abstract
- During birth, when the maternal supply of glucose is occluded, there is a drastic fall in blood glucose in the newborn. This stimulus triggers the non-neurogenic release of catecholamines from adrenomedullary chromaffin cells, which restores blood glucose homeostasis. In this report we present preliminary data showing that glucosensing is present in neonatal chromaffin cells from adrenal slices but absent in chromaffin cells from juvenile slices. Moreover, we show that the aglycemia-evoked rise in intracellular Ca2+ is robust in neonatal chromaffin cells but blunted in juvenile chromaffin cells. Lastly, we show that the Kir6.2 subunit of the KATP channel, is upregulated in the adrenal medulla in juvenile animals providing a potential mechanism for the developmental regulation of glucosensing.