Development of adrenergic nerve terminals: The effects of decentralization

Abstract

The effect of decentralization (deafferentation) on the ontogeny of adrenergic nerve terminals was studied in the rat iris. Transection of the cholinergic trunk, which innervates the superior cervial ganglion (SCG), in 2–3-day-old rats, inhibited the developmental increase in iris nerve terminal density, as indicated by fluorescence microscopy. However, terminal varicosities, containing the norepinephrine (NE) storage vesicles, appeared larger and more brightly fluorescent in decentralized irides. Tyrosine hydroxylase, localized to nerve terminal cytoplasm, developed to only 40% of normal in decentralized irides. In contrast, dopamine-ß-hydroxylase, which is localized to NE storage vesicles in varicosities, developed normally. The ability to accumulate and store [ 3H]NE was examined in control and decentralized terminals in the presence or absence of reserpine. This drug inhibits NE storage capacity without primarily affecting accumulation itself. Decentralization reduced the in vitro uptake of NE to 54%, measured after reserpine pretreatment; in contrast, apparent uptake of transmitter was reduced to only 76% in vehicle-treated rats. These results suggest that decentralization prevents the normal development of nerve terminal membrane without markedly interfering with vesicular storage capacity. This contention was supported by the observation that in vitro retention of [ 3H]NE over time was actually increased in decentralized irides. Our results suggest that the ontogeny of different subcellular structures is affected differently by deafferentation. The transsynaptic regulation of nerve terminal maturation appears to be most critical in younger rats, since decentralization exerts most marked effects when performed during the perinatal period.