Immunocytochemical techniques were used to investigate the distribution of gamma-aminobutyric acidA (GABAA) receptors in the rat primary somatosensory cortex (SI). Monoclonal antibody 62-3G1 (de Blas et al., 1988; Victorica et al., 1988), which recognizes an epitope common to the beta 2 and beta 3 subunits of the GABAA receptor, produces staining of small punctate structures throughout the neuropil, and around somata and linear processes in all laminae of SI. Receptor immunostaining is relatively intense in upper lamina I and in lamina IV, where patches of intense receptor staining are interleaved with narrow zones of moderate immunoreactivity. Staining is lightest in lamina Vb, where stained puncta appear to be aligned with radially oriented processes, and moderate in the remaining laminae. Tangential sections through lamina IV reveal that each large cortical barrel encompasses several patches of intense receptor staining that are aligned with the corners or edges of individual barrels; interbarrel septa are moderately of intense cytochrome oxidase (CO) histochemical staining. A similar correspondence is apparent between a complex lattice of dense receptor clustering and a plexus of dark CO staining in the cortical trunk representation. Six to eight weeks of tactile deprivation produced by simple whisker trimming have no visible effect on GABAA receptor distribution. This is the case for rats whose whiskers were trimmed only during adulthood and for rats deprived from the day of birth until examination 6-8 weeks later. However, electrocautery ablation of whisker follicles leads to a marked decline in GABAA receptor immunoreactivity in cortical barrels associated with the ablated follicles. Our findings indicate that there is reasonable, though not perfect, correspondence between the distribution of GABAA receptors and the distribution of GABA-containing neurons and terminals in rat SI. These elements are associated with regions of intense oxidative metabolic activity revealed by CO staining. The density of GABAA receptors is reduced in lamina IV following complete loss of peripheral afferent input. However, less severe tactile deprivation, which is known to affect cortical neuron responsiveness, produces little or no change in receptor distribution.