Summary
The release of noradrenaline (NA) from the sympathetic nerve endings (varicosities) is discussed in relation to the economy of the amine storage granules, their content of NA, and the rate of contribution of new granules to the nerve terminals via intra-axonal transport.
I. Different models for the involvement of amine storage granules in release are considered mainly on the basis of quantitative data on the amount of NA released per nerve impulse. The conclusion is drawn that granules in all probability can be used several times for transmitter release at nerve activity and that newly synthesized NA plays an important role at this release. Also the transmitter “quantum” seems to be far less than the total content of NA in a single granule.
II. The marked increase of the NA amount released from the sympathetic nerve endings at nerve activity after α-receptor blockade has been studied. Various previous explanations for this phenomenon appear at present to be unlikely. The current view is that the results are better explained as due to an increase in the amount of transmitter released per nerve impulse from the nerve endings. This indicates that the amount of transmitter released per nerve impulse is not constant but may vary due to regulation via local feed-back mechanisms. In consequence α-receptor blockers are unsuitable as tools for quantitative studies on the physiological, “true” release of transmitter at nerve activity.
III. Studies on the recovery of different functions in the nerve terminals after a large dose of reserpine indicate that granules formed in the cell bodies and recently downtransported to the nerve terminals via intra-axonal transport are probably capable not only of storing endogenous NA but also of uptake-retention of small amounts of 3H-NA and of preferential release of the transmitter at nerve activity. These last-mentioned functions appear to be lost rather soon after the arrival of the new granules to the nerve terminals. The capacity to store endogenous NA seems, however, to be a long-lasting capacity.
This functional heterogenicity of the nerve terminal amine storage granules is discussed in relation to morphological and biochemical differences in granules from the axons and from the nerve terminals. A factor of importance for the agening of the granules may be release of granuler proteins during nerve activity.
The results support the view (section I) that the granules are not fully consumed at transmitter release following a normal nerve impulse, but that release occurs via partial exocytosis which may cause a change of properties of the storage particles.
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Häggendal, J. (1974). Some Aspects of the Release of the Adrenergic Transmitter. In: Csillik, B., Kappers, J.A. (eds) Neurovegetative Transmission Mechanisms. Journal of Neural Transmission, vol 11. Springer, Vienna. https://doi.org/10.1007/978-3-7091-8341-0_8
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