NeuroD1 expression RG7112 correlates well with granule cell differentiation in the cerebellum, showing stable levels in the internal granular layer until adulthood. Despite a near uniform cytoarchitecture, some genes are differentially expressed among the cerebellar lobes. Preferential posterior cerebellum defects in granule cells were reported in the global absence of NeuroD1. A conditional granule cell precursor-selective NeuroD1 knock-out model resulted in elimination of the granule cells in the central lobes and anomalies in the Purkinje cells. Although these results vary, depending on when and where NeuroD1 is deleted during the cerebellar development, the genetically modified mice support the interactions between Purkinje and granule cells during the acquisition and maintenance of their final phenotypes. GAD67 catalyzes the conversion of L-glutamate into c�C aminobutyric acid, the principal inhibitory neurotransmitter that can also exercise an excitatory influence in the immature brain, and on hippocampal neuronal precursors promoting adult neurogenesis. GAD67 is encoded by a single gene, distinct from Gad65. Different protein forms derived from alternative splicing of GAD67 mRNAs and with specific developmental expression patterns have been reported. The transcription factor Egr1, a known regulator of genes associated with synaptic plasticity and memory, was also found to induce Gad67 expression in hippocampal neurons. Roybon et al. proposed that basic helix-loop-helix transcription factors influence GABAergic or glutamatergic neuronal differentiation in a compensatory and cross-regulatory manner. Specifically these authors showed that NeuroD1, a Neostigmine Bromide downstream effector of neurogenins, can abrogate the GABAergic phenotype directed by Mash1 facilitating the glutamatergic fate. A direct inhibitory role of NeuroD1 on Gad67 was not ruled out. It is well known that neurogenesis and cell proliferation increase in the neonatal brain in response to ischemic injury and that multiple brain areas function as reservoirs of brain precursor cells. The contribution of progenitor pools to recovery in the immature brain, which displays a window of plasticity, has been addressed in other reports.