Acute unilateral ureteral distension inhibits glutamate-dependent spinal pelvic-urethra reflex potentiation via GABAergic neurotransmission in anesthetized rats.
The effects of an acute increase in intraureteral pressure (IUP) on pelvic-urethra reflex potentiation were examined in urethane-anesthetized rats by recording the external urethral sphincter electromyogram activities evoked by the pelvic afferent stimulation. Compared with a single action potential elicited by the test stimulation (TS; characterized by an intensity that evoked a constant reflex response without facilitation, 1/30 Hz, 1.03 +/- 0.12 spikes/stimulation, n = 7), the repetitive stimulation [RS; identical stimulation intensity as the TS (1 Hz)] significantly induced spinal reflex potentiation (SRP; 16.90 +/- 2.00 spikes/stimulation, P < 0.01, n = 7). Such SRP was significantly attenuated by intrathecal 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo (F) quinoxaline [NBQX; a glutamatergic alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionat (AMPA) receptor antagonist] and d-2-amino-5-phosphonovalerate [APV; a glutamatergic N-methyl-d-aspartate (NMDA) antagonist; the spike number per stimulation: 11.0 +/- 0.70 for NBQX, 1.01 +/- 0.30 for APV, and 16.90 +/- 2.0 for RS, respectively, n = 7, P < 0.01]. Acute stepwise elevations of IUP gradually attenuated and eventually abolished the RS-induced SRP (16.80 +/- 1.30, 17.00 +/- 1.30, 16.30 +/- 1.30, 10.50 +/- 1.80, 8.80 +/- 1.90, 3.50 +/- 1.60, 0.80 +/- 0.20, 0.70 +/- 0.20, and 0.20 +/- 0.10 spikes/stimulation at intraureteral pressure of 0, 2.5, 5, 7.5, 10, 12.5, 15, 17.5, and 20 cmH(2)O, respectively, n = 7). Intrathecal NMDA (a glutamatergic NMDA receptor agonist) and bicuculline (a GABA receptor antagonist) both reversed the abolition of RS-induced SRP caused by unilateral ureteral distension (14.0 +/- 4.04 and 8.00 +/- 1.53 spikes/stimulation, respectively, n = 7, P < 0.01). All the results suggested unilateral ureteral distension might compensatorily relax the urethra via GABAergic inhibition of NMDA-dependent SRP.
Chen
Kuo-Jung
KJ
Institute of Medicine, College of Medicine, Chung-Shan Medical University,Taichung, Taiwan.
Peng
Hsien-Yu
HY
Cheng
Chen-Li
CL
Chen
Cheng-Hsu
CH
Liao
Jiuan-Miaw
JM
Ho
Yu-Cheng
YC
Liou
Jung-Tong
JT
Tung
Kwong-Chung
KC
Hsu
Tien-Huan
TH
Lin
Tzer-Bin
TB
D000200:Action Potentials / Q000187:drug effects; D000344:Afferent Pathways / Q000187:drug effects; D000758:Anesthesia; D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D004576:Electromyography; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005260:Female; D018756:GABA Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000378:metabolism* / Q000494:pharmacology; D006874:Hydrostatic Pressure; D017774:Long-Term Potentiation / Q000187:drug effects; D016202:N-Methylaspartate / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012018:Reflex / Q000187:drug effects / Q000502:physiology*; D013127:Spinal Nerves / Q000187:drug effects / Q000503:physiopathology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D014513:Ureter / Q000294:innervation / Q000503:physiopathology*; D014521:Urethra / Q000187:drug effects / Q000294:innervation / Q000503:physiopathology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D016202:N-Methylaspartate; D001640:Bicuculline