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1
Sun, Shu-Yu, Wei Wang, and Harold D. Schultz. "Activation of cardiac afferents by arachidonic acid: relative contributions of metabolic pathways." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 1 (July 1, 2001): H93—H104. http://dx.doi.org/10.1152/ajpheart.2001.281.1.h93.
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Arachidonic acid (AA) is metabolized via cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P-450 (CP450) pathways to a variety of bioactive products. The sensitivity of cardiac afferent endings to AA and its metabolites, especially those derived from LOX and CP450 pathways, is currently unclear. We examined AA-induced activation of cardiac vagal chemosensitive afferents in non- and postischemic hearts in rats and evaluated the relative contributions of the three metabolic pathways to the effects. Epicardial application of AA activated the cardiac afferents dose dependently in both nonischemic and postischemic hearts, with afferent responses greater in the latter condition. In nonischemic hearts, the afferent response to AA was abolished only after simultaneous administration of indomethacin and 17-octadecynoic acid (COX and CP450 inhibitors, respectively). Nordihydroguaiaretic acid (a LOX inhibitor) had no effect on the afferent response to AA. In postischemic hearts, abolition of the afferent response to AA required simultaneous blockade of all three pathways. None of the AA metabolic inhibitors affected resting activity of cardiac afferents in nonischemic hearts, but each suppressed afferent activity during ischemia-reperfusion. Most COX metabolites, CP450 metabolites, and 5-LOX metabolites tested were capable of activating cardiac afferents. The 12-LOX metabolites and 15-LOX metabolites had no effect on afferent activity. These data indicate that in the nonischemic heart, basal AA metabolism does not contribute to resting afferent activity, but AA is capable of activating cardiac afferents via COX and CP450 but not LOX pathways. During ischemia-reperfusion, all three metabolic pathways contribute to activation of cardiac vagal afferents with an enhanced responsiveness to AA. Our results suggest that induction of the 5-LOX pathway contributes to the enhanced sensitivity of cardiac vagal afferents to AA in the ischemic condition.
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Nelson, David W., James W. Sharp, Mark S. Brownfield, Helen E. Raybould, and Denise M. Ney. "Localization and Activation of Glucagon-Like Peptide-2 Receptors on Vagal Afferents in the Rat." Endocrinology 148, no. 5 (May 1, 2007): 1954–62. http://dx.doi.org/10.1210/en.2006-1232.
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Glucagon-like peptide-2 (GLP-2) is a nutrient-dependent proglucagon-derived hormone that stimulates intestinal growth through poorly understood paracrine and/or neural pathways. The relationship between GLP-2 action and a vagal pathway is unclear. Our aims were to determine whether 1) the GLP-2 receptor (GLP-2R) is expressed on vagal afferents by localizing it to the nodose ganglia; 2) exogenous GLP-2 stimulates the vagal afferent pathway by determining immunoreactivity for c-fos protein in the nucleus of the solitary tract (NTS); and 3) functional ablation of vagal afferents attenuates GLP-2-mediated intestinal growth in rats maintained with total parenteral nutrition (TPN). A polyclonal antibody against the N terminus of the rat GLP-2R was raised and characterized. The GLP-2R was localized to vagal afferents in the nodose ganglia and confirmed in enteroendocrine cells, enteric neurons, and nerve fibers in the myenteric plexus using immunohistochemistry. Activation of the vagal afferent pathway, as indicated by c-fos protein immunoreactivity in the NTS, was determined by immunohistochemistry after ip injection of 200 μg human GLP-2. GLP-2 induced a significant 5-fold increase in the number of c-fos protein immunoreactive neurons in the NTS compared with saline. Ablation of vagal afferent function by perivagal application of capsaicin, a specific afferent neurotoxin, abolished c-fos protein immunoreactivity, suggesting that activation of the NTS due to GLP-2 is dependent on vagal afferents. Exogenous GLP-2 prevented TPN-induced mucosal atrophy, but ablation of vagal afferent function with capsaicin did not attenuate this effect. This suggests that vagal-independent pathways are responsible for GLP-2 action in the absence of luminal nutrients during TPN, possibly involving enteric neurons or endocrine cells. This study shows for the first time that the GLP-2R is expressed by vagal afferents, and ip GLP-2 activates the vagal afferent pathway.
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Xu, Linjing, and G. F. Gebhart. "Characterization of Mouse Lumbar Splanchnic and Pelvic Nerve Urinary Bladder Mechanosensory Afferents." Journal of Neurophysiology 99, no. 1 (January 2008): 244–53. http://dx.doi.org/10.1152/jn.01049.2007.
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Sensory information from the urinary bladder is conveyed via lumbar splanchnic (LSN) and sacral pelvic (PN) nerves to the spinal cord. In the present report we compared the mechanosensitive properties of single afferent fibers in these two pathways using an in vitro mouse bladder preparation. Mechanosensitive primary afferents were recorded from the LSN or PN and distinguished based on their response to receptive field stimulation with different mechanical stimuli: probing (160 mg to 2 g), stretch (1–25 g), and stroking of the urothelium (10–1,000 mg). Four different classes of afferent were recorded from the LSN and PN: serosal, muscular, muscular/urothielial, and urothelial. The LSN contained principally serosal and muscular afferents (97% of the total sample), whereas all four afferent classes of afferent were present in the PN (63% of which were muscular afferents). In addition, the respective proportions and receptive field distributions differed between the two pathways. Both low- and high-threshold stretch-sensitive muscular afferents were present in both pathways, and muscular afferents in the PN were shown to sensitize after exposure to an inflammatory soup cocktail. The LSN and PN pathways contain different populations of mechanosensitive afferents capable of detecting a range of mechanical stimuli and individually tuned to detect the type, magnitude, and duration of the stimulus. This knowledge broadens our understanding of the potential roles these two pathways play in conveying mechanical information from the bladder to the spinal cord.
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Kirk, M. D. "Presynaptic inhibition in the crayfish CNS: pathways and synaptic mechanisms." Journal of Neurophysiology 54, no. 5 (November 1, 1985): 1305–25. http://dx.doi.org/10.1152/jn.1985.54.5.1305.
