We found that several microRNAs associated with normal neuronal differentiation are significantly down regulated in medulloblastoma. Of these microRNA 128a was strongly down regulated. While the role of miR-128a has been investigated in astrocytic tumors such as glioblastoma, its role in neuronal tumors such as medulloblastoma is not known. Given the range of retinal cell types expressing Sez-6 and the role Sez-6 plays in shaping the dendritic arbor and excitatory connectivity in cortical pyramidal neurons, it was surprising that ERG analyses failed to reveal any functional consequences of Sez-6 absence in the retina. As a mass electrical potential, the ERG trace represents the summed activity of the entire retinal circuitry. It is therefore possible that single cell electrophysiological analysis would be required to detect putative functional abnormalities in subsets of amacrine cells that may arise from Sez-6 gene inactivation. Examples in the literature of normal ERG responses in gene knockout mice include the G-substrate, mouse retinal degeneration B2 and transthyretin null mouse lines. Like Sez-6, G-substrate and rdgB2 are expressed in subsets of amacrine and ganglion cells. The normal ERG responses in the rdgB2 and transthyretin knockout mice were attributed to likely functional compensation mechanisms and this explanation could well apply to the results obtained here. Sez-6 is a member of a gene family and the two closest family members are also expressed in eye. Two other genes showed significantly altered expression levels on micro-arrays from CD inflamed smokers as compared to the CD inflamed never-smokers: PGM2L1 was 1.6 fold downregulated, whereas KCNJ2 was upregulated by a factor 2.4. Our results imply that the cholinergic reinforcement of visual stimuli 1) would be provided by the adequately-timed cortical release of ACh from the basal forebrain terminals and 2) would be sufficient for visual learning. These implications are further supported by previous work that ACh is released in cortex during numerous learning paradigms, or visual stimulation. This release might be induced by sensory feed-forward influxes or by top-down control, in which ACh mediates top-down attention mechanisms elicited by higher cognitive areas through basal forebrain activation. This interplay MDV3100 between stimulus driven and top-down input to modulate neuronal activity has been addressed by computational neurosciences. In the computational model, the authors suggest that a reinforcement signal combined with an attention feedback signal, called attention-gated reinforcement learning, could model the cortical integration and mapping of sensory stimuli. The long-term mechanisms involving NMDAR and probably LTP pathways shown in the present study.