Molecular biological studies of neurons in the central nervous system relating to the recovery from micturition disorders in rats with central nervous damage

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1. Effects of intrathecal injections of tamsulosin (adrenergic α1A receptor antagonist) and naftopidil (adrenergicα1D receptor antagonist), on isovolumetric cystometry were investigated in rats with or without thoracic cord injury (TCI). Intrathecal injection of naftopidil transiently stopped bladder contraction, and decreased the amplitude of bladder contractions when large dose of naftopidil was administrated in rats with or without TCI. The volume of mRNA of adrenergic α1D in the lumbosacral cord did not change even after TCI. Therefore, adrenergic α1D receptors were located in both afferent and efferent limbs of the micturition reflex pathway, and serum catecholamines may also act on the spinal cord and facilitate micturition reflex.2. Cystometry and electrical myography of the external urethral sphincter were examined in TCI cats with or without autograft of the adrenal medulla into the sacral cord. In autografted cats, detrusorsphincter dyssynergia during bladder contraction improved, and tyrosine hydroxylase immuno-reactive cells were recognized in the sacral cord. Therefore, catecholamines projecting to the sacral cord may relax the urethra.3. Isovolumetric cystometry was performed before and after cerebral infarction (CI) in rats, and glutamate and glycine levels in the central nervous system were also measured. The frequency of bladder contractions increased 1-7 days after CI, but it returned to the control level 2-8 weeks after CI. Glutamate level in the cerebrum decreased, and glycine levels in the brainstem, cervicothoracic cord, and lumbosacral cord decreased after CI. However, glycine level in the lumbosacral cord returned to the control level 4-8 weeks after CI. Therefore, the frequency of bladder contractions may be depended on the glycine level in the lumbosacral cord.