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Figure 9 | Bioelectronic Medicine

Figure 9

From: Impact of Bioelectronic Medicine on the Neural Regulation of Pelvic Visceral Function

Figure 9

Model showing putative circuitry and neurotransmitters involved in inhibition of reflex bladder overactivity elicited by TNS in a cat with an intact spinal cord. Bladder overactivity is elicited by intravesical infusion of dilute acetic acid and is mediated by both spinal and supraspinal pathways triggered by both Aδ and C-fiber bladder afferents. Note that TNS does not inhibit reflex bladder activity in the acute spinal cord transected preparation shown in Figure 8. It is likely that the inhibition occurs at a supraspinal site. Tibial nerve afferents activate (presumably by the releases of glutamate and stimulation of glutamatergic receptors) a spinal tract neuron that transmits information to the brain (left side). The receptors may be mGluR2/3 subtypes because LY341495, an mGluR2/3 antagonist, suppresses TNS inhibition. Because naloxone, an opioid receptor antagonist, blocks TNS inhibition, it is likely that the inhibition of the supraspinal micturition reflex pathway occurs at the level of the PAG-PMC and is mediated by release of an opioid peptide. Activation of opioid receptors in the brain with drugs suppresses reflex bladder activity, and intracerebroventricular injection of naloxone enhances bladder reflexes, indicating that the reflexes are tonically suppressed by endogenously released opioid peptides. *Excitatory glutamatergic transmission at the tibial nerve afferent terminal or in the micturition reflex pathway in the spinal cord.

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