The Journal of Neuroscience, December 1, 1998, 18(23):10016-10029
Activation of CNS Circuits Producing a Neurogenic Cystitis:
Evidence for Centrally Induced Peripheral Inflammation
Luc
Jasmin1, 2,
Gabriella
Janni2,
Herbert
J.
Manz4, and
Samuel D.
Rabkin1, 3
Departments of 1 Neurosurgery, 2 Cell
Biology, 3 Microbiology and Immunology, and
4 Pathology, Georgetown University Medical Center,
Washington, DC 20007
We present a model of neurogenic cystitis induced by viral
infection of specific neuronal circuits of the rat CNS. Retrograde infection by pseudorabies 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 themselves or of circuits
distant from these rarely produced cystitis. Absence 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 integrity of
central bladder-related circuits is necessary for the appearance of
bladder inflammation, because only CNS lesions affecting bladder circuits, i.e., bilateral dorsolateral or ventrolateral funiculectomy, as well as bilateral lesions of Barrington's nucleus/locus coeruleus area, prevented bladder inflammation. The close proximity in the CNS of
noninfected visceral circuits to infected somatic neurons would thus
permit a bystander effect, leading to activation of the sensory and
autonomic circuits innervating the bladder and resulting in a
neurogenic inflammation localized to the bladder. The present study
indicates that CNS dysfunction can bring about a peripheral inflammation.
Key words:
neuroimmune process; herpesviridae infection; nitric-oxide synthase; mad itch; urinary bladder; pain
Copyright © 1998 Society for Neuroscience 0270-6474/98/182310016-14$05.00/0
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