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1Department of Physiology, College of Medicine, 7Department of Obstetrics and Gynecology, Chung-Shan Medical University Hospital, Chung-Shan Medical University, 2Department of Cosmetic Science, Providence University, 3Division of Urology, Department of Surgery, Taichung Veterans General Hospital, and 8Department of Veterinary Medicine, College of Veterinary Medicine, Chung-Hsing University, Taichung; Departments of 4Biotechnology and 5Medical Engineering, Ming-Chuan University, Taoyuan; and 6School of Medicine, Kao-Hsiung Medical University, Kaohsiung, Taiwan
Submitted 30 July 2006 ; accepted in final form 5 January 2007
The purposes of this study were to investigate whether the pelvic nerve-to-external urethra sphincter (EUS) reflex potentiation can be induced under physiological conditions and to determine whether glutamatergic neurotransmission is involved in the reflex potentiation. Stimulation-evoked reflex activities, during rhythmic bladder contractions caused by a continuous saline infusion, in 21 anesthetized rats were recorded with/without the intrathecal administration of 10 µl of CNQX (a glutamatergic AMPA receptor antagonist; 100 µM) and APV( a glutamatergic NMDA receptor antagonist; 100 µM). Reflex activities became potentiated following the increment of intravesical pressure (IVP) during the storage phase (2.39 ± 0.28 spikes/mmHg, n = 21) and the ascending period of the voiding phase (1.46 ± 0.35 spikes/mmHg, n = 21) and decreased following the decrement of IVP during the descending period of the voiding phase (1.50 ± 0.33 spikes/mmHg, n = 21). Although it is characterized by a low IVP, a postvoiding reflex potentiation in stimulation-evoked activities was elicited at the critical period after a voiding contraction had just finished (23.95 ± 8.96 spikes/mmHg, n = 21). The slope of the regression line of evoked activities vs. the IVP during the storage phase was significantly (P < 0.01) higher than that of the ascending and descending periods of the voiding phase, but there was no statistical difference between the ascending and the descending periods (P > 0.05). In addition, the slope of the regression line of posttetanic reflex potentiation was significantly higher than that of the storage phase (P < 0.01). All the slopes of the regression lines decreased after intrathecal CNQX administration (from 3.15 ± 0.44, 2.10 ± 0.57, 2.13 ± 0.53, and 21.30 ± 3.41 to 0.83 ± 0.31, 0.74 ± 0.12, 0.76 ± 0.12, and 4.31 ± 3.71 spikes/mmHg in storage, ascending and descending period of the voiding phase, and postvoiding potentiation, respectively; all P < 0.01, n = 10). The slopes of the regression lines became almost horizontal after intrathecal APV administration (from 3.15 ± 0.44, 2.10 ± 0.57, 2.13 ± 0.53, and 21.30 ± 3.41 to 0.16 ± 0.12, 0.21 ± 0.07, 0.18 ± 0.05, and 0.23 ± 0.76 spikes/mmHg in storage, ascending and descending period of voiding phase, and postvoiding potentiation, respectively; all P < 0.01, n = 10). Our results suggest that a potentiation in the pelvic nerve-to-EUS reflex can be induced under physiological conditions and the glutamatergic mechanism appears to be involved in this reflex potentiation.
postvoiding potentiation; posttetanic potentiation; glutamate
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