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I studied the pathways that produce primary afferent depolarization (PAD) and presynaptic inhibition during crayfish escape behavior. Simultaneous intracellular recordings were obtained from interneurons and primary afferent axons in the neuropil of the sixth abdominal ganglion. In several experiments, a sucrose-gap recording of PAD accompanied the intracellular impalements. I have identified PAD-producing inhibitory interneurons (PADIs) that are fired by a single impulse in the lateral (LG) or medial (MG) giant, escape-command axons; the PADIs appear to be directly responsible for presynaptic inhibition of primary afferent input to identified mechanosensory interneurons. PADI spikes, elicited by injection of depolarizing current, produced unitary PAD with constant short latency (mean = 0.97 +/- 0.12 SD ms). The unitary PADs were capable of following PADI impulses one for one at frequencies greater than 100 Hz, and the amplitude of unitary PAD was increased by injection of chloride into the afferent terminals. Therefore, the PADIs appear to directly produce an increase in chloride conductance in the primary afferent terminals. Intracellular injections of Lucifer yellow or horseradish peroxidase (HRP) revealed three morphological types of PADI. Their axonal branches and terminals are bilateral and overlap extensively with the innervation fields of all 10 sensory roots of the sixth ganglion. The three morphological types of PADI were physiologically indistinguishable. In several cases, the impaled PADI was shown to produce unitary PAD in more than one afferent of a given root as well as in afferents of adjacent roots. Therefore, the PADIs appear to diverge widely and contact many afferents in all of the sixth-ganglion sensory roots. Stimulation, caudal to the fifth ganglion, of an MG that had been interrupted rostral to the fifth ganglion produced no PAD in sixth-ganglion afferents. Also, stimulation of an MG or an LG in a surgically isolated sixth abdominal ganglion failed to produce PAD. Therefore, the pathway between the MGs and PADIs is activated exclusively within the rostral abdominal ganglia. Direct stimulation in the second and third abdominal ganglia of the segmental giants (SGs) produced a polysynaptic, suprathreshold response in the PADIs. This response was compound and was not due to the activity of the identified corollary discharge interneurons, CDI-2 and CDI-3, that are fired by the SGs. Therefore, the primary input to the PADIs must come from other, unidentified CDIs that are driven by the SGs. PADIs were not fired by shocks to the sensory portions of any peripheral roots even though these shocks produced PAD.(ABSTRACT TRUNCATED AT 400 WORDS)
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Friemert, B., S. Franke, A. Gollhofer, L. Claes, and M. Faist. "Group I Afferent Pathway Contributes to Functional Knee Stability." Journal of Neurophysiology 103, no. 2 (February 2010): 616–22. http://dx.doi.org/10.1152/jn.00172.2009.
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The hamstring reflex response has been suggested to play a substantial role in knee joint stabilization during anterior tibial translation. The present study was performed to determine which afferent pathways contribute to the hamstring reflex as well as the potential effects of specific afferent pathways on functional knee stability. Short- and medium-latency hamstring reflexes (SLR and MLR) were evoked by anterior tibial translation in 35 healthy subjects during standing with 30° knee flexion. Nerve cooling, tizanidine, and ischemia were employed to differentiate afferent pathways. Two hours of thigh cooling ( n = 10) resulted in a significant increase in MLR latency and, to a lesser extent, SLR latency. No significant changes were recorded in reflex sizes or maximum tibial translation. The ingestion of tizanidine ( n = 10), a suppressor of group II afferents, strongly reduced the MLR size while SLR size or latency of both reflex responses was not significantly affected. Maximum tibial translation was unchanged [5.3 ± 1.9 to 4.8 ± 2 (SD) mm; P = 0.410]. Ischemia in the thigh ( n = 15) led to a highly significant depression in SLR size (89 ± 4%; P < 0.001) but only a slight and not significant decline of MLR size. In these subjects maximum tibial translation increased significantly (6.9 ± 1.6 to 9.4 ± 3.2 mm; P = 0.028). It is concluded that the hamstring SLR is mediated by Ia afferents, while group II afferents mainly contribute to the MLR. Suppression of SLR may increase maximum anterior tibial translation, thus indicating a possible functional role of Ia afferents in knee joint stabilization.
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Liu, C. Y., M. H. Mueller, D. Grundy, and M. E. Kreis. "Vagal modulation of intestinal afferent sensitivity to systemic LPS in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 292, no. 5 (May 2007): G1213—G1220. http://dx.doi.org/10.1152/ajpgi.00267.2006.
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The central nervous system modulates inflammation in the gastrointestinal tract via efferent vagal pathways. We hypothesized that these vagal efferents receive synaptic input from vagal afferents, representing an autonomic feedback mechanism. The consequence of this vagovagal reflex for afferent signal generation in response to LPS was examined in the present study. Different modifications of the vagal innervation or sham procedures were performed in anesthetized rats. Extracellular mesenteric afferent nerve discharge and systemic blood pressure were recorded in vivo before and after systemic administration of LPS (6 mg/kg iv). Mesenteric afferent nerve discharge increased dramatically following LPS, which was unchanged when vagal efferent traffic was eliminated by acute vagotomy. In chronically vagotomized animals, to eliminate both vagal afferent and efferent traffic, the increase in afferent firing 3.5 min after LPS was reduced to 3.2 ± 2.5 impulses/s above baseline compared with 42.2 ± 2.0 impulses/s in controls ( P < 0.001). A similar effect was observed following perivagal capsaicin, which was used to eliminate vagal afferent traffic only. LPS also caused a transient hypotension (<10 min), a partial recovery, and then persistent hypertension that was exacerbated by all three procedures. Mechanosensitivity was increased 15 min following LPS but had recovered at 30 min in all subgroups except for the chronic vagotomy group. In conclusion, discharge in capsaicin-sensitive mesenteric vagal afferents is augmented following systemic LPS. This activity, through a vagovagal pathway, helps to attenuate the effects of septic shock. The persistent hypersensitivity to mechanical stimulation after chronic vagal denervation suggests that the vagus exerts a regulatory influence on spinal afferent sensitization following LPS.
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Mazzone, Stuart B., and Bradley J. Undem. "Vagal Afferent Innervation of the Airways in Health and Disease." Physiological Reviews 96, no. 3 (July 2016): 975–1024. http://dx.doi.org/10.1152/physrev.00039.2015.
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Vagal sensory neurons constitute the major afferent supply to the airways and lungs. Subsets of afferents are defined by their embryological origin, molecular profile, neurochemistry, functionality, and anatomical organization, and collectively these nerves are essential for the regulation of respiratory physiology and pulmonary defense through local responses and centrally mediated neural pathways. Mechanical and chemical activation of airway afferents depends on a myriad of ionic and receptor-mediated signaling, much of which has yet to be fully explored. Alterations in the sensitivity and neurochemical phenotype of vagal afferent nerves and/or the neural pathways that they innervate occur in a wide variety of pulmonary diseases, and as such, understanding the mechanisms of vagal sensory function and dysfunction may reveal novel therapeutic targets. In this comprehensive review we discuss historical and state-of-the-art concepts in airway sensory neurobiology and explore mechanisms underlying how vagal sensory pathways become dysfunctional in pathological conditions.
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Webster, W. Andrew, and Michael J. Beyak. "The long chain fatty acid oleate activates mouse intestinal afferent nerves in vitro." Canadian Journal of Physiology and Pharmacology 91, no. 5 (May 2013): 375–79. http://dx.doi.org/10.1139/cjpp-2012-0138.
