Effects of thyroid deficiency on the development of cholinergic, GABA, dopaminergic and glutamate neuron markers and DNA concentrations in the rat corpus striatum.

The effects of propylthiouracil (PTU)-induced thyroid deficiency on the postnatal development of synaptic markers for cholinergic, GABA, dopaminergic and glutamate neurons in the rat corpus striatum were investigated. Similar effects were also assessed on β-alanine uptake by fine prisms and on DNA concentrations in striatal samples from 3- and 6-week-old rats. Thyroid deficiency (Tx) in rats markedly impaired the development of choline acetyltransferase activity and [(3)H]spiroperidol and [(3)H]-glutamate binding capacities. In contrast, small but significant increases were evident in γ-aminobutyric acid uptake and glutamate decarboxylase activity. β-Alanine uptake, a possible glial marker, was increased by up to 50% in samples from the Tx rats compared to controls. Consistent with deficits in striatal weight and greater DNA concentrations in the striatum of the Tx rats those neuronal markers which showed impairments on a mg tissue basis manifest even greater impairments expressed per whole striatum. Present findings suggest differential effects on neuronal markers, with the greatest impairments in the presynaptic markers for cholinergic interneurons in striatum during neonatal thyroid deficiency. The differential sensitivity on neuronal markers of the relatively late onset of thyroid deficiency seems likely to reflect the timing of the morphological differentiation of cholinergic and the other neurons in striatum.