Like other parts of the nervous system, the assembly of sympathetic neuronal circuits (which control autonomic bodily functions, including sweating) involves a series of differentiation steps. The final step in sweat gland innervation is a noradrenergic to cholinergic neurotransmitter phenotype switch. Stanke and co-workers now report that target-dependent signalling through the cytokine receptor subunit gp130 mediates this developmental change in the sympathetic neurons that innervate mouse sweat glands (see p. ). They show that cytokines that act through gp130 are present in sweat glands and that the conditional deletion of gp130 in sympathetic neurons prevents the switch from a noradrenergic to cholinergic neurotransmitter phenotype; the differentiation of cholinergic sympathetic neurons innervating other targets is also mediated by gp130. Surprisingly, gp130-depleted mice have functional sweat glands,indicating that cholinergic neurotransmission is not needed for the acquisition and maintenance of sweat gland secretory responsiveness, as previously believed.