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Vagal afferents innervating the gastrointestinal tract serve an important nutrient-sensing function, and these signals contribute to satiety. Detection of nutrients occurs largely through the release of mediators from specialized enteroendocrine cells within the mucosa of the gastrointestinal tract. The signaling pathways leading to vagal afferent activation are not clear; however, previous in-vivo studies have implicated a role for cholecystokinin (CCK). We used an in vitro intestinal afferent extracellular recording preparation to study the effect of luminal perfusion of the long chain fatty acid oleate on mouse intestinal afferent activity. Oleate activated intestinal afferents in a concentration-dependent fashion, with an EC50 value of approximately 25 mmol/L. The L-type calcium channel blocker nicardipine attenuated the effect of oleate. Vagotomy resulted in a significant (>60%) reduction of the responses to both oleate and CCK. The CCK-1 receptor antagonist lorglumide nearly abolished responses to CCK and oleate. Our experiments therefore suggest that oleate activates intestinal afferents, with vagal afferents primarily involved; however, nonvagal fibres also contribute. The activation is dependent on CCK release, likely via activation of L-type channels on mucosal enteroendocrine cells, finally resulting in activation of CCK-1 receptors on the afferent terminals.
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Joris, Philip X., and Tom C. T. Yin. "Envelope Coding in the Lateral Superior Olive. III. Comparison With Afferent Pathways." Journal of Neurophysiology 79, no. 1 (January 1, 1998): 253–69. http://dx.doi.org/10.1152/jn.1998.79.1.253.
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Joris, Philip X. and Tom C. T. Yin. Envelope coding in the lateral superior olive. III. Comparison with afferent pathways. J. Neurophysiol. 79: 253–269, 1998. Binaural cues for spatial localization of complex high-frequency sounds are interaural level and time differences (ILDs and ITDs). We previously showed that cells in the lateral superior olive (LSO) are sensitive to ITDs in the envelope of sinusoidally amplitude-modulated (AM) signals up to a modulation frequency of only ∼800 Hz. To understand the limitations in this ITD-sensitivity, we here compare responses to monaural modulation in LSO and its input pathways, derived from cochlear nucleus and medial nucleus of the trapezoid body. These pathways have marked functional and morphological specializations, suggestive of adaptations for timing. Afferent cell populations were identified on the basis of electrophysiological signatures, and for each population, average firing rate and synchronization to AM tones were compared with auditory-nerve fibers and LSO cells. Except for an increase in modulation gain in some subpopulations, synchronization of LSO afferents was very similar to that in auditory nerve fibers in its dependency on sound pressure level (SPL), modulation depth, and modulation frequency. Distributions of cutoff frequencies of modulation transfer functions were largely coextensive with the distribution in auditory nerve. Group delays, measured from the phase of the response modulation as a function of modulation frequency, showed an orderly dependence on characteristic frequency and cell type and little dependence on SPL. Similar responses were obtained to a modulated broadband carrier. Compared with their afferents, LSO cells synchronized to monaurally modulated stimuli with a higher gain but often over a narrower range of modulation frequencies. Considering the scatter in afferent and LSO cell populations, ipsi- and contralateral responses were well matched in cutoff frequency and magnitude of delays. In contrast to their afferents, LSO cells show a decrease in average firing rate at high modulation frequencies. We conclude that the restricted modulation frequency range over which LSO cells show ITD-sensitivity does not result from loss of envelope information along the afferent pathway but is due to convergence or postsynaptic effects at the level of the LSO. The faithful transmission of envelope phase-locking in LSO afferents is consistent with their physiological and morphological adaptations, but these adaptations are not commensurate with the rather small effects of physiological ITDs reported previously, especially when compared with effects of ILDs. We suggest that these adaptations have evolved to allow a comparison of instantaneous amplitude fluctuations at the two ears rather than to extract interaural timing information per se.
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Ryan, Stephen, and Philip Nolan. "Superior laryngeal and hypoglossal afferents tonically influence upper airway motor excitability in anesthetized rats." Journal of Applied Physiology 99, no. 3 (September 2005): 1019–28. http://dx.doi.org/10.1152/japplphysiol.00776.2004.
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Upper airway (UA) muscle activity is stimulated by changes in UA transmural pressure and by asphyxia. These responses are reduced by muscle relaxation. We hypothesized that this is due to a change in afferent feedback in the ansa hypoglossi and/or superior laryngeal nerve (SLN). We examined 1) the glossopharyngeal motor responses to UA transmural pressure and asphyxia and 2) how these responses were changed by muscle relaxation in animals where one or both of these afferent pathways had been sectioned bilaterally. Experiments were performed in 24 anesthetized, thoracotomized, artificially ventilated rats. Baseline glossopharyngeal activity and its response to UA transmural pressure and asphyxia were moderately reduced after bilateral section of the ansa hypoglossi ( P < 0.05). Conversely, bilateral SLN section increased baseline glossopharyngeal activity, augmented the response to asphyxia, and abolished the response to UA transmural pressure. Muscle relaxation reduced resting glossopharyngeal activity and the response to asphyxia ( P < 0.001). This occurred whether or not the ansa hypoglossi, the SLN, or both afferent pathways had been interrupted. We conclude that ansa hypoglossi afferents tonically excite and SLN afferents tonically inhibit UA motor activity. Muscle relaxation depressed UA motor activity after section of the ansa hypoglossi and SLN. This suggests that some or all of the response to muscle relaxation is mediated by alterations in the activity of afferent fibers other than those in the ansa hypoglossi or SLN.
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Montgomery, J., D. Bodznick, and M. Halstead. "Hindbrain signal processing in the lateral line system of the dwarf scorpionfish Scopeana papillosus." Journal of Experimental Biology 199, no. 4 (April 1, 1996): 893–99. http://dx.doi.org/10.1242/jeb.199.4.893.
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Recordings were made from primary afferent fibres and secondary projection neurones (crest cells) in the mechanosensory lateral line system of the dwarf scorpionfish. Crest cells were identified by antidromic stimulation from the contralateral midbrain. Differences between primary afferent fibre and crest cell response characteristics are indicative of signal processing by the neuronal circuitry of the medial octavolateralis nucleus. There are a number of differences between primary afferent fibres and crest cells. Primary afferents have relatively high levels of spontaneous activity (mean close to 40 impulses s-1) and many of them are strongly modulated by ventilation. By contrast, crest cells have a much lower rate of spontaneous activity that is not obviously modulated by ventilation. Primary afferents show a simple tonic response to a maintained stimulus, whereas crest cells show a variety of temporal response properties, but in general show a phasic/tonic response to the same prolonged stimulus. Afferents are most sensitive to frequencies of stimulation around 100 Hz; in contrast, crest cells show a strong suppression of activity at this frequency. Crest cells are most responsive around 50 Hz. These afferent/secondary comparisons show similarities with those reported for allied electrosensory and auditory pathways.
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Loening-Baucke, V., N. W. Read, and T. Yamada. "Further evaluation of the afferent nervous pathways from the rectum." American Journal of Physiology-Gastrointestinal and Liver Physiology 262, no. 5 (May 1, 1992): G927—G933. http://dx.doi.org/10.1152/ajpgi.1992.262.5.g927.
