Early barbiturate treatment eliminates peak serum thyroxine levels in neonatal mice and produces ultrastructural damage in the brains of adults

Serum thyroxine levels peak sharply at the end of the second postnatal week in mice. Treating neonatal mice with barbiturates (PhB) completely eliminates this marked thyroxine (T 4) peak without significantly affecting nonpeak levels at other ages. PhB treatment at this same time also establishes or induces long-lasting degenerative processes that continue to result in ultrastructural neural deficits in adults, long after treatment has been discontinued. Similar neural deficits have been observed in animals which were deficient in T 4 during this same period of development.