Abstract
The effect of thyroid status on noradrenergic synaptic function in the mature rat brain was examined by measuring presynaptic alpha 2- and post-synaptic beta-adrenoceptors. Repeated triiodothyronine (T3) administration to rats (100 micrograms/kg X 14 days: hyperthyroid) caused an 18% increase in striatal beta-adrenoceptors as shown by [3H]-dihydroalprenolol binding with no change in membranes from cerebral cortex or hypothalamus. In contrast, hypothyroidism (propylthiouracil, PTU X 14 days) produced significant 12% and 30% reductions in striatal and hypothalamic beta-adrenoceptors respectively with no change in the cerebral cortex. Presynaptic alpha 2-adrenoceptor function was measured in the two dysthyroid states using the clonidine-induced hypoactivity model. Experimental hyperthyroidism increased the degree of clonidine-induced hypoactivity, and suggests increased presynaptic alpha 2-adrenoceptor function compared with control rats, whereas hypothyroidism suppressed presynaptic alpha 2-adrenoceptor function. These results show firstly that changes in thyroid status in the mature rat may produce homeostatic alterations at central noradrenergic synapses as reflected by changes in pre- and post-synaptic adrenoceptor function. Secondly, there appear to be T3-induced changes in beta-adrenoceptors in the striatum where changes in dopaminergic neuronal activity have previously been demonstrated.
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