The effect of postnatal thyroid deficiency on chdlinergic and associated neurons in the pat corpus striatum

The consequences of p r ~ i t h i o u r a c i l (PTU)-treatment on the postnatal d e v e l o ~ n t of the striatal preand postsynapticmarkers for cholinergic, dopa~ne, GABA and glutamate neurons and on 8-alanine transport were investigated. To assess effects on cell n ~ r s and acquisition, DNA concentratior~ were n~su red in striatal san~oles from 3and 6-w~ek-old control and treated neoPates. P~J-treatraent in rats markedly in,paired the development of choline acetyltransferase activity, choline uptake (Kalaria et al, 19817, l~C-acetylcholine synthesis, and 3 Hspiroperidol and 3 H ~ l u ~ t e binding. In contrast, two-vray ANOVAR revealed significant increases in GABAuptake and g l u ~ t e decarhoxylase activity and in ~alanine uptake in sab les from the treated neonates. Consistent with deficits in striatal weight and greater DNA concentrations in the s t r i a t~ of PTU-treated neonates those neuronal markers which showed in~pairments on a mg tissue basis n~nifest even greater ~oairments expressed per whole striation. These findings suggest impaired arborlzation of cholinergic interneurons in the striatum during neonatal thyroid deficiency. The differential sensitivity on neuronal markers of the onset of postnatal thyroid deficiency seems likely to reflect the timing of the morphological differentiation of cholinergic and associated neurons in the striatum. There appear to be final adjustments in the development of the circuitry of neurons relative to overall growth of the str iatumduring thyroid deficiency.