Embryonic brain development is a complex process in which expression patterns of receptors and transcription factors control the generation of many different cell types from a common precursor, as well as their subsequent temporal and spatial distribution within different regions of the brain. Although these programs are tightly regulated to ensure formation of functional neuronal networks, the external cues that govern these processes are still largely unknown. The p75 neurotrophin receptor (p75 NTR) has been identified as a key regulator in the development of a range of cell types, including neural progenitors of the peripheral nervous system. As a cell surface receptor, p75 NTR can initiate direct environment-to-cell communication and coordinate important aspects of neurogenesis including survival, proliferation, specification, migration, and/or differentiation. However, the function of p75 NTR in development of the central nervous system had not been studied comprehensively. The aim of the thesis is to elucidate the role of p75 NTR in brain development and, more specifically, to investigate how neocortical progenitor fate is regulated by p75 NTR using conditional p75 NTR knockout mice. We found that p75 NTR is most highly expressed during cortical development in post-mitotic neuronal cells, but that loss of p75 NTR expression during embryogenesis in progenitor cells has widespread ramifications on the development of the neocortex and basal ganglia due to effects on progenitor populations. Specifically, p75 NTR expression is required for the survival of neuron-specified intermediate progenitor cells (IPCs) and for the generation of appropriate numbers of pyramidal cortical neurons and parvalbumin (PV)-positive interneurons. Without p75 NTR expression, a significant number of IPCs die prior to, or in the process of, undergoing neurogenic divisions, resulting in a depletion of the progenitor pool and subsequent reduction in neuronal production. Furthermore, loss of p75 NTR expression in progenitors of the medial ganglionic eminences (MGE) reduces their ability to generate interneurons in culture and to differentiate into a PV-expressing subtype. In vivo, loss of p75 NTR in the MGE selectively reduces the production of PV-expressing interneurons, presumably caused by reduced activity of the nuclear factor κB (NF-κB) pathway. These results demonstrate that p75 NTR expression is required for normal cortical development by facilitating survival of cortical IPCs.