain Res.
(1974) - et al.
High-affinity uptake systems for glycine, glutamic. and aspartic acids in synaptosomes of rat central nervous tissues
Brain Res.
(1972) - et al.
Protein measurement with the Folin phenol reagent
J. biol. Chem.
(1951) - et al.
Structural requirements for the inhibition of L-glutamate uptake by glia and nerve endings
Brain Res.
(1975) - et al.
Synaptic morphology and cytoplasmic densities: rapid post-mortem effects
Tissue & Cell
(1974) Effects of tissue storage and freezing on brain glutamate uptake
Life Sci.
(1981)
Stimulation-dependent uptake of glutamic acid by hippocampal slices
Brain Res.
(1981)
The structural specificity of the high affinity uptake of L-glutamate and L-aspartate by rat brain slices
J. Neurochem.
(1972)
Competitive inhibition of GABA uptake in rat brain slices by some GABA analogues of restricted conformation
J. Neurochem.
(1972)
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Molecular actions and therapeutic potential of lithium in preclinical and clinical studies of CNS disorders
2010, Pharmacology and TherapeuticsCitation Excerpt :Initial research in animal models of HD found that lithium neuroprotection is mediated through Bcl-2 induction and GSK-3β inhibition. The striatal infusion of quinolinic acid (QA), a neuronal excitotoxin that causes the death of medium-sized spiny neurons by activating NMDA receptors, and produces many of the neuroanatomical changes found in HD, has been frequently used as an animal model for investigating this disease (Foster et al., 1983; Schwarcz & Whetsell, 1982). In this rat excitotoxic model of HD, lithium treatment at doses within the therapeutic range (0.5 and 1.0 mEq/kg) markedly reduces the size of QA-induced striatal lesions (Wei et al., 2001) and the loss of striatal medium-sized neurons (Senatorov et al., 2004).
Dysfunction of brain kynurenic acid metabolism in Huntington's disease: focus on kynurenine aminotransferases
1995, Journal of the Neurological SciencesAge-related changes in binding to excitatory amino acid uptake site in temporal cortex of human brain
1992, Developmental Brain ResearchRegion-specific loss of glutamate innervation in Alzheimer's disease
1987, Neuroscience Letters
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