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Neonatal hypothyroidism impairs structural maturation in the brain and results in diminished electrical activities and energy metabolism. We recently found that glucose utilization (CMRglc) is markedly depressed throughout the brain in mice with targeted mutations in thyroid hormone receptor α1 (TRα1), but not TRβ. Previous studies had shown that CMRglc increases linearly with spike frequency in the afferent pathways to synapse-rich regions in neuropil, but not in neuronal cell bodies. To determine whether the decreased CMRglc in mutant TRα1PV/+ mice reflected lesser synaptic density or reduced functional activity in existing synapses, we stimulated vibrissae unilaterally and measured CMRglc bilaterally in four stations of the whisker-to-barrel cortex pathway. Baseline CMRglc (unstimulated side) was markedly lower in all four stations in the TRα1PV/+ mutants than in wild-type controls, even though Northern blot and immunohistochemical examinations showed normal Na+,K+-adenosine triphosphatase expression and neuronal differentiation. Despite the lower baseline CMRglc, however, vibrissal stimulation evoked percent increases in CMRglc in the TRα1PV/+ mutants that were as great as those in wild-type mice. These results indicate that in the TRα1PV/+ mutants there it is a reduction in synaptic density that is responsible for the decrease in CMRglc, but functionality of existing synapses is retained.

Functional Activation of Cerebral Metabolism in Mice with Mutated Thyroid Hormone Nuclear Receptors