L. Jasmin et al., ACTIVATION OF CNS CIRCUITS PRODUCING A NEUROGENIC CYSTITIS - EVIDENCEFOR CENTRALLY INDUCED PERIPHERAL INFLAMMATION, The Journal of neuroscience, 18(23), 1998, pp. 10016-10029
We present a model of neurogenic cystitis induced by viral infection o
f specific neuronal circuits of the rat CNS. Retrograde infection by p
seudorabies virus (PRV) of neuronal populations neighboring those that
innervate the bladder consistently led to a localized immune response
in the CNS and bladder inflammation. Infection of bladder circuits th
emselves or of circuits distant from these rarely produced cystitis. A
bsence of virus in bladder and urine ruled out an infectious cystitis.
Total denervation of the bladder, selective C-fiber deafferentation,
or bladder sympathectomy prevented cystitis without affecting the CNS
disease, indicating a neurogenic component to the inflammation. The in
tegrity of central bladder-related circuits is necessary for the appea
rance of bladder inflammation, because only CNS lesions affecting blad
der circuits, i.e., bilateral dorsolateral or ventrolateral funiculect
omy, as well as bilateral lesions of Barrington's nucleus/locus coerul
eus area, prevented bladder inflammation. The close proximity in the C
NS of noninfected visceral circuits to infected somatic neurons would
thus permit a bystander effect, leading to activation of the sensory a
nd autonomic circuits innervating the bladder and resulting in a neuro
genic inflammation localized to the bladder. The present study indicat
es that CNS dysfunction can bring about a peripheral inflammation.