The Subplate and Its Role in the GABA System in the Prefrontal Cortex
Abstract
During early brain development, the subplate relays thalamocortical afferents. Lesions to the subplate have been implicated in developmental abnormalities of cortical GABAergic circuits. This thesis examined the effects of subplate lesions in the prefrontal cortex of rats on the expression of GABA markers (parvalbumin and GAD67) and GABA synapse maturation [potassium-chloride cotransporter (KCC2) and sodium-potassium- chloride cotransporter (NKCC1)] with relevance to the characterization of a rat model for schizophrenia. Lesions were made on postnatal day 1 (P1). Lesioned and control rats were sacrificed between P5 and P90 and immunolabelled for parvalbumin, GAD67, KCC2, and NKCC1. We found decreased parvalbumin expression in lesioned animals, validating our subplate lesion model in impaired interneuron development. GAD67, KCC2, and NKCC1 levels were unchanged at all timepoints studied compared to control. Despite this, decreased parvalbumin expression may alter cortical E/I balance, as previously seen in behavioral abnormalities of this animal model.