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To evaluate the visceral afferents from the rectum, we recorded cerebral evoked potentials (EPs) in 26 healthy subjects after electrical stimulation of the rectum, pudendal nerve, and posterior tibialis nerve. We found two distinctly different EPs after rectal stimulation, with differences in latencies and pattern. In 13 subjects (group 1), the EP after rectal stimulation had multiple prominent peaks with early onset latencies ranging from 22 to 29 ms (mean 26 ms). In 13 subjects (group 2), the EP after rectal stimulation had a trifid configuration due to a very prominent negative peak between 97 and 108 ms (mean 101 ms) and longer onset latencies ranging from 50 to 61 ms (mean 55 ms). Latencies after pudendal nerve and posterior tibialis nerve stimulation were similar in the two groups. On further study, we found that both types of afferent pathways are present in the distal colon, since both types of EPs were found in the same subjects either in the rectum or in the rectum and sigmoid. We speculate that the early onset EP is a visceral pathway using the same afferents as the pudendal nerve because the early onset EP after rectal stimulation appears similar in number of peaks and interpeak latencies to EPs recorded after pudendal nerve stimulation, and the late onset EP is a visceral pathway using afferents along the pelvic nerve. Early onset EPs were also recorded after sigmoid stimulation, suggesting that both kinds of EPs are visceral afferents.
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BLATTEIS, CLARK M., ELMIR SEHIC, and SHUXIN LI. "Afferent Pathways of Pyrogen Signalinga." Annals of the New York Academy of Sciences 856, no. 1 MOLECULAR MEC (September 1998): 95–107. http://dx.doi.org/10.1111/j.1749-6632.1998.tb08318.x.
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de Groat, W. C. "Neuropeptides in pelvic afferent pathways." Experientia 43, no. 7 (July 1987): 801–13. http://dx.doi.org/10.1007/bf01945358.
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Harrington, Andrea M., Sonia Garcia Caraballo, Jessica E. Maddern, Luke Grundy, Joel Castro, and Stuart M. Brierley. "Colonic afferent input and dorsal horn neuron activation differs between the thoracolumbar and lumbosacral spinal cord." American Journal of Physiology-Gastrointestinal and Liver Physiology 317, no. 3 (September 1, 2019): G285—G303. http://dx.doi.org/10.1152/ajpgi.00013.2019.
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The distal colon is innervated by the splanchnic and pelvic nerves, which relay into the thoracolumbar and lumbosacral spinal cord, respectively. Although the peripheral properties of the colonic afferent nerves within these pathways are well studied, their input into the spinal cord remain ill defined. The use of dual retrograde tracing from the colon wall and lumen, in conjunction with in vivo colorectal distension and spinal neuronal activation labeling with phosphorylated MAPK ERK 1/2 (pERK), allowed us to identify thoracolumbar and lumbosacral spinal cord circuits processing colonic afferent input. In the thoracolumbar dorsal horn, central projections of colonic afferents were primarily labeled from the wall of the colon and localized in laminae I and V. In contrast, lumbosacral projections were identified from both lumen and wall tracing, present within various dorsal horn laminae, collateral tracts, and the dorsal gray commissure. Nonnoxious in vivo colorectal distension evoked significant neuronal activation (pERK-immunoreactivity) within the lumbosacral dorsal horn but not in thoracolumbar regions. However, noxious in vivo colorectal distension evoked significant neuronal activation in both the thoracolumbar and lumbosacral dorsal horn, with the distribution of activated neurons correlating to the pattern of traced projections. Dorsal horn neurons activated by colorectal distension were identified as possible populations of projection neurons or excitatory and inhibitory interneurons based on their neurochemistry. Our findings demonstrate how colonic afferents in splanchnic and pelvic pathways differentially relay mechanosensory information into the spinal cord and contribute to the recruitment of spinal cord pathways processing non-noxious and noxious stimuli. NEW & NOTEWORTHY In mice, retrograde tracing from the colon wall and lumen was used to identify unique populations of afferent neurons and central projections within the spinal cord dorsal horn. We show that there are pronounced differences between the spinal cord regions in the distribution pattern of colonic afferent central projections and the pattern of dorsal horn neuron activation evoked by colorectal distension. These findings demonstrate how colonic afferent input influences spinal processing of colonic mechanosensation.
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Zhao, Weiying, A. Daniel Martin, and Paul W. Davenport. "Detection of inspiratory resistive loads in double-lung transplant recipients." Journal of Applied Physiology 93, no. 5 (November 1, 2002): 1779–85. http://dx.doi.org/10.1152/japplphysiol.00210.2002.
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The afferent pathways mediating respiratory load perception are still largely unknown. To assess the role of lung vagal afferents in respiratory sensation, detection of inspiratory resistive loads was compared between 10 double-lung transplant (DLT) recipients with normal lung function and 12 healthy control (Nor) subjects. Despite a similar unloaded and loaded breathing pattern, the DLT group had a significantly higher detection threshold (2.91 ± 0.5 vs. 1.55 ± 0.3 cmH2O · l−1 · s) and Weber fraction (0.50 ± 0.1 vs. 0.30 ± 0.1) compared with the Nor group. These results suggest that inspiratory resistive load detection occurs in the absence of vagal afferent feedback from the lung but that lung vagal afferents contribute to inspiratory resistive load detection response in humans. Lung vagal afferents are not essential to the regulation of resting breathing and load compensation responses.
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Smid, Scott D., Richard L. Young, Nicole J. Cooper, and L. Ashley Blackshaw. "GABABR expressed on vagal afferent neurones inhibit gastric mechanosensitivity in ferret proximal stomach." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 6 (December 1, 2001): G1494—G1501. http://dx.doi.org/10.1152/ajpgi.2001.281.6.g1494.
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GABAB-receptor (GABABR) agonists reduce transient lower esophageal sphincter relaxation (TLESR) and reflux episodes through an action on vagal pathways. In this study, we determined whether GABABR are expressed on vagal afferent neurones and whether they modulate distension-evoked discharge of vagal afferents in the isolated stomach. Vagal mehanoreceptor activity was recorded following distensions of the isolated ferret proximal stomach before and after perfusion with the GABABR-selective agonists baclofen and 3-aminopropylphosphinic acid (3-APPiA). Retrograde labeling and immunohistochemistry were used to identify GABABR located on vagal afferent neurones in the nodose ganglia. Vagal afferent fibers responded to isovolumetric gastric distension with an increase in discharge. The GABAB-receptor agonists baclofen (5 × 10−5 M) and 3-APPiA (10−6 to 10−5 M) but not muscimol (GABAA-selective agonist: 1.3 × 10−5 M) significantly decreased afferent distension-response curves. The effect of baclofen (5 × 10−5 M) was reversed by the GABAB-receptor antagonist CGP 62349 (10−5 M). Over 93% of retrogradely labeled gastric vagal afferents in the nodose ganglia expressed immunoreactivity for the GABABR. GABABR expressed on vagal afferent fibers directly inhibit gastric mechanosensory activity. This is likely a contributing mechanism to the efficacy of GABAB-receptor agonists in reducing TLESR and reflux episodes in vivo.
