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Effect of Repeated Treatment with a γ‐Aminobutyric Acid Receptor Agonist on Postnatal Neural Development in Rats
Author(s) -
Meier Eddi,
Jørgensen Ole Steen,
Schousboe Arne
Publication year - 1987
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.1471-4159.1987.tb01015.x
Subject(s) - glutamate decarboxylase , glutamatergic , agonist , neural cell adhesion molecule , glutamate receptor , aminobutyric acid , receptor , chemistry , medicine , endocrinology , pharmacology , biology , biochemistry , enzyme , cell , cell adhesion
The effect of treatment with the γ‐aminobutyric acid (GABA) agonist tetrahydroisoxazolo[5,4‐ c ]pyridin‐3‐ol (THIP) on neural development was monitored in rats by following the expression of the neuron‐specific proteins neural cell adhesion molecule (NCAM), D1, and D3 as well as the enzymes glutamate decarboxylase (GAD) and glutamate dehydrogenase (GLDH). As judged from the effect of the treatment on the expression of NCAM and GAD, GABA agonists have the capacity to accelerate and enhance neuronal development during the early postnatal period. However, as judged from the expression of D1‐and D3‐protein some adverse late effects may result from prolonged treatment with high doses of GABA agonists. The decrease in GLDH specific activity observed in THIP‐treated rats during their late postnatal development possibly indicates a repression of glutamatergic neurons.