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. 1984 Feb:347:741-9.
doi: 10.1113/jphysiol.1984.sp015093.

Functional, structural and chemical correlates of sprouting of intact preganglionic sympathetic axons in the guinea-pig

Functional, structural and chemical correlates of sprouting of intact preganglionic sympathetic axons in the guinea-pig

F Fonnum et al. J Physiol. 1984 Feb.

Abstract

Intact preganglionic axons can sprout and form new functional synaptic connexions with neurones in the partially denervated superior cervical ganglion of the guinea-pig (Maehlen & Njå, 1981). In the present work we have examined to what extent the degree of sprouting, as measured by intracellular recording, is paralleled by changes in ultrastructural and neurochemical parameters. The mean number of preganglionic axons innervating each neurone, as estimated by intracellular recording from ganglion cells during stimulation of the individual ventral roots, was reduced from about eleven to about two immediately after the partial denervation. However, 5-7 weeks after the operation, when sprouting was complete, each neurone was innervated on average by about seven axons. The estimated mean amplitude of the synaptic potential elicited by each innervating axon (about 5 mV) was only slightly increased after sprouting. Counts of the number of synaptic profiles per unit area of electron microscopical sections of the ganglion were reduced to about 15% of normal 3-4 days after the operation, and increased to about 60% of normal after sprouting (5-7 weeks). The activity of the enzyme choline acetyltransferase was about 20% of the normal value in ganglia examined 3-4 days after partial denervation. After sprouting (5-7 weeks), this value was increased to about 35% of that in normal ganglia. These results show that intact preganglionic sympathetic axons have a substantial growth potential. However, the increase in the choline acetyltransferase activity was smaller than the increase in electrophysiological and ultrastructural measurements. Therefore, compensatory axonal branching and synapse formation may cause a reduction in the supply of choline acetyltransferase to each presynaptic terminal from the parent soma.

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