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Karlsson, J. A., G. Sant'Ambrogio, and J. Widdicombe. "Afferent neural pathways in cough and reflex bronchoconstriction." Journal of Applied Physiology 65, no. 3 (September 1, 1988): 1007–23. http://dx.doi.org/10.1152/jappl.1988.65.3.1007.
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Cough and bronchoconstriction are airway reflexes that protect the lung from inspired noxious agents. These two reflexes can be evoked both from the larynx and tracheobronchial tree and also from some extrarespiratory sites. Within the airways, certain sites are particularly sensitive to stimulation of cough (larynx and points of proximal airway branching), whereas bronchoconstriction can be triggered from the whole of the tracheobronchial tree. In the larynx, "irritant" receptors with myelinated afferents mediate cough and bronchoconstriction. Little seems to be known about laryngeal nonmyelinated afferents and their reflexes. In the tracheobronchial tree and lung, slowly adapting stretch receptors (SARs) and rapidly adapting stretch receptors (RARs) have opposing effects on airway tone, the former mediating bronchodilation and the latter bronchoconstriction. In cough, on the other hand, they operate concurrently, a mediatory role for RARs and a facilitatory role for SARs. C-fiber endings (bronchial and pulmonary) mediate bronchoconstriction. Inhalation of so-called "selective" C-fiber stimulants induces cough, but excitation of RARs has not been eliminated, and the possibility also exists that the cough is secondary to other lung actions mediated by these nerve endings. Although cough and bronchoconstriction may be mediated by the same type of receptor, they seem to have separate afferent neural pathways.
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PAUL, D. H., and B. L. ROBERTS. "Spinal Neuronal activity During the Pectoral Fin Reflex of the Dogfish: Pathways For Reflex Generation and Cerebellar Control." Journal of Experimental Biology 148, no. 1 (January 1, 1990): 403–14. http://dx.doi.org/10.1242/jeb.148.1.403.
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ingle units were recorded from the spinal cord of decerebrate dogfish (Scyliorhinus canicula) during pectoral fin reflexes (PFR) evoked by electrical pulse trains to the fin. The units were classified as primary afferent neurones, motoneurones or interneurones. Motoneurones discharged for limited (and various) periods during the reflex at latencies of 20 ms or more. There was no evidence for monosynaptic activation by primary afferents. Short-latency (S) units received monosynaptic input from fast-conducting afferents at latencies (<20 ms) appropriate for pre-motor interneurones. However, excitation of individual S-units by intracellular current injection never evoked motoneurone discharges, suggesting that convergence is necessary for motoneurone activation. Intracellular recordings from S-units which discharged for periods longer than the duration of the afferent volley generated by the fin stimulus showed that they receive other inputs in addition to those from primary afferent fibres. Intermediate-latency (I) units had similar properties to S-units except for a longer latency (>30ms), which ruled out monosynaptic excitation by fast-conducting afferents. Antidromic activation of S- and I-units by high spinal stimulation was rarely seen and orthodromic driving was also uncommon. A significant number of interneurones with latencies greater than 60 ms (L-units) were antidromically activated by high spinal stimulation. Their discharges were often long-lasting (>1 s) and we suggest that they may provide input to the cerebellum during the PFR.
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Dellon, A. Lee, and Amin S. Herati. "Review of Bladder Pain and Referred T12–L2 Input as One Etiology for Interstitial Cystitis." Journal of Reconstructive Microsurgery Open 04, no. 02 (July 2019): e58-e63. http://dx.doi.org/10.1055/s-0039-1696954.
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Abstract Background The etiology of interstitial cystitis (IC)/bladder pain syndrome (BPS) remains a mystery. Based on two patients, whose IC/BPS was relieved by resection of injured iliohypogastric (IH) and ilioinguinal (II) nerves, injured by endoscopic prostatectomy in the first patient and a stretch/traction injury in the second patient, a referred pain pathway is hypothesized that can be applied to patients with IC/BPS and previous abdominal wall surgery/injury. Methods The known neurophysiology of bladder function was reviewed as were the pathways for accepted referred pain syndromes. Results Perception of bladder filling occurs by impulses generated from stretch receptors in the bladder wall, traveling along visceral afferent fibers that enter the thoracolumbar spinal cord at T12, L1, and L2, the same location as the sympathetic outflow to the viscera and the same location as some of the visceral afferents from the bladder. The II and IH nerves originate from T12, L1, and sometimes L2 somatic, dorsal root ganglia. It is hypothesized that somatic afferent pain impulses, from the lower abdominal wall, are misinterpreted as visceral afferent impulses from the bladder, giving rise to the urinary frequency and urgency of IC/BPS. Resecting injured cutaneous afferents (II and IH) permitted long-term IC/BPS relief in the first patient for 59 months and in the second patient for 30 months. Neural inputs from the sacral visceral afferents and sacral somatic afferents did not appear to be involved in this referred pain pathway. Conclusion Nerve blocks of the T12 -L2 spinal nerves in patients with bladder pain who also have had abdominal wall surgery/injury may identify IC/BPS patients for whom resection of the II and IH nerves may prove beneficial in obtaining lasting IC/BPS relief.
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Urch, Catherine. "Normal Pain Transmission." Reviews in Pain 1, no. 1 (August 2007): 2–6. http://dx.doi.org/10.1177/204946370700100102.
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• Acute (normal) pain transmission is part of a survival response to prevent tissue damage and attend to and protect damaged tissue. • A cycle of afferent transmission, response to stimuli, followed by temporary hypersensitivity, then attenuation and resolution occurs. • Primary afferent, spinal cord ascending and descending pathways are fixed; however the response elicited is highly dynamic and not a linear relationship with input intensity. • Somatic inputs are topographically accurate, in contrast to diffuse visceral inputs. • Primary afferents code differentially for stimuli (heat, acid, pressure etc) and intensity. • The dorsal horn allows extensive modulation of initial inputs, either excitation or inhibition. • Higher CNS areas allow extensive modulation of inputs, account for the conscious recognition of pain: the intensity, location, emotional and memory aspects. • Descending pathways arising from midbrain regions can be inhibitory or excitatory.
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Partosoedarso, Elita R., Richard L. Young, and L. Ashley Blackshaw. "GABAB receptors on vagal afferent pathways: peripheral and central inhibition." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 4 (April 1, 2001): G658—G668. http://dx.doi.org/10.1152/ajpgi.2001.280.4.g658.
