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. 2013 Apr 10;305(2):R126–R133. doi: 10.1152/ajpregu.00572.2012

Fig. 6.

Fig. 6.

Putative opioid receptor and group II mGluR mechanisms underlying the inhibitory effect of TNS on overactive bladder reflexes induced by nociceptive stimulation of the bladder with AA. Reflex pathways (right) show spinal and supraspinal circuits mediating excitatory input to the bladder activated by C-fiber and Aδ bladder afferents, respectively; an interneuronal pathway (left) mediating TNS-induced inhibition of the bladder reflexes. Interneuron-1 activated by tibial afferents releases opioid peptides and glutamate, which inhibit interneuron-3 on the spinal micturition reflex pathway by activating opioid receptors (*) and group II mGluR (#), respectively. Activation of interneuron-5 by the tibial afferent modulates TNS inhibition by eliciting GABAergic/glycinergic inhibition of interneuron-1. Presynaptic group II mGluR at sites (#) on the interneuronal-5 pathway suppress transmitter release. Block of these receptors with LY341495 enhances the inhibitory modulation of interneuron-1 and reduces TNS inhibition of the micturition reflex. Opioid receptor (*) and group II mGluR (#) mechanisms in micturition centers (PAG/PMC) in the brain stem may also contribute to TNS inhibition. The spinal mechanism for TNS enkephalinergic inhibition of the supraspinal micturition reflex pathway is not included in this figure.