THALAMIC AND BASAL FOREBRAIN AFFERENTS MODULATE THE DEVELOPMENT OF PARVALBUMIN AND CALBINDIN D28K IMMUNOREACTIVITY IN THE BARREL CORTEX OF THE RAT

In the adult barrel cortex of the rat the calcium-binding proteins cal bindin D28k (CALB) and parvalbumin (PARV) are found in separate popula tions of GABAergic nonpyramidal neurons. In layers II to IV of the bar rel cortex most PARV-immunoreactive neurons are likely to derive from a subpopulation of CALB-immunoreactive neurons whose CALB immunoreacti vity ceases when they begin to express PARV between the second and thi rd postnatal weeks. The aim of this study was to investigate the influ ence of subcortical afferents on the neurochemical differentiation of cortical PARV- and CALB-immunoreactive nonpyramidal neurons during dev elopment of the barrel cortex. We produced unilateral excitotoxic lesi ons with a single injection of ibotenic acid (0.5 mu l, 0.05 M) in dif ferent subcortical nuclei in 7- to 8-day-old rats. Lesions involving t he ventroposterior thalamic nuclei resulted in delayed development of PARV and CALB immunoreactivity in the barrel cortex. One week after ib otenic acid injections a transient decrease in the number of PARV-immu noreactive neurons in layer IV was observed, together with increased n umbers of CALB-immunoreactive neurons in all cortical layers. The numb er of nonpyramidal neurons displaying coexistence of PARV and CALB in the lesioned hemisphere also increased compared with the numbers in th e control hemisphere or control littermates. In contrast, lesions affe cting the globus pallidus, zona incerta and reticular thalamic nucleus transiently increased the number of PARV-immunoreactive neurons in la yers II and III, but had no effect on the number of CALB-positive cell s. From 3 weeks onwards no differences were found between control and lesioned hemispheres after injections into either the ventroposterior thalamic nuclei or the magnocellular basal forebrain. These results su ggest that CALB and PARV expression in nonpyramidal cortical neurons c an be reversibly modulated in opposite directions by different cortica l afferents during postnatal development.