J. Neurochem. (2011) 117, 61–70. Abstract Galanin (GAL) is a neuropeptide which is up‐regulated following neuronal axotomy or inflammation. One subtype of GAL receptor (GalR2) is reported to be expressed in the brain’s immune cell population, microglia. In the present study, we investigated the effect of GAL on microglial migration and compared the mechanism with that of bradykinin (BK). GAL significantly increased the migration of rat cultured microglia at 0.1 pM. The GAL‐induced signal cascade was partly similar to that induced by BK. It was not dependent on Gi/o protein but involved activation of protein kinase C, phosphoinositide 3‐kinase and Ca2+‐dependent K+ channels. However, reverse‐mode activation of the Na+/Ca2+‐exchanger 1 was not involved in GAL‐induced microglial migration, unlike BK‐induced migration. Likewise, nominally‐free extracellular Ca2+ inhibited BK‐induced migration but not GAL‐induced migration. An inositol‐1,4,5‐triphosphate receptor antagonist significantly inhibited GAL‐induced migration. GAL‐induced Ca2+ signaling did not induce nitric oxide synthase expression, but up‐regulated class II major histocompatibility complex expression. These results indicate that activation of inositol‐1,4,5‐triphosphate receptor and increase in intracellular Ca2+ are important for GAL‐induced migration and immunoreactivity in microglia. The differences in down‐stream signal transduction induced by GAL and BK suggest that GAL and BK may control distinct microglial functions under pathological conditions.

IDilazep, a coronary dilator, has been reported to potentiate the negative inotropic and negative chronotropic responses of guinea-pig atria to adenosine. Studies were made on the mechanism of the potentiating action of dilazep with special reference to the degradation and uptake of adenosine. 2 The negative inotropic actions of adenosine and adenine nucleotides, such as ATP, ADP, AMP and cyclic AMP, on guinea-pig atria were selectively and dose-dependently augmented by dilazep at concentrations insufficient to produce any effect alone (0.01 to 1 tM). 4 Adenosine (10 pM to 10 mM) was degraded to inosine and hypoxanthine during incubation with atrial tissue; dilazep (0.1 to 10 pM) retarded the disappearance of adenosine and the formation of inosine and hypoxanthine. 5 These results suggest that dilazep potentiates the negative inotropic effect of adenosine on guineapig atria by preventing both its accumulation by atrial tissue and degradation by deaminase.

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