Model-based analysis of the acute effects of transcutaneous magnetic spinal cord stimulation on micturition after spinal cord injury in humans
Fig 3
Enhanced model simulation of normal bladder control during storage (A) and voiding (B). The elements of the network controlling storage and voiding are highlighted (thick lines) in A (storage) and B (voiding). The activities of Nodes 4, 8 and 9 are shown sequentially in separate panels (1–3). The activity shown represents the simulated changes in membrane potential at each node, which resembles somatic neuronal activity. The activities of Nodes 4, 8 and 9 during urine storage (A and C1-3), Nodes 4 simulates volume-dependent sympathetic inhibition of detrusor contraction (C1; note that the bladder volume was increased in three large steps—each step indicated by an arrowhead below the tracing of nodal activity and each step associated with a commensurate increased in nodal activity); parasympathetic activity stimulating detrusor contraction, which is inhibited during urine storage is shown in C2; and sphincter contraction originating from the Nucleus of Onuf as represented by Node 9 as shown in C3. Activity of the PSC and inactivity of the PAG during urine storage mean that detrusor muscle relaxes and sphincter muscle contracts. During voiding, the PAG is activated, which in turn activates the PMC, the detrusor contracts (note high activity in the parasympathetic preganglionic Node 8 (D2), and the sphincter relaxes so that activity in Node 9 is reduced. In order to permit the detrusor to contract, sympathetic inhibition of the detrusor is withdrawn, and Node 4 is quiet, thereby enabling urine to flow out of the bladder during detrusor contraction. This figure was created in part with BioRender.com.