
<ArticleTitle>Biphasic response to human <prot>galanin</prot> of extracellular acidification in human Bowes melanoma cells.</ArticleTitle>
<AbstractText>The metabolic response of <prot><prot>galanin</prot> <prot>GAL1</prot> receptor</prot> subtype, endogenously expressed in human Bowes melanoma (HBM) cells, was investigated. Cytosensor microphysiometry was used to determine the extracellular acidification rate. A biphasic response, consisting of a rapid increase in the extracellular acidification rate followed by a decrease below the basal level, was observed after perfusion with human <prot>galanin</prot>. The magnitude and the rate of onset of both phases were dependent on the <prot>galanin</prot> concentration. The increase in the extracellular acidification rate (maximum of 25% of basal level; -log(EC(50))=7.23+/-0.14) was transient, whereas the following decrease (maximum of 40% of basal level; -log(EC(50))=7.77+/-0.23) was sustained. The EC(50) values for the increase and decrease were in a similar range. After consecutive <prot>galanin</prot> administration, the magnitude of the response was the same as for the unexposed cells, indicating the absence of <prot><prot>galanin</prot> receptor</prot> desensitization or internalization in HBM cells. Responses were blocked by pretreatment with <prot>pertussis toxin</prot> and phorbol-12-myristate-13-acetate (PMA), indicating a G-protein/<prot>protein kinase C</prot> signalling pathway. Our microphysiometry results show a biphasic response of the extracellular acidification rate mediated by the <prot><prot>galanin</prot> receptor</prot> expressed in HBM cells which has not been described previously for any other endogenously expressed neuropeptide receptor.</AbstractText>
