The neural circuitry that controls urination, or micturition, is complex and highly distributed. It involves pathways at various levels of the brain, the spinal cord, and the peripheral nervous system and is under the mediation of multiple neurotransmitters.[1] To fully understand the role that the Pontine Micturition Center (PMC) plays in regulating urination requires a basic understanding of the structures and innervations involved.

The mechanisms of storing and eliminating urine depend on the coordinated activity of the two functional units of the lower urinary tract: the urinary bladder and urinary outlet. The bladders' primary function is storing urine and contracting to void the stored urine. It is comprised mainly of smooth muscle, namely the detrusor muscle. The urinary outlet through which urine passes upon exiting the bladder consists of:

• The bladder neck
• The urethra
• The urethral sphincters 

If either of the sphincters contracts, the urethra is blocked, and urine will not flow out.[2]

As a summary of innervation of these structures:

• Sympathetic innervation originates in the thoracic spine and serves to inhibit urination. Sympathetic nerves inhibit the detrusor muscle and activate the internal sphincter to contract.
• Parasympathetic innervation originates in the sacrum and serves to promote urination. Parasympathetic nerves activate the detrusor muscle causing it to contract and relax the internal sphincter.
• Both of these innervations act on the internal sphincter, which is made of smooth muscle and is an extension of the detrusor muscle.
• Both innervations are autonomic and involuntary.[1]

In contrast to the previous autonomic pathways, a third innervation is that of the somatic motor nerves, which originate in the sacrum. These nerves act primarily on the external urethral sphincter, which is composed of striated muscle, and under voluntary control. When the somatic nerves stimulate the sphincter, it contracts and prevents urine from flowing.[1] 

The PMC, also known as Barrington's nucleus, is located in the brainstem and works with other regions of the brain to coordinate micturition. The primary role of the PMC when it is activated is to stimulate urination. It achieves this through activation of parasympathetic neurons, triggering the detrusor muscle to contract and indirectly inhibits the somatic nerves that maintain the external sphincter closed in contraction.[3]

The Pontine micturition center(PMC) is located in the medial dorsal pons, close to, or includes the lateral dorsal tegmental nucleus and locus coeruleus.[4] Upon stimulation, PMC exerts dual effects of producing detrusor muscle contraction and urethral sphincter relaxation with consequent micturition. External urethral sphincter relaxation is mediated indirectly by suppressing Onuf's nucleus located in the sacral spinal cord. A PET(positron emission tomography) scan is the imaging modality that detects how tissues and organs are functioning by measuring blood flow, the extent of oxygen and sugar use. Increased blood flow has been demonstrated by PET scan in right dorsomedial pons during voiding. In contrast, PET scan during withholding of urine showed higher blood flow in the right ventral pons.[5][6] There are also suggestions that specific nuclei that control micturition predominantly exist in the right pons.[4] The pontine micturition center (PMC) coordinates the mechanical process of micturition, thus the sphincter and detrusor muscle activities of the urinary bladder. Afferents from the bladder relay on the PMC before to higher brain centers. And the higher brain centers of micturition communicate with PMC through the periaqueductal gray matter to either provoke or suppress the voiding reflex. When the urinary bladder becomes distended, the stretch receptors of the bladder wall transmits an afferent signal to the pons, which subsequently notifies the brain. This afferent signal results in a perception of bladder fullness or desire to urinate. The higher brain determines the appropriateness of initiating voiding reflex. Under typical situations, the higher brain suppresses PMC by transmitting inhibitory signals via the periaqueductal gray matter. Upon the PMC inhibition, the urge to urinate disappears, which allows delaying voiding until finding a socially acceptable place and time. In an appropriate time and place, the brain withdraws the suppression of the PMC, which allows initiating a micturition reflex. Regardless, the individual may consciously contract the pelvic floor muscles to keep the external urethral sphincter closed or suppress the voiding urgency by distracting techniques. 

Periaqueductal gray(PAG) of the mesencephalon has a potential role in integrated movement patterns of both the somatic as well as the autonomic nervous system. PAG exerts its impact on micturition by its neural projections to the PMC. In fact, no direct connections exist between PAG and the sacral cord motoneurons.  The central PAG receives afferents from the sacral cord, which in turn sends projections to the PMC. The PAG does not play an essential role in micturition reflex rather transmits afferent signals of the full bladder to higher brain centers. PAG serves only as a relay station during transmission of afferents from the bladder to the PMC. However, PMC is responsible for switching from urine storage to the voiding phase of the bladder.

A variety of neurotransmitters operate in the central control of the micturition. These neurotransmitters can categorize as excitatory such as glutamic acid, tachykinins, PACAP (pituitary-adenylate-cyclase-activating polypeptide), NO and ATP or inhibitory such as GABA  glycine, enkephalins. Glutamate binds with NMDA and non-NMDA receptors and is the essential neurotransmitters in reflex pathways controlling the bladder and the urethral sphincter. Inhibitory neurotransmitters exert a tonic inhibition in the PMC and as well as in the spinal cord.

During the third week of development, the notochord forms in the mesoderm, which in turn stimulates the differentiation of its overlying ectoderm to neuroectoderm. Later neuroectoderm thickens to form the neural plate. Neural folds form bilateral edges of the neural plate and then approach and fuse in the midline to form the neural tube. The cephalic end of the neural tube gives rise to three primary brain vesicles, prosencephalon, mesencephalon, and rhombencephalon. The rhombencephalon gives rise to the adult hindbrain by further division into secondary brain vesicles, metencephalon, and myelencephalon. Pons and cerebellum derive from the metencephalon, whereas medulla derives from the myelencephalon. Thus pontine micturition center is a part of the metencephalon of hindbrain vesicle.[7] However, reflex voiding is eventually modulated by the influence of higher brain centers until the nervous system has matured postnatally. During the prenatal period, before full maturation of the nervous system, bladder evacuation occurs by non-neural mechanisms and at later stages of development, by primitive reflex pathways at the spinal cord level. Extensive synaptic remodeling in the parasympathetic nucleus of the sacral cord and within the higher brain is an essential factor in the postnatal maturation of micturition reflexes.[1]

The pons is perfused by three sets of arteries, anteromedial, lateral, and dorsal. The anteromedial branches arise from the terminal portion of vertebral arteries and basilar artery. In contrast, the lateral branches derive from the anterior inferior cerebellar artery, superior cerebellar artery, and long pontine arteries. Finally, the dorsal group of arteries arise from the terminal superior cerebellar artery and nourish the locus coeruleus, the mesencephalic nucleus of the trigeminal nerve(CN V), and superior cerebellar peduncle. Blood supply to the pontine micturition center mostly derived from the perforating branches dorsal arteries, also, may receive the collateral circulation from the perforating branches of the anteromedial and lateral group of arteries.[8]