The neural control of micturition involves complex interactions between the brain, spinal cord, and peripheral nervous system, with multiple neurotransmitters playing key roles. In adults, neurological diseases or injuries can lead to involuntary micturition, causing urinary incontinence. The lower urinary tract includes the urinary bladder (reservoir) and the urethra and urethral sphincter (outlet), which are controlled by coordinated neural circuits. The bladder has two modes of operation: storage and elimination, and its control is distinct from other visceral organs due to its reliance on central nervous system (CNS) control and unique neural mechanisms. The peripheral innervation of the urinary tract involves autonomic (sympathetic and parasympathetic) and somatic (pudendal) pathways. Sympathetic nerves release noradrenaline, which relaxes the bladder and contracts the urethra, while parasympathetic nerves release acetylcholine, causing bladder contraction. Sensory nerves convey information about bladder fullness to the spinal cord, and the urothelium, the inner lining of the bladder, has sensory and signaling properties that allow it to respond to chemical and mechanical stimuli. The CNS pathways involved in micturition include connections between the brain and spinal cord, with specific regions such as the pontine micturition centre (PMC) and periaqueductal grey (PAG) playing key roles. These areas regulate bladder activity through complex interactions, including the modulation of reflex pathways and the integration of sensory input. The regulation of bladder filling and voiding involves reflex mechanisms that switch between storage and voiding modes, with the PMC and PAG being central to this process. Neurotransmitters such as glutamic acid, tachykinins, and ATP are involved in the central control of the lower urinary tract, with various receptors mediating their effects. Neuroplasticity and pathology, including spinal cord injury (SCI), can disrupt these pathways, leading to conditions such as neurogenic detrusor overactivity (NDO). Treatments such as botulinum toxin A (BoNT/A) and vanilloids (e.g., capsaicin, resiniferatoxin) have been explored for their ability to reduce detrusor overactivity and improve bladder function. New therapies for neurogenic bladder dysfunction include the use of botulinum toxin A, which can temporarily block neurotransmitter release and reduce detrusor overactivity. Additionally, the use of vanilloids has shown promise in desensitizing bladder afferents and improving symptoms in patients with detrusor overactivity. Improved bladder emptying in conditions such as prostatic hypertrophy is also a focus of research, with studies exploring the role of nitric oxide (NO) in sphincter relaxation and the potential of phosphodiesterase inhibitors in modulating NO signaling. Overall, the complex neural control of mThe neural control of micturition involves complex interactions between the brain, spinal cord, and peripheral nervous system, with multiple neurotransmitters playing key roles. In adults, neurological diseases or injuries can lead to involuntary micturition, causing urinary incontinence. The lower urinary tract includes the urinary bladder (reservoir) and the urethra and urethral sphincter (outlet), which are controlled by coordinated neural circuits. The bladder has two modes of operation: storage and elimination, and its control is distinct from other visceral organs due to its reliance on central nervous system (CNS) control and unique neural mechanisms. The peripheral innervation of the urinary tract involves autonomic (sympathetic and parasympathetic) and somatic (pudendal) pathways. Sympathetic nerves release noradrenaline, which relaxes the bladder and contracts the urethra, while parasympathetic nerves release acetylcholine, causing bladder contraction. Sensory nerves convey information about bladder fullness to the spinal cord, and the urothelium, the inner lining of the bladder, has sensory and signaling properties that allow it to respond to chemical and mechanical stimuli. The CNS pathways involved in micturition include connections between the brain and spinal cord, with specific regions such as the pontine micturition centre (PMC) and periaqueductal grey (PAG) playing key roles. These areas regulate bladder activity through complex interactions, including the modulation of reflex pathways and the integration of sensory input. The regulation of bladder filling and voiding involves reflex mechanisms that switch between storage and voiding modes, with the PMC and PAG being central to this process. Neurotransmitters such as glutamic acid, tachykinins, and ATP are involved in the central control of the lower urinary tract, with various receptors mediating their effects. Neuroplasticity and pathology, including spinal cord injury (SCI), can disrupt these pathways, leading to conditions such as neurogenic detrusor overactivity (NDO). Treatments such as botulinum toxin A (BoNT/A) and vanilloids (e.g., capsaicin, resiniferatoxin) have been explored for their ability to reduce detrusor overactivity and improve bladder function. New therapies for neurogenic bladder dysfunction include the use of botulinum toxin A, which can temporarily block neurotransmitter release and reduce detrusor overactivity. Additionally, the use of vanilloids has shown promise in desensitizing bladder afferents and improving symptoms in patients with detrusor overactivity. Improved bladder emptying in conditions such as prostatic hypertrophy is also a focus of research, with studies exploring the role of nitric oxide (NO) in sphincter relaxation and the potential of phosphodiesterase inhibitors in modulating NO signaling. Overall, the complex neural control of m