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To investigate GABAB receptors along vagal afferent pathways, we recorded from vagal afferents, medullary neurons, and vagal efferents in ferrets. Baclofen (7–14 μmol/kg iv) reduced gastric tension receptor and nucleus tractus solitarii neuronal responses to gastric distension but not gastroduodenal mucosal receptor responses to cholecystokinin (CCK). GABAB antagonists CGP-35348 or CGP-62349 reversed effects of baclofen. Vagal efferents showed excitatory and inhibitory responses to distension and CCK. Baclofen (3 nmol icv or 7–14 μmol/kg iv) reduced both distension response types but reduced only inhibitory responses to CCK. CGP-35348 (100 nmol icv or 100 μmol/kg iv) reversed baclofen's effect on distension responses, but inhibitory responses to CCK remained attenuated. They were, however, reversed by CGP-62349 (0.4 nmol icv). In conclusion, GABAB receptors inhibit mechanosensitivity, not chemosensitivity, of vagal afferents peripherally. Mechanosensory input to brain stem neurons is also reduced centrally by GABAB receptors, but excitatory chemosensory input is unaffected. Inhibitory mechano- and chemosensory inputs to brain stem neurons (via inhibitory interneurons) are both reduced, but the pathway taken by chemosensory input involves GABAB receptors that are insensitive to CGP-35348.
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Zhang, Weirong, and Paul W. Davenport. "Activation of thalamic ventroposteriolateral neurons by phrenic nerve afferents in cats and rats." Journal of Applied Physiology 94, no. 1 (January 1, 2003): 220–26. http://dx.doi.org/10.1152/japplphysiol.00334.2002.
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It has been demonstrated that phrenic nerve afferents project to somatosensory cortex, yet the sensory pathways are still poorly understood. This study investigated the neural responses in the thalamic ventroposteriolateral (VPL) nucleus after phrenic afferent stimulation in cats and rats. Activation of VPL neurons was observed after electrical stimulation of the contralateral phrenic nerve. Direct mechanical stimulation of the diaphragm also elicited increased activity in the same VPL neurons that were activated by electrical stimulation of the phrenic nerve. Some VPL neurons responded to both phrenic afferent stimulation and shoulder probing. In rats, VPL neurons activated by inspiratory occlusion also responded to stimulation on phrenic afferents. These results demonstrate that phrenic afferents can reach the VPL thalamus under physiological conditions and support the hypothesis that the thalamic VPL nucleus functions as a relay for the conduction of proprioceptive information from the diaphragm to the contralateral somatosensory cortex.
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Young, Richard L., Amanda J. Page, Tracey A. O'Donnell, Nicole J. Cooper, and L. Ashley Blackshaw. "Peripheral versus central modulation of gastric vagal pathways by metabotropic glutamate receptor 5." American Journal of Physiology-Gastrointestinal and Liver Physiology 292, no. 2 (February 2007): G501—G511. http://dx.doi.org/10.1152/ajpgi.00353.2006.
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Metabotropic glutamate receptors (mGluR) are classified into group I, II, and III mGluR. Group I (mGluR1, mGluR5) are excitatory, whereas group II and III are inhibitory. mGluR5 antagonism potently reduces triggering of transient lower esophageal sphincter relaxations and gastroesophageal reflux. Transient lower esophageal sphincter relaxations are mediated via a vagal pathway and initiated by distension of the proximal stomach. Here, we determined the site of action of mGluR5 in gastric vagal pathways by investigating peripheral responses of ferret gastroesophageal vagal afferents to graded mechanical stimuli in vitro and central responses of nucleus tractus solitarius (NTS) neurons with gastric input in vivo in the presence or absence of the mGluR5 antagonist 2-methyl-6-(phenylethynyl)pyridine (MPEP). mGluR5 were also identified immunohistochemically in the nodose ganglia and NTS after extrinsic vagal inputs had been traced from the proximal stomach. Gastroesophageal vagal afferents were classified as mucosal, tension, or tension-mucosal (TM) receptors. MPEP (1–10 μM) inhibited responses to circumferential tension of tension and TM receptors. Responses to mucosal stroking of mucosal and TM receptors were unaffected. MPEP (0.001–10 nmol icv) had no major effect on the majority of NTS neurons excited by gastric distension or on NTS neurons inhibited by distension. mGluR5 labeling was abundant in gastric vagal afferent neurons and sparse in fibers within NTS vagal subnuclei. We conclude that mGluR5 play a prominent role at gastroesophageal vagal afferent endings but a minor role in central gastric vagal pathways. Peripheral mGluR5 may prove a suitable target for reducing mechanosensory input from the periphery, for therapeutic benefit.
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Ramachandran, Ramnarayan, and Stephen G. Lisberger. "Transformation of Vestibular Signals Into Motor Commands in the Vestibuloocular Reflex Pathways of Monkeys." Journal of Neurophysiology 96, no. 3 (September 2006): 1061–74. http://dx.doi.org/10.1152/jn.00281.2006.
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Parallel pathways mediate the rotatory vestibuloocular reflex (VOR). If the VOR undergoes adaptive modification with spectacles that change the magnification of the visual scene, signals in one neural pathway are modified, whereas those in another are not. By recording the responses of vestibular afferents and abducens neurons for vestibular oscillations at frequencies from 0.5 to 50 Hz, we have elucidated how vestibular signals are processed in the modified versus unmodified VOR pathways. For the small stimuli we used (±15°/s), the afferents with the most regular spontaneous discharge fired throughout the cycle of oscillation even at 50 Hz, whereas afferents with more irregular discharge showed phase locking. For all afferents, the firing rate was in phase with stimulus head velocity at low frequencies and showed progressive phase lead as frequency increased. Sensitivity to head velocity increased steadily as a function of frequency. Abducens neurons showed highly regular spontaneous discharge and very little evidence of phase locking. Their sensitivity to head velocity during the VOR was relatively flat across frequencies; firing rate lagged head velocity at low frequencies and shifted to large phase leads as stimulus frequency increased. When afferent responses were provided as inputs to a two-pathway model of the VOR, the output of the model reproduced the responses of abducens neurons if the unmodified and modified VOR pathways had frequency-dependent internal gains and included fixed time delays of 1.5 and 9 ms. The phase shifts predicted by the model provide fingerprints for identifying brain stem neurons that participate in the modified versus unmodified VOR pathways.
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Burgard, Edward C., Mathew O. Fraser, and Karl B. Thor. "Serotonergic modulation of bladder afferent pathways." Urology 62, no. 4 (October 2003): 10–15. http://dx.doi.org/10.1016/s0090-4295(03)00590-9.
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Almeida, Tatiana F., Suely Roizenblatt, and Sergio Tufik. "Afferent pain pathways: a neuroanatomical review." Brain Research 1000, no. 1-2 (March 2004): 40–56. http://dx.doi.org/10.1016/j.brainres.2003.10.073.
