Transecting the hypogastric nerve to uncover the bladder-inhibitory pathways involved with saphenous nerve stimulation in anesthetized rats

2020 ◽  
Vol 226 ◽  
pp. 102672
Author(s):  
Karly S. Franz ◽  
Paul B. Yoo
1991 ◽  
Vol 66 (2) ◽  
pp. 460-472 ◽  
Author(s):  
J. C. Leahy ◽  
R. G. Durkovic

1. We previously demonstrated in the spinal cat that superficial peroneal cutaneous nerve stimulation produced strong reflex contraction in tibialis anterior (TA) and semitendinosus (St) muscles but unexpectedly produced mixed effects in another physiological flexor muscle, extensor digitorum longus (EDL). The goal of the present study was to further characterize the organization of ipsilateral cutaneous reflexes by examining the postsynaptic potentials (PSPs) produced in St, TA, and EDL motoneurons by superficial peroneal and saphenous nerve stimulation in decerebrate, spinal cats. 2. In TA and St motoneurons, low-intensity cutaneous nerve stimulation that activated only large (A alpha) fibers [i.e., approximately 2-3 times threshold (T)], typically produced biphasic PSPs consisting of an initial excitatory phase and subsequent inhibitory phase (EPSP, IPSP). Increasing the stimulus intensity to activate both large (A alpha) and small (A delta) myelinated cutaneous fibers supramaximally (15-45 T) tended to enhance later excitatory components in TA and St motoneurons. 3. In EDL motoneurons, 2-3 T stimulation of the superficial peroneal nerve evoked initial inhibition (of variable magnitude) in 7/10 EDL motoneurons tested, with either excitation (n = 2) or mixed effects (n = 1) observed in the remaining EDL motoneurons. Saphenous nerve stimuli produced excitation either alone, or preceded by an inhibitory phase in EDL. Increasing the stimulus intensity enhanced later inhibitory influences from superficial peroneal and excitatory influences both from superficial peroneal and saphenous nerve inputs in EDL motoneurons. 4. Short-latency (less than 1.8 ms) EPSPs were observed in a few motoneurons in all reflex pathways examined, except for EPSPs in EDL motoneurons evoked by saphenous stimulation. IPSPs with central latencies less than 1.8 ms were also produced by both saphenous (TA, n = 1; EDL, n = 2) and superficial peroneal (EDL, n = 4) nerve stimulation. 5. The results, in comparison with other reports employing spinal and nonspinal preparations, suggest that removal of influences from higher centers reveals inhibitory circuits from the superficial peroneal and saphenous nerves to EDL motoneurons in the spinal preparation. The inhibitory inputs observed are thought to reflect the activation of "specialized" reflex pathways. Additionally, the demonstration of short-latency EPSPs and IPSPs suggest that the minimal linkage in both the excitatory and inhibitory cutaneous reflex pathways examined is disynaptic. The results are discussed in relation to previous studies on classically conditioned flexion reflex facilitation in spinal cat.


1984 ◽  
Vol 246 (4) ◽  
pp. F387-F394
Author(s):  
K. Inokuchi ◽  
K. U. Malik

We studied the contribution of prostaglandins to the actions of bradykinin at the renal vascular adrenergic neuroeffector junction by examining the effect of the peptide on the decrease in renal blood flow elicited by renal nerve stimulation and injected norepinephrine in pentobarbital-anesthetized rats with or without pretreatment with the cyclooxygenase inhibitors sodium meclofenamate or indomethacin. Infusion of bradykinin, 10 ng X kg-1 X min-1, into the renal artery reduced both the basal and the rise in renal vascular resistance produced by nerve stimulation or norepinephrine. The prostaglandin precursor arachidonic acid, 5 micrograms X kg-1 X min-1, infused into the renal artery, also reduced renal vascular resistance and the vasoconstrictor response elicited by either adrenergic stimulus. In animals pretreated with either sodium meclofenamate or indomethacin, the effect of arachidonic acid, but not that of bradykinin, to produce renal vasodilation and to attenuate adrenergically induced renal vasoconstriction was abolished. These data suggest that bradykinin produces renal vasodilation and inhibits the renal vasoconstrictor effect of adrenergic stimuli in the rat kidney in vivo by a mechanism unrelated to prostaglandin synthesis.


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