This study utilized neuronal c-fos expression to examine the spinal pathways involved in processing nociceptive and non-nociceptive afferent input from the lower urinary tract (LUT) of the urethane-anesthetized rat. C-fos protein was detected immunocytochemically in only a small number of cells (< 2 cells/L6 section) in control animals. However, chemical irritation with 1% acetic acid or mechanical stimulation of the LUT markedly increased the number of c-fos-positive neurons (56-180 cells/L6 section) in four regions of the caudal lumbosacral (L6-S1) spinal cord: medial dorsal horn (MDH), lateral dorsal horn, dorsal commissure (DCM), and sacral parasympathetic nucleus (SPN). Only small numbers of c-fos-positive cells were detected in rostral lumbar segments, a region that is thought to receive nociceptive input from the LUT via afferent pathways in sympathetic nerves. The distribution of c-fos-positive cells in the L6 spinal cord varied according to the stimulus (i.e., urethral catheter, bladder distension, or chemical irritation). Distension of the urinary bladder increased the number of c-fos-positive cells mainly in DCM and SPN regions of the cord. In contrast, irritation of the LUT increased c-fos expression largely in DCM and MDH areas. Spinal cord transection (T8 level) did not alter the c-fos expression induced by a catheter or chemical irritation, indicating that gene expression was mediated by spinal pathways. Denervation experiments showed that c-fos expression was induced by activation of afferent pathways in the pelvic and pudendal nerves. These results suggest that neurons in several regions of the spinal cord are involved in processing afferent input from different parts of the LUT. Neurons in the DCM appear to have an important role since they respond to both nociceptive and non-nociceptive inputs and to visceral (pelvic nerve) and somatic (pudendal nerve) afferent pathways. Thus, these neurons may be involved in the mechanisms of visceral-somatic referred pain.
The distribution of nitric oxide synthase immunoreactivity (NOS-IR) and the changes in this distribution after peripheral axotomy were examined in lumbosacral afferent and preganglionic neurons (PGNs) innervating the pelvic viscera of the male rat. The visceral neurons in L6-S1 and L1-L2 dorsal root ganglia (DRG) and in the spinal cord were identified by retrograde axonal transport following injection of Fluorogold (FG) into the major pelvic ganglion (MPG). Axotomy was performed by removing the MPG on one side 2–4 weeks prior to sacrificing the animals. A differential distribution of NOS-IR was detected in DRG cells at different segmental levels of control animals. Significantly greater numbers of NOS-IR cells were present in thoracic (T8, T10, T12; 30–44 cell profiles/section) and rostral lumbar DRGs (L1-L2; 3–15 NOS-IR cell profiles/section) compared to caudal lumbosacral (L5-S1) DRGs (0.2–0.7 cell profiles/section). A significant increase in the number of NOS-IR cells was detected in the L6-S1 DRG (p < or = 0.001; 11 NOS-IR cell profiles/section) but not in the L2 or L5 DRG ipsilateral to axotomy. In these ganglia, an average of 37.0 +/- 4.0% (L6) and 20.6 +/- 2.2% (S1), respectively, of FG-labeled pelvic afferent neurons were NOS-IR compared to 1.1 +/- 0.5% (L6) and 2.5 +/- 1.4% (S1) contralateral to the axotomy. Following axotomy, a significantly greater percentage of dye-labeled pelvic visceral afferents in the L1 and L2 DRG also exhibited NOS-IR in comparison to the contralateral side. Following axotomy, NOS-IR fibers were detected along the lateral edge of the dorsal horn extending from Lissauer's tract to the region of the sacral parasympathetic nucleus (SPN) on the ipsilateral side of the L6 and S1 spinal segments. These NOS-IR fibers were not detected in adjacent spinal segments (L4, L5, or S2). Axotomy also changed the numbers of NADPH-d-positive and NOS-IR cells in the region of the SPN in the L6 spinal segment. Contralateral to the axotomy 38.3 +/- 4.0% of PGNs in the L6 spinal segment were colabeled with NOS-IR; however, ipsilateral to axotomy, a significantly greater percentage (61.0 +/- 3.0%; p < or = 0.01) of PGNs exhibited NOS-IR. Axotomy did not alter the distribution of PGNs in the S1 segment exhibiting NOS-IR. These results indicate that NOS-IR in visceral afferent and PGNs is plastic and can be upregulated by peripheral nerve injury.
