Spinal glutamatergic NMDA-dependent pelvic nerve-to-external urethra sphincter reflex potentiation caused by a mechanical stimulation in anesthetized rats.
The current study investigates whether the spinal pelvic nerve-to-external urethra sphincter (EUS) reflex potentiation can be induced by a mechanical stimulation and whether the glutamatergic mechanism is involved in yielding such a reflex potentiation. The external urethra sphincter electromyogram (EUSE) activity, evoked by a single or by repetitive pelvic nerve stimulation, in 30 anesthetized rats was recorded with/without bladder saline distension. Without saline distension (0 cmH(2)O), a single pulse nerve stimulation evoked a single action potential in the reflex activity, whereas repetitive pelvic stimulation and saline distension (6 approximately 20 cmH(2)O) both elicited a long-lasting reflex potentiation (20.05 +/- 3.21 and 75.01 +/- 9.87 spikes/stimulation, respectively). The saline distension-induced pelvic nerve-to-EUS reflex potentiation was abolished by D-2-amino-5-phosphonovalerate [APV; a glutamatergic N -methyl-D-aspartic acid (NMDA) receptor antagonist; 100 microM, 10 microl, 1.72 +/- 0.31 spikes/stimulation] and attenuated by 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo (F) quinoxaline [NBQX; a glutamatergic alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate (AMPA) receptor antagonist; 100 microM, 10 microl, 26.16 +/- 7.27 spikes/stimulation], but was not affected by bicuculline (a GABAergic antagonist; 100 microM, 10 microl, 53.62 +/- 15.54 spikes/stimulation). Intrathecal administration of glutamate (31.12 +/- 8.25 spikes/stimulation, 100 microM, 10 microl) and NMDA (26.25 +/- 4.12 spikes/stimulation, 100 microM, 10 microl) both induced a long-lasting pelvic nerve-to-EUS reflex potentiation without saline distension, which was similar to the findings observed from saline distension only. The duration of the contraction wave of the urethra was elongated by the saline distension-induced pelvic nerve-to-EUS reflex potentiation, whereas the peak pressure of the contraction wave was not affected. Our findings suggest that saline distension in the bladder elicits a pelvic nerve-to-EUS reflex potentiation and the glutamatergic mechanism contributes to the presence of such a reflex potentiation.
Liao
Jiuan-Miaw
JM
Department of Physiology, College of Medicine, Chung-Shan Medical University Hospital, Chung-Shan Medical University, Taichung, Taiwan.
Huang
Pei-Chen
PC
Pan
Shwu-Fen
SF
Chen
Mei-Jung
MJ
Tung
Kwong-Chung
KC
Peng
Hsien-Yu
HY
Shyu
Jyh-Cherng
JC
Liou
Ying-Ming
YM
Chen
Gin-Den
GD
Lin
Tzer-Bin
TB
D000200:Action Potentials / Q000502:physiology; D000758:Anesthesia; D000818:Animals; D004106:Dilatation; D004576:Electromyography; D005260:Female; D018755:GABA Agonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000502:physiology*; D007278:Injections, Spinal; D018482:Muscle, Skeletal / Q000502:physiology; D010388:Pelvis / Q000294:innervation*; D010525:Peripheral Nerves / Q000502:physiology*; D010812:Physical Stimulation; D011312:Pressure; D051381:Rats; D017208:Rats, Wistar; D018091:Receptors, AMPA / Q000037:antagonists & inhibitors; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors / Q000502:physiology*; D012018:Reflex / Q000502:physiology*; D013119:Spinal Cord Injuries / Q000503:physiopathology; D014521:Urethra / Q000294:innervation* / Q000502:physiology
D018755:GABA Agonists; D018756:GABA Antagonists; D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid