IN humans, trauma to a peripheral nerve may be followed by chronic pai
n syndromes which are only relieved by blockade of the effects of symp
athetic impulse traffic1-4. It is presumed that, after the lesion, nor
adrenaline released by activity of sympathetic postganglionic axons ex
cites primary afferent neurons by activating alpha-adrenoceptors2,5, g
enerating signals that enter the 'pain pathways' of the central nervou
s system. The site of coupling is unclear. In some patients local anae
sthesia of the relevant peripheral nerve6 does not alleviate pain, imp
lying that ectopic impulses arise either within the central nervous sy
stem, or in proximal parts of the primary afferent neurons. In experim
entally lesioned rats, activity can originate within the dorsal root g
anglia7,8. Here we report that, after sciatic nerve ligation, noradren
ergic perivascular axons in rats sprout into dorsal root ganglia and f
orm basket-like structures around large-diameter axotomized sensory ne
urons; sympathetic stimulation can activate such neurons repetitively.
These unusual connections provide a possible origin for abnormal disc
harge following peripheral nerve damage. Further, in contrast to the s
prouting of intact nerve terminals into nearby denervated effector tis
sues in skin9,10, muscle11, sympathetic ganglia12 and sweat glands13,
the axons sprout into a target which has not been-partially denervated
.