Partial urethral ligation in female Wistar rats produces changes in the neural control of the lower urinary tract including bladder hyperactivity and facilitation of a spinal micturition reflex pathway. To gain insight into the mechanisms underlying these changes, axonal tracing studies were conducted to examine the postganglionic efferent limb of the micturition reflex pathway which originates in the major pelvic ganglion (MPG). Forty microliters of the tracer Fluoro-Gold (4%) were injected into the right side of the bladder in urethral-obstructed (n = 10) and control (n = 4) rats 6 weeks after urethral ligation or sham surgery. As a control Fast blue (40 microliters, 5%) was injected into the colon to label neurons in the MPG innervating the intestine. Obstructed rats exhibited a 6-fold increase (p less than 0.001) in bladder weight (0.848 gm) compared to controls (0.148 gm). A significant increase (p less than 0.001) in the size of labeled bladder postganglionic neurons in the MPG was noted in obstructed rats (576.4 microns 2, n = 4) as compared to controls (299.6 microns 2). However, labeled, colon postganglionic neurons in the MPG in obstructed (312.9 microns 2) rats were not enlarged compared to controls (359.4 microns 2). Neuronal hypertrophy was not associated with a change in the number of labeled MPG neurons in control and obstructed groups.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of vasoactive intestinal polypeptide (VIP) in the superior cervical ganglion of the cat were studied in vitro and in vivo with sucrose gap and multiunit recording, respectively. At a dose of 0.03 to 0.12 nanomole, VIP produced a dose-dependent, prolonged (3 to 15 minutes) depolarization of the ganglion and enhanced the ganglionic depolarization elicited by the muscarinic agonist acetyl-beta-methylcholine. At a dose of 1.8 to 10 nanomoles, the peptide enhanced and prolonged the postganglionic discharge elicited by acetyl-beta-methylcholine, enhanced muscarinic transmission in ganglia treated with an anticholinesterase agent, and enhanced the late muscarinic discharge elicited by acetylcholine. VIP did not affect the early nicotinic discharge elicited by acetylcholine or by electrical stimulation of the preganglionic nerve. It is concluded that VIP has a selective facilitatory action on muscarinic excitatory mechanisms in the superior cervical ganglion of the cat.
1. In adult cats, postganglionic nerve fibres on the surface of the bladder were isolated and multiunit activity of these fibres was recorded. In these cats, the urinary bladder was cannulated and intravesical pressure was also recorded. 2. ATP, APPCP, ADP, AMP and adenosine depress transmission in vesical parasympathetic ganglia equipotently; however, 2-chloroadenosine was 10-fold more potent than ATP. 3. 2-chloroadenosine, ATP, ADP, AMP, adenosine and APPCP inhibit neurally evoked bladder contractions in the same order or potency with which they depress pelvic ganglionic transmission; however, adenine, inosine, IMP and ITP were ineffective. 4. 3',5'-cyclic AMP and dibutyryl cAMP produced little or no effect on bladder activity. 5. ATP and APPCP produced a transient rise in intravesical pressure at doses 2 to 50 times the dose needed for inhibition, presumably through ATP (P2) receptors. APPCP was 10 to 20 times more potent in exciting the bladder than ATP. 6. Theophylline and caffeine effectively antagonized purinergic effects mediated through adenosine (P1) receptors on both pelvic ganglia and bladder smooth muscle. 7. ATP inhibition of TMA-evoked bladder contractions and postganglionic nerve firing suggests that purinergic inhibition occurs, at least in part, at a postsynaptic site in the ganglia.
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