Most of them also manifest hypersensitivity to NSAIDs, and their asthma remains poorly controlled

uently, the genes that are expressed in both regions were excluded. For example, the potassium channels and Parv performed on brain sections of transgenic GlyT2-EGFP mice revealed the presence of several axons and axon terminals in the hypothalamic region encompassing the parvafox nucleus. The merged image shows GlyT2-EGFP-positive terminals around the perikaryon and the dendrites of a Parv-positive neuron. Three-dimensional reconstruction by Imaris reveals several EGFP-positive terminals on the dendrite, as well as on the cell body of the Parv-neuron. Kcnab3, Kcnc1, Kcnc2, and Kcnk1), which are responsible for the high firing rates of Parv-positive neurons in the cortex and the hippocampus, were recognized as being expressed in the parvafox nucleus by the ABA-ISH-database screening but not by the gene-microarray analysis. Nevertheless, a detailed comparison of the long list of expressed genes in the gene-microarrays of both mice revealed that approximately 40% of those that were registered in the study of were also enriched in the gene-microarray of the parvafox nucleus. For some genes, no in-situ-hybridization data exist as yet in the ABA-ISH. For others, screening of the ABA-ISH database yielded negative results, even though the expression of such genes in the hypothalamus has been demonstrated by in-situ hybridization or immunohistochemistry in other reports. Lowlevel transcripts may be below the threshold of detection by in situ hybridization techniques, and more sensitive techniques such as qRT-PCR may be needed to validate their expression in the parvafox nucleus. Hence, falsely negative results partially account for the discrepant findings. On the other hand, it is also conceivable that the genearray technique yields falsely-positive or falsely-negative results. The former may arise from the non-specific binding of cDNAs to homologous oligonucleotide probes, and the latter from the privileged amplification of certain mRNAs at the expense of others. Hence, taking into account the combined results of the three approaches maximizes the reliability of the information we have gained. The counterchecking of findings revealed by a gene-microarray analysis against those disclosed by in-situ hybridization and in the B database, is a legitimate mean of predicting the expression profiles of the neurons in the parvafox nucleus. Albeit so, it represents only a first approximation: the definitive allocation of gene-expression activity to a specific 2353-45-9 chemical information sub-population of neurons awaits the instigation of antibodies against the corresponding proteins for a definitive immunohistological confirmation of their localization to specific sub-population of neurons. Furthermore, functional in-vitro studies investigating for example the effects of blocking glycinergic transmission or applying locally the corresponding neurotransmitter will be needed to confirm the physiological roles of the genes of interest. The glycinergic inhibitory system is particularly powerful in the spinal cord and the brainstem, where virtually all immunoreactive cell-bodies are located. However, glycine-immunoreactive fibers and terminals have been observed in various parts of the brain by different authors and glycine-induced PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19815048 chloride-currents were discovered already in 1989 in dissociated hypothalamic neurons. Functional glycine receptors have been detected in higher brain centers, 12 Szabolcsi et al. Parvalbumin-Neurons of the Parvafox Receive Glycinergic Input such as the hipp