Neurourology and urodynamics vol:30 issue:6 pages:855-856
41st Annual Meeting of the International-Continence-Society (ICS) Glasgow, SCOTLAND, AUG 29-SEP 02, 2011
Hypothesis / aims of study
Since decades, the bladder contraction upon instillation of ice-cold saline in the bladder has been used in the clinic as a diagnostic test for neurogenic detrusor overactivity (NDO). Similar bladder contractions have been shown in urethane anaesthetized cats, guinea pigs and rats with intact neuraxis (1). This bladder cooling reflex is also present in a significant percentage of patients with other urological conditions, such as overactive bladder (OAB) (2). It is hypothesized that this bladder cooling reflex is mediated via unmyelinated afferent C-fibers, which is different than the normal micturition reflex, which is controlled via the myelinated afferent Aδ-fibers. The presence of the reflex could indicate emerging C-fiber function and could reflect modifications that occur in pathological states. The exact neuronal mechanism and the cellular origin and molecular nature of the cold sensors underlying this reflex are unknown.
The TRP superfamily represents a diverse group of ion channels which are regulated by a wide range of physical and chemical stimuli. A subset of the TRP superfamily exhibits particularly high sensitivity to changes in temperature. Expression of the cold-activated TRPA1 and TRPM8 has been reported in afferent neurons of the lower urinary tract (3).
The infliction of a spinal cord injury (SCI) in rats is well described and leads to NDO. We decided to test the bladder cooling reflex in urethane anaesthetized and in SCI rats. We hypothesized that TRPA1 plays a crucial role in the bladder cooling reflex. The long term purpose of this study will be to ameliorate the therapeutic arsenal to relieve patients with NDO and OAB.