16 research outputs found
Photoaffinity labeling of a 33 kDa protein subunit of the δ-opioid receptor in neuroblastoma and hybrid cell lines
Effects of GM1 and 2-Deoxy-2,3-dehydro-N-acetylneuraminic acid (NeuAc2en) on neuroblastoma (Neuro 2a) and human glioma cells (U1242 MG)
Effects of cell density on the neutral glycolipid composition of cultured human brain and glioma cells
Deletion of the neuropeptide Y (NPY) Y(1) receptor gene reveals a regulatory role of NPY on catecholamine synthesis and secretion
The contribution of neuropeptide Y (NPY), deriving from adrenal medulla, to the adrenosympathetic tone is unknown. We found that in response to NPY, primary cultures of mouse adrenal chromaffin cells secreted catecholamine, and that this effect was abolished in cultures from NPY Y(1) receptor knockout mice (Y(1)−/−). Compared with wild-type mice (Y(1)+/+), the adrenal content and constitutive release of catecholamine were increased in chromaffin cells from Y(1)−/− mice. In resting animals, catecholamine plasma concentrations were higher in Y(1)−/− mice. Comparing the adrenal glands of both genotypes, no differences were observed in the area of the medulla, cortex, and X zone. The high turnover of adrenal catecholamine in Y(1)−/− mice was explained by the enhancement of tyrosine hydroxylase (TH) activity, although no change in the affinity of the enzyme was observed. The molecular interaction between the Y(1) receptor and TH was demonstrated by the fact that NPY markedly inhibited the forskolin-induced luciferin activity in Y(1) receptor-expressing SK-N-MC cells transfected with a TH promoter sequence. We propose that NPY controls the release and synthesis of catecholamine from the adrenal medulla and consequently contributes to the sympathoadrenal tone