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Imig, J. D., and P. C. Deichmann. "Afferent arteriolar responses to ANG II involve activation of PLA2 and modulation by lipoxygenase and P-450 pathways." American Journal of Physiology-Renal Physiology 273, no. 2 (August 1, 1997): F274—F282. http://dx.doi.org/10.1152/ajprenal.1997.273.2.f274.
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Activation of angiotensin receptors activates phospholipase A2 (PLA2) in various tissues, resulting in the release of arachidonic acid and formation of vasoactive metabolites. The present study examined the role of the lipoxygenase and cytochrome P-450 pathways by evaluating the effects of PLA2, cyclooxygenase, lipoxygenase, and epoxygenase inhibition on the afferent arteriolar responses to angiotensin II (ANG II) and norepinephrine in the vitro perfused rat juxtamedullary nephron preparation. ANG II (0.01-100 nM) resulted in a dose-dependent afferent arteriolar vasoconstriction ranging from 3 +/- 1 to 32 +/- 2% (n = 47). Norepinephrine at 0.01, 0.1, and 1.0 microM also decreased afferent arteriolar diameter by 5 +/- 1, 17 +/- 1, and 34 +/- 2%, respectively (n = 43). In the presence of arachidonyl trifluoromethyl ketone (AACOCF3, 20 microM), a PLA2 inhibitor, afferent arteriolar vasoconstriction to ANG II (100 nM) was attenuated, and the diameter decreased by 23 +/- 4% (n = 7). The cyclooxygenase inhibitor, indomethacin (10 microM), and the cyclooxygenase-2 inhibitor, NS-398 (10 microM), did not affect the afferent arteriolar response to ANG II. The lipoxygenase inhibitor biacalein (1 microM) attenuated the afferent arteriolar response to ANG II, and vessel diameter decreased by 11 +/- 5% (n = 6) in response to 100 nM ANG II. On the other hand, miconazole (1 microM), a selective epoxygenase inhibitor, enhanced the afferent arteriolar vasoconstriction to 100 nM ANG II. 17-Octadecynoic acid (17-ODYA, 1 microM), an inhibitor of hydroxylase and epoxygenase metabolism of arachidonic acid, also increased the responsiveness of the afferent arteriole. PLA2, lipoxygenase, or cytochrome P-450 inhibition had no effect on the afferent arteriolar vasoconstriction to norepinephrine. The afferent arteriolar vasoconstrictor response to norepinephrine (0.1 microM) was enhanced by indomethacin or NS-398, and diameter decreased by 25 +/- 3% and 28 +/- 4%, respectively. Results of this study suggest that metabolites of the cyclooxygenase pathway attenuate the afferent arteriolar vasoconstrictor effect of norepinephrine. Furthermore, these data suggest that activation of PLA2 is involved in part of the afferent arteriolar response to ANG II and that metabolites of the lipoxygenase pathway augment and metabolites of the epoxygenase pathway attenuate the afferent arteriolar vasoconstrictor effect of ANG II.
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Ménard, Ariane, Hugues Leblond, and Jean-Pierre Gossard. "Sensory Integration in Presynaptic Inhibitory Pathways During Fictive Locomotion in the Cat." Journal of Neurophysiology 88, no. 1 (July 1, 2002): 163–71. http://dx.doi.org/10.1152/jn.2002.88.1.163.
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The aim of this study is to understand how sensory inputs of different modalities are integrated into spinal cord pathways controlling presynaptic inhibition during locomotion. Primary afferent depolarization (PAD), an estimate of presynaptic inhibition, was recorded intra-axonally in group I afferents ( n = 31) from seven hindlimb muscles in L6–S1 segments during fictive locomotion in the decerebrate cat. PADs were evoked by stimulating alternatively low-threshold afferents from a flexor nerve, a cutaneous nerve and a combination of both. The fictive step cycle was divided in five bins and PADs were averaged in each bin and their amplitude compared. PADs evoked by muscle stimuli alone showed a significant phase-dependent modulation in 20/31 group I afferents. In 12/20 afferents, the cutaneous stimuli alone evoked a phase-dependent modulation of primary afferent hyperpolarization (PAH, n = 9) or of PADs ( n = 3). Combining the two sensory modalities showed that cutaneous volleys could significantly modify the amplitude of PADs evoked by muscle stimuli in at least one part (bin) of the step cycle in 17/31 (55%) of group I afferents. The most common effect (13/17) was a decrease in the PAD amplitude by 35% on average, whereas it was increased by 17% on average in the others (4/17). Moreover, in 8/13 afferents, the PAD reduction was obtained in 4/5 bins i.e., for most of the duration of the step cycle. These effects were seen in group I afferents from all seven muscles. On the other hand, we found that different cutaneous nerves had quite different efficacy; the superficial peroneal (SP) being the most efficient (85% of trials) followed by Saphenous (60%) and caudal sural (44%) nerves. The results indicate that cutaneous interneurons may act, in part, by modulating the transmission in PAD pathways activated by group I muscle afferents. We conclude that cutaneous input, especially from the skin area on the dorsum of the paw (SP), could subtract presynaptic inhibition in some group I afferents during perturbations of stepping (e.g., hitting an obstacle) and could thus adjust the influence of proprioceptive feedback onto motoneuronal excitability.
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Wang, Yu, and Li Ye. "The Afferent Function of Adipose Innervation." Diabetes 73, no. 3 (February 20, 2024): 348–54. http://dx.doi.org/10.2337/dbi23-0002.
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Adipose tissue innervation is critical for regulating metabolic and energy homeostasis. While the sympathetic efferent innervation of fat is well characterized, the role of sensory or afferent innervation remains less explored. This article reviews previous work on adipose innervation and recent advances in the study of sensory innervation of adipose tissues. We discuss key open questions, including the physiological implications of adipose afferents in homeostasis as well as potential cross talk with sympathetic neurons, the immune system, and hormonal pathways. We also outline the general technical challenges of studying dorsal root ganglia innervating fat, along with emerging technologies that may overcome these barriers. Finally, we highlight areas for further research to deepen our understanding of the afferent function of adipose innervation.
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Wildman, M. "Connections between thoraco-coxal proprioceptive afferents and motor neurons in the locust." Journal of Experimental Biology 203, no. 3 (February 1, 2000): 435–45. http://dx.doi.org/10.1242/jeb.203.3.435.
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The position of the coxal segment of the locust hind leg relative to the thorax is monitored by a variety of proprioceptors, including three chordotonal organs and a myochordotonal organ. The sensory neurons of two of these proprioceptors, the posterior joint chordotonal organ (pjCO) and the myochordotonal organ (MCO), have axons in the purely sensory metathoracic nerve 2C (N2C). The connections made by these afferents with metathoracic motor neurons innervating thoraco-coxal and wing muscles were investigated by electrical stimulation of N2C and by matching postsynaptic potentials in motor neurons with afferent spikes in N2C. Stretch applied to the anterior rotator muscle of the coxa (M121), with which the MCO is associated, evoked sensory spikes in N2C. Some of the MCO afferent neurons make direct excitatory chemical synaptic connections with motor neurons innervating the thoraco-coxal muscles M121, M126 and M125. Parallel polysynaptic pathways via unidentified interneurons also exist between MCO afferents and these motor neurons. Connections with the common inhibitor 1 neuron and motor neurons innervating the thoraco-coxal muscles M123/4 and wing muscles M113 and M127 are polysynaptic. Afferents of the pjCO also make polysynaptic connections with motor neurons innervating thoraco-coxal and wing muscles, but no evidence for monosynaptic pathways was found.
