Plasticity of cerebral metabolic whisker maps in adult mice after whisker follicle removal--I. Modifications in barrel cortex coincide with reorganization of follicular innervation.

We investigated alterations of the metabolic whisker map of barrel cortex after the removal of the follicles of left whiskers C1, C2 and C3 in adult albino mice. The quantitative autoradiographic [14C]deoxyglucose method was used to measure local cerebral metabolic rates for glucose in barrel cortex of mice two, four, eight, 64, 160 and 250 days after the lesion. Metabolic rates were measured in three groups of animals: (i) mice with lesions that had all whiskers clipped; (ii) mice with lesions that had left whiskers B1-3 and D1-3 stimulated; and (iii) unoperated mice that had left whiskers B1-3 and D1-3 stimulated. Compared with the metabolic rates in barrels C1-3 of stimulated unoperated mice, barrels C1-3 of stimulated mice with lesions showed the first discernible increase in metabolic rate four days after the lesion. The increase became distinct at 64 days, but attained statistical significance only approximately 160 days after the lesion. The lesion per se, i.e. without whisker stimulation, caused only a small increase in metabolic rate in barrels C1-3 accounting for not more than one fourth of the increase in metabolic rate measured after whisker deflection. The removal of whisker follicles C1-3 led, therefore, to an enlargement of the metabolic representations of the adjacent whiskers into the barrels deprived by the lesion. The gradual consolidation of the alterations of the metabolic whisker map coincided with the regeneration of follicular nerves in the whiskerpad. We detected anomalous deep nerves innervating follicles surrounding the lesion at approximately 64 days, and the number of myelinated nerve fibres in the deep nerves of these follicles was increasing with increasing time after the lesion. The coincidence of peripheral and central change suggests that the reorganization of the innervation of the sensory periphery plays an important role in the persistent alterations of the cortical somatotopy in adults following a lesion in the sensory periphery.