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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ventral medullary surface (VMS) is a site of the medullary chemoreceptor neurons which sense excess protons (H+) derived from hypercapnia and facilitate respiration. We hypothesized that expression of genes involved in H+-sensitivity is higher in the VMS than in other central nervous system areas. By using the differential display technique, we differentiated the mRNAs of VMS neurons from those of cerebral cortical neurons. Seventeen clones of interest were isolated, and sequence analysis revealed that one of these clones had an encoding nuclear transcription factor, MafG. MafG is a member of Maf protein family, and the founding member of the family (v-Maf) was originally discovered as the transduced transforming component of avian musculoaponeurotic fibrosarcoma virus, AS42. The rat MafG was composed of 162 amino acid residues and was conserved among the primary structures of various species. Expression of rat mafG mRNA is high in the VMS, heart and skeletal muscle while the cerebral cortex, cerebellum, liver, stomach and intestine show moderate expression. To determine whether the expression of mafG mRNA is induced by hypercapnic stimulation, 7% CO2 in air was inhaled to rats for 5 min. We found that the hypercapnic stimulation induced the gene expression of mafG. These results suggest that MafG may be involved in H+-sensitivity and respiratory regulation in the VMS.
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PMID:Cloning of MafG homologue from the rat brain by differential display and its expression after hypercapnic stimulation. 1072 42

Significant advances have been made in understanding how neurons sense and respond to acidosis at the cellular level. Decrease in pH of the cerebrospinal fluid followed by hypercapnia (increased arterial CO2) is monitored by the chemosensory neurons of the medulla oblongata. Then the intracellular signalling pathways are activated to regulate specific gene expression, which leads to a hyperventilatory response. However, little is known about molecular details of such cellular responses. Recent studies have identified several transcription factors such as c-Jun, Fos and small Maf proteins that may play critical roles in the brain adaptation to hypercapnia. Hypercapnic stimulation also activates c-Jun NH2-terminal kinase (JNK) cascade via influx of extracellular Ca2+ through voltage-gated Ca2+ channels. In addition, several transmembrane proteins including Rhombex-29 (rhombencephalic expression protein-29 kDa) and Past-A (proton-associated sugar transporter-A) have been implicated in regulation of H+ sensitivity and brain acidosis-mediated energy metabolism, respectively. This review discusses current knowledge on the signalling mechanisms and molecular basis of neuronal adaptation during acidosis.
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PMID:Molecular responses to acidosis of central chemosensitive neurons in brain. 1576 22