Anatomy of the central neural pathways controlling the lower urinary tract

This paper will review the central nervous control of the lower urinary tract.

Neuroanatomical, electrophysiological and pharmacological techniques have provided information about the neural circuitry and the neurotransmitters involved in the neural control of voiding.

Storage of urine is dependent in part upon spinal reflex mechanisms that activate sympathetic and somatic pathways to the urethral outlet as well as tonic inhibitory systems in the brain that suppress the parasympathetic outflow to the urinary bladder. Voiding is mediated by inhibition of sympathetic and somatic reflex pathways and activation of a spinobulbospinal parasympathetic reflex pathway passing through a micturition center in the rostral pons. Studies in animals indicate that glutamic acid is the major excitatory transmitter in the micturition reflex pathway and that a number of other transmitter mechanisms (noradrenergic, dopaminergic and GABAergic) modulate glutamatergic transmission. Damage to the brain or spinal cord can induce bladder hyperactivity by reducing central inhibitory mechanisms or by promoting a reorganization of spinal reflex pathways.

The central nervous regulation of the lower urinary tract is mediated by simple on-off switching circuits in the brain and spinal cord that are under voluntary control. Interruption of central inhibitory mechanisms can unmask primitive voiding reflexes that trigger bladder hyperactivity.