Adult rat barrel cortex plasticity occurs at 1 week but not at 1 day after vibrissectomy as demonstrated by the 2-deoxyglucose method.

Stimulation of a single facial vibrissa in rats receiving [14C]2-deoxyglucose leads to increased local cerebral glucose utilization in the corresponding contralateral barrel of lamina IV of the first somatosensory cortex (SmI). In the adult rat, the metabolic representation of such a barrel enlarges 2 months after removal of all other vibrissal follicles but enlargement is prevented by prior removal of SmI norepinephrine. Here, the early time course of such enlargement and how this was affected by cortical norepinephrine manipulations were examined in adult rats. One day after total vibrissal follicle removal with sparing of the central (C3) vibrissa, neither the areal extent nor absolute glucose utilization in the stimulated, spared C3 cortical barrel were changed. However, 7 days after follicle removal, the spared C3 barrel was enlarged by 41%, although absolute glucose utilization remained constant. This delayed onset of enlargement is compatible with either a structural or neurochemical change in barrel circuitry following vibrissal deafferentation. With ipsilateral locus coeruleus lesions but intact vibrissae, there was progressive enlargement of stimulated C3 barrel areas with increasing cortical norepinephrine depletion (r = 0.864) suggesting a suppressive effect of norepinephrine on activity spread in barrels with intact vibrissal afferents. Previously shown blockade of chronic (2 month) vibrissectomy-induced barrel enlargement by norephinephrine depletion suggested an additional effect on plasticity. Even though acute (1 day) follicle removal here produced no change in spared C3 barrel area, addition of norepinephrine depletion produced a surprising 40% decrease in barrel area. Thus, barrel plasticity assessed by 2-deoxyglucose reflects a complex interaction between barrel metabolic activity and the extent of vibrissal and noradrenergic afferent input.