Perisomatic CF synapses peaked at P9, when pericellular nests were most developed and CF-spine synapses constituted 88% of the total perisomatic synapses. Thereafter, they diminished substantially by P15 and had almost disappeared by P20, Donepezil hydrochloride whereas BF synapses increased reciprocally. Thus, changes in the density and compo sition of perisomatic CF synapses correspond to a developmental switch in the CF innervation mode; namely, CF-spine synapses increase during the pericellular nest stage, decrease during the capuchon stage, and are IM-12 effectively gone in the dendritic stage. During the early postnatal period transmitter receptor expression on the Purkinje cell somata also switches from glutamatergic to GABAergic. Our work documents varied responses to hypoxic and hypoxicischemic stimuli, involving cerebellar neurons of glutamatergic and GABAergic nature. These responses are summarized as follows: a decreased number of migrating and resident NeuroD1-positive granule cells in the ML and IGL, respectively, of the posterior cerebellar lobes from animals that suffered hypoxia or hypoxia-ischemia, with an apparent recovery to control levels when the treatments were combined. Moreover, NeuroD1 protein expression in the nuclear fraction from the whole cerebellum was affected by hypoxic-ischemic challenge, and again returned to control levels when the preconditioning stimulus was applied 24 hours prior. Interestingly, total NeuroD1 expression in Pc cerebella was not different from that in control pups. GAD67-expressing Purkinje cells decreased in number in all three treatment groups, and a substantial percentage of the remaining cells evinced altered features, including diminished branching of their dendritic trees, pyknotic nuclei, and axial rotation. The expression of a potentially dimeric form of the truncated GAD67 protein in the cytoplasmic extracts from whole cerebella also fell in the Pc and L groups, while the PcL animals recovered to control levels. A decrease in Purkinje cell GAD67 mRNA expression was reported in autistic individuals, suggesting that reduced Purkinje cell GABA input to the cerebellar nuclei potentially disrupts cerebellar output to higher association cortices affecting motor and/or cognitive function.