Adaptive differentiation of avian exocrine cells alters their pHi response to mAChR activation.

Muscarinic receptor-mediated changes in intracellular pH (pHi) were measured in isolated 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein-loaded cells, suspended in bicarbonate-containing media, from the exocrine nasal gland of freshwater-fed ducklings (Anas platyrhynchos). The pHi recovery from an acid load was sensitive to amiloride, required sodium ions in the external medium, and was independent of added bicarbonate. These findings are consistent with the hypothesis that the pHi recovery was mediated by a Na+/H+ exchanger. Muscarinic activation of cells resulted in a sustained cytosolic alkalinization that was sensitive to atropine and that was blocked by amiloride. Activation of protein kinase C (PKC) or inhibition of protein phosphatases mimicked the effect of receptor activation on pHi, whereas inhibitors of PKC blocked the response, indicating that phosphorylation of a major pHi control mechanism results in a shift of pHi to more alkaline values. In contrast, fully differentiated salt gland cells isolated from nasal glands of salt-stressed ducklings responded to muscarinic receptor activation with a transient cytosolic acidification. These findings raise the question whether the cytosolic alkalinization in muscarinic acetylcholine receptor-activated naive cells may serve as a signal or a permissive factor for the initiation of adaptive growth and/or differentiation processes observed in the salt glands of salt-stressed birds.