Observed in sound-evoked cortical response in the auditory cortex. Mecamylamine inhibits both a4b2 and a7 nAChRs that are located on thalamocortical terminals and cortical GABAergic neurons. An important prerequisite for the interconversion between complementary subsets is a transcriptional permissiveness of those genes whose transcription characterizes the Masitinib respective differentiation state. The creation of the permissive state of a differentiation specific gene might rely on mechanisms related e.g. to activation of primary response genes, which are regulated at the level of transcript elongation and processing. Alternatively, transcription of differentiation-specific genes might be attenuated, but still weakly active and rapidly switched to a more active state upon activation of respective signaling cascades, initiating and accompanying the transition into another differentiation state. In this scenario, the regulation of transcriptional activity might be exerted by transcription factors acting in concert with signaling pathways. For instance, a transient inflammatory signaling cascade activated by Src kinase in human MCF10A cells triggers a Lin28B/let-7 mediated epigenetic switch resulting in engagement of transcription factor STAT3 and acquirement of fully transformed phenotype and CSC properties. Activation of nAChRs located on the thalamocortical afferents increase thalamic input. Inhibition of these receptors should result in the reduction of incoming signals from the thalamus which is in agreement with the abolishment of VEP amplitude enhancement under mecamylamine conditions in the current study. Inhibition of nAChRs located on the GABAergic cells may not be sufficient to explain these results since inhibition of these receptors should also result in reducing the inhibitory drive within the intracortical network, thereby lowering the threshold for eliciting a cortical response. In addition, it has been shown that mecamylamine could transiently inhibit the NMDAR in vitro at the concentration used in the present study. It is possible that the blockade of CCh induced long-term effect on VEPs by mecamylamine in our study could result from an inhibition of the NMDAR located on the glutamatergic cells. It is possible, however, that the tumor suppressors can be localized in a region showing chromosomal amplification in tumor cells. One example is a potential tumor suppressive gene, GSDMA, is localized in a chromosomal region amplified in gastric cancer cells. This gene is downregulated in the human gastric cancers even though the gene showed amplification in tumor cells. In the case of the miR-185, epigenetic silencing of the miRNA might occur prior to the gene amplification of the chromosome 22q21.1 region. Further investigation clearly needs to address these questions thoroughly. Therefore, we decided to investigate microRNA function in medulloblastoma.