Neonatal sensory deprivation induces selective changes in the quantitative distribution of GABA-immunoreactive neurons in the rat barrel field cortex.

Modified activity of the rat vibrissae from birth to adulthood induces profound alterations of the responsiveness and selectivity of neurons in the contralateral somatosensory barrel field cortex of adult rats. Because these functional properties are under the control of the intracortical inhibitory mechanisms, we investigated the effects of unilateral removal of face pad vibrissae on the quantitative distribution of intracortical gamma-aminobutyric acid (GABA)-immunoreactive neurons in the rat contralateral and ipsilateral barrel field cortices. This distribution was then compared to a population of control animals. For the entire cortical depth, no significant changes in the density (7,700/mm3 vs. 7,400/mm3), proportion (13.6% vs. 14.4%), or size (11.7 microns vs. 12.5 microns) of GABA-immunoreactive neurons were found in the left contralateral vs. the right ipsilateral barrel field cortex. However, in cortical layer IV, contralateral to the deprivation, the density and proportion of GABA-immunoreactive neurons were lower (6,300/mm3 vs. 13,900/mm3, 6.0% vs. 13.6%; P < 0.01), and these neurons were larger (mean projected height of 15.1 microns vs. 10.8 microns; P < 0.01) than in the ipsilateral barrel field cortex, suggesting a specific loss of GABA expression in a subpopulation of small intracortical neurons. In addition to changes in the contralateral layer IV, GABA-immunoreactive neurons located in the ipsilateral granular layer were also affected. Indeed, their numerical density (13,900/mm3) and proportion (13.6%) were higher (P < 0.01) than in both hemispheres of control animals (average of 10,050/mm3 and 9.4%). On the other hand, GABA-immunoreactive neurons in the ipsilateral layer V were less numerous (5,600/mm3, 15.0%) than in both sides of the controls (average of 10,300/mm3, 22.0%; P < 0.01). Thus, our results show that a unilateral sensory deprivation induces highly selective changes in the intracortical GABA inhibitory circuitry of both hemispheres. These changes are located directly at the input of thalamic afferents and at an output layer of corticofugal and commissural axons and could result in a profound reorganization of the excitatory and inhibitory drives of both sides of the sensory-deprived barrel field cortex.