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GABA CONTENT AND GLUTAMIC ACID DECARBOXYLASE ACTIVITY IN BRAIN OF HUNTINGTON'S CHOREA PATIENTS AND CONTROL SUBJECTS 1
Author(s) -
Urquhart Nadine,
Perry T. L.,
Hansen Shirley,
Kennedy Janet
Publication year - 1975
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1975.tb03679.x
Subject(s) - chorea , glutamate decarboxylase , putamen , globus pallidus , caudate nucleus , substantia nigra , endocrinology , medicine , glutamate receptor , aromatic l amino acid decarboxylase , neuroscience , basal ganglia , dopamine , chemistry , biology , central nervous system , enzyme , biochemistry , dopaminergic , receptor , disease
—GABA contents are significantly decreased in the caudate nucleus, putamen‐globus pallidus, substantia nigra, and occipital cortex in autopsied brain from Huntington's chorea patients, as compared to values in the same regions from control subjects who have died without neurological disease. Homocarnosine levels are lower in choreic than in control brain, but only in the putamen‐globus pallidus and the cerebellar cortex are the differences significant. Activity of the enzyme which synthesizes GABA, glutamic acid decarboxylase, is reduced in the brains of some choreic patients, but may be equally low in brain of control subjects, even though the latter exhibit normal brain GABA content. Low glutamic acid decarboxylase activity in autopsied human brain is not uniquely characteristic of Huntington's chorea. No evidence was found in this study for an inhibitor of glutamic acid decarboxylase in choreic brain, nor for the presence of an isoenzyme with decreased affinity for glutamate. GABA aminotransferase, the enzyme which degrades GABA, was equally active in control and choreic brain; therefore, increased activity of this enzyme cannot account for the low brain GABA levels in Huntington's chorea.