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Temporal Analysis of Changes in C-FosImmunoreactivity (IR) Induced by Traumatic Brain Injury (TBI) in Rat BrainStructures Relevant to Micturition
Benjamin J. Moody, Undergraduate student, Kalev Freeman, MD, PhD, Katarina Zvarova, MD, PhD.
University of Vermont, Burlington, VT, USA.
BACKGROUND:
Lower urinary tract symptoms and dysfunction are frequent in TBI patient. Urinary incontinence, with an incidence ranging from 50% to 62%, followed by urinary retention, with incidence of approximately 8%, are the most frequent lower urinary tract symptoms reported in the literature. While a relationship between TBI and bladder dysfunction has been established, underlying pathomechanism remains unclear. The present study was undertaken to test the hypothesis that dysregulation of signal transmission contributes to the altered bladder function in animal model of TBI.
METHODS:
Control and lateral fluid-percussion TBI animals were examined. Experimental urodynamics and immunohistochemical techniques using a specific antibody against c-fos protein were used to map and correlate changes in the neuronal activity of brain structures associated with micturition, with changes in urodynamic parameters.
RESULTS:
TBI induced a significant increase in c-Fos-like IR in locus coeruleus - Barrington nucleus (LC-BN) complex (66.5±10.3 versus 5.5±3.2, p<0.001) and pontine nucleus incertus (NI) both in pars compacta ([Nic] 78.25±8.53 versus 11.33±1.54 neurons, p<0.001) and pars dissipata (NId) (16.0±5.5 versus 1.7±2.4 neurons, p<0.001). Decrease (ventrolateral [vl] 18.8±10.8 versus 48.0±19.1 neurons, p<0.001) and increase (dorsal raphe [DR] 27.3±12.3 versus 12.0±6.0 neurons, p<0.001) in neuronal activity were detected in periaquadactual grey (PAG). The injury-induced changes were coupled to a urinary retention followed by prolonged bladder filling and overdistention.
CONCLUSIONS:
These results provide immunohistochemical evidence for TBI-induced alterations in neuronal activity in central micturition regulating circuits/areas and showing that LC-BN, DR and NI activation is associated with an inhibition of voiding behavior. It suggests for the first time that traumatic brain injury-induced dysregulation in neuronal activity may alter information processing about the bladder fullness, possibly through modulation of the LC-NE response to bladder afferent impulse transmission. Chemical coding of the associated brain neuronal circuitry activated by TBI and discrimination between the injury stress- and bladder afferent-activated stimuli remains to be elucidated.
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