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GluR-A and GluR-B AMPA receptor subunits and NR1 but not NR GluR-A and GluR-B AMPA receptor subunits and NR1 but not NR2 NMDA receptor subunits (566). Conversely, motoneurons within the urethral sphincter nucleus express all four AMPA receptor subunits (GluR-A, -B, -C, and -D) in conjunction with moderate amounts of NR2A and NR2B also as high levels of NR1 receptor subunits. It seems most likely that thisCompr Physiol. Author manuscript; out there in PMC 2015 June Groat et al.Pagedifference in expression accounts for the different sensitivity of bladder and sphincter reflexes to glutamatergic antagonists. Glutamate also plays a role as an excitatory transmitter in the afferent limb on the micturition reflex. C-fos expression induced in spinal interneurons by activation of bladder afferents is suppressed by the administration of each NMDA and non-NMDA glutamatergic receptor antagonists (55,298,300). In contrast to excitatory effects of glutamate by means of ionotropic glutamatergic receptors (NMDA and AMPA/kinate), activation metabotropic glutamatergic receptors (mGluRs) within the spinal cord has inhibitory effects on the descending limb of the micturition reflex simply because a group I/II mGluR agonist applied towards the spinal cord in the lumbosacral level suppresses reflex bladder contractions too as those induced by PMC stimulation in rats (621). It has also been reported that mGluRs are involved in inhibition of the excitatory pathway to the EUS because a group I/II mGluR antagonist applied into the lumbosacral intrathecal space drastically facilitates the EMG activity of your EUS in rats (719). During synaptic transmission, glutamate released from presynaptic nerve terminals is cleared from the synaptic cleft into presynaptic nerve terminals and adjacent astrocytes, by means of glutamate transporters. A current study demonstrated that intrathecal application of a nonselective inhibitor of glutamate transporters, L-trans-pyrrolidine-2,4-dicarboxylic acid (L-trans-PDC) that increases endogenous glutamate concentration at nerve terminals, delays the onset of micturition by increasing intermicturition intervals and pressure thresholds in rats under urethane anesthesia (273). Inhibitory amino acids (GABA, glycine, and glycine transporter)--Intrathecal injection of either GABAA or GABAB agonists increases bladder capacity and decreases voiding stress and efficiency in regular rats (279, 501) as well as suppresses DO in rats induced with intravesical application of oxyhemoglobin, an NO scavenger (501) or spinal cord injury (435). Furthermore, intravenous or intrathecal application of a GABA reuptake inhibitor (tiagabine) that increases endogenous GABA concentrations reportedly inhibits typical micturition in rats (500). In a ) (Lu et al., 2017) in brain edema. Nonetheless, it remains unclear whether or not compact clinical study in three subjects, intrathecal administration of a GABAB receptor agonist (baclofen) increased the volume threshold for inducing the micturition reflex (89). Intrathecally administered baclofen also developed phaclofen-sensitive inhibition of distention-evoked micturition in conscious rats that appears to be resistant to capsaicin (substance P depletion) and parachlorophenylalanine (5hydroxytryptamine depletion) pretreatment (234). Because baclofen also inhibits field stimulation-evoked release of CGRP from primary afferent terminals in dorsal horn slices, one particular probable mechanism of action of GABAergic inhibition is suppression of transmitter release from main afferent terminals within the spinal cord. Preceding studies also showed that glycine, a different inhibitory amino acid, acting on.