Degeneration Of Adrenergic Nerves Research Articles

The polypeptide chain composition of β-crystallin

1.1. Degeneration of nerve terminals of the submaxillary gland of the rat proceeds at a faster rate after crushing adrenergic nerves close to the gland than after ganglionectomy.2.2. Bretylium, pargyline, nialamide and clorgyline delayed degeneration to the same extent after either type of denervation.3.3. Chlorpromazine and pentobarbitone also delayed adrenergic degeneration, effect related to the hypothermai induced by these drugs.4.4. Colchicine applied on the nerve trunk innervating the right gland delayed not only degeneration of the ipsilateral nerve terminals but the contralateral gland as well.5.5. From the data obtained it seems probable that the drugs tested delay adrenergic nerve degeneration at the levels of nerve terminals. This effect is not related to lysosomal stabilization.

Degeneration of adrenergic nerves produced by 6-hydroxydopamine

6-Hydroxydopamine (6-OH-DA) has been shown to deplete adrenergic nerves very rapidly of endogenous noradrenaline (NA). Its action is probably more rapid than any other known drug. The depletion is more pronounced in the terminals than in the main axons and nerve cell bodies. The iris was found to be a very sensitive organ, while the vas deferens was less sensitive. The depletion may be due partially or solely to destruction of the nerves by 6-OH-DA or some metabolite, taken up by the axon membrane pump into the adrenergic nerves. The destruction of the nerves would thus make the nerves unable to retain endogenous NA. At the same time the nerves cannot take up and store α-methyl-NA. This inhibition of uptake is not due to direct interference by 6-OH-DA with the uptake mechanisms of the cell membrane, but the inhibition of uptake occurs simultaneously with the disappearance of endogenous NA. Therefore, our data indicate a degenerative destruction of the sympathetic nerves, and suggest that 6-OH-DA might be used in achieving a chemical sympathectomy.