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Chappell, R. L., and F. J. Rosenstein. "Pharmacology of the skate electroretinogram indicates independent ON and OFF bipolar cell pathways." Journal of General Physiology 107, no. 4 (April 1, 1996): 535–44. http://dx.doi.org/10.1085/jgp.107.4.535.
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Organization of afferent information into parallel ON and OFF pathways is a critical feature of the vertebrate visual system. All afferent visual information in the vertebrate retina reaches the inner plexiform layer (IPL) via bipolar cells. It is at the bipolar cell level that separation of ON and OFF information first appears for afferent information from cones. This may also hold true for the rod pathway of cold-blooded vertebrates, but not for mammals. The all-rod retina of the skate presents an opportunity to examine such pathways in a retina having but a single class of photoreceptor. Immunocytochemical evidence suggests that both ON and OFF bipolar cells are present in the skate retina. We examined the pharmacology of the skate electroretinogram (ERG) to test the hypothesis that independent ON and OFF bipolar cell pathways are functional as rod afferent pathways from outer to inner plexiform layer in the skate. 100 microM 2-amino-4-phosphonobutyric acid (APB) reversibly blocked the skate ERG b-wave. A small d-wave-like OFF component of the ERG revealed by DC recording of response to a prolonged (10 s) flash of light was reduced or blocked by 5 mM kynurenic acid (KYN). We found that addition of 200 microM picrotoxin to the Ringer's solution revealed prominent ON and OFF components of the skate ERG while reducing the c-wave. These ON and OFF components were reversibly blocked by 100 microM APB and 5 mM KYN, respectively. Reversible block of the OFF component by KYN was also accomplished in the presence of 500 microM N-methyl-DL-aspartate. From these findings, we conclude that ON and OFF bipolar cells are likely to be functional as parallel afferent interplexiform pathways in the all-rod retina of the skate.
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Kadekawa, Katsumi, Tsuyoshi Majima, Takahiro Shimizu, Naoki Wada, William C. de Groat, Anthony J. Kanai, Momokazu Goto, Mitsuharu Yoshiyama, Kimio Sugaya, and Naoki Yoshimura. "The role of capsaicin-sensitive C-fiber afferent pathways in the control of micturition in spinal-intact and spinal cord-injured mice." American Journal of Physiology-Renal Physiology 313, no. 3 (September 1, 2017): F796—F804. http://dx.doi.org/10.1152/ajprenal.00097.2017.
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We examined bladder and urethral sphincter activity in mice with or without spinal cord injury (SCI) after C-fiber afferent desensitization induced by capsaicin pretreatment and changes in electrophysiological properties of mouse bladder afferent neurons 4 wk after SCI. Female C57BL/6N mice were divided into four groups: 1) spinal intact (SI)-control, 2) SI-capsaicin pretreatment (Cap), 3) SCI-control, and 4) SCI-Cap groups. Continuous cystometry and external urethral sphincter (EUS)-electromyogram (EMG) were conducted under an awake condition. In the Cap groups, capsaicin (25, 50, or 100 mg/kg) was injected subcutaneously 4 days before the experiments. In the SI-Cap group, 100 mg/kg capsaicin pretreatment significantly increased bladder capacity and decreased the silent period duration of EUS/EMG compared with the SI-control group. In the SCI-Cap group, 50 and 100 mg/kg capsaicin pretreatment decreased the number of nonvoiding contractions (NVCs) and the duration of reduced EUS activity during voiding, respectively, compared with the SCI-control group. In SCI mice, hexamethonium, a ganglionic blocker, almost completely blocked NVCs, suggesting that they are of neurogenic origin. Patch-clamp recordings in capsaicin-sensitive bladder afferent neurons from SCI mice showed hyperexcitability, which was evidenced by decreased spike thresholds and increased firing rate compared with SI mice. These results indicate that capsaicin-sensitive C-fiber afferent pathways, which become hyperexcitable after SCI, can modulate bladder and urethral sphincter activity in awake SI and SCI mice. Detrusor overactivity as shown by NVCs in SCI mice is significantly but partially dependent on capsaicin-sensitive C-fiber afferents, whereas the EUS relaxation during voiding is enhanced by capsaicin-sensitive C-fiber bladder afferents in SI and SCI mice.
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Qin, Chao, Margaret J. Chandler, Kenneth E. Miller, and Robert D. Foreman. "Responses and Afferent Pathways of Superficial and Deeper C1–C2 Spinal Cells to Intrapericardial Algogenic Chemicals in Rats." Journal of Neurophysiology 85, no. 4 (April 1, 2001): 1522–32. http://dx.doi.org/10.1152/jn.2001.85.4.1522.
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Electrical stimulation of vagal afferents or cardiopulmonary sympathetic afferent fibers excites C1–C2spinal neurons. The purposes of this study were to compare the responses of superficial (depth <0.35 mm) and deeper C1–C2 spinal neurons to noxious chemical stimulation of cardiac afferents and determine the relative contribution of vagal and sympathetic afferent pathways for transmission of noxious cardiac afferent input to C1–C2 neurons. Extracellular potentials of single C1–C2 neurons were recorded in pentobarbital anesthetized and paralyzed male rats. A catheter was placed in the pericardial sac to administer a mixture of algogenic chemicals (0.2 ml) that contained adenosine (10− 3 M), bradykinin, histamine, serotonin, and prostaglandin E2(10− 5 M each). Intrapericardial chemicals changed the activity of 20/106 (19%) C1–C2 spinal neurons in the superficial laminae, whereas 76/147 (52%) deeper neurons responded to cardiac noxious input ( P < 0.01). Of 96 neurons responsive to cardiac inputs, 48 (50%) were excited (E), 41 (43%) were inhibited (I), and 7 were excited/inhibited (E-I) by intrapericardial chemicals. E or I neurons responsive to intrapericardial chemicals were subdivided into two groups: short-lasting (SL) and long-lasting (LL) response patterns. In superficial gray matter, excitatory responses to cardiac inputs were more likely to be LL-E than SL-E neurons. Mechanical stimulation of the somatic field from the head, neck, and shoulder areas excited 85 of 95 (89%) C1–C2 spinal neurons that responded to intrapericardial chemicals; 31 neurons were classified as wide dynamic range, 49 were high threshold, 5 responded only to joint movement, and no neuron was classified as low threshold. For superficial neurons, 53% had small somatic fields and 21% had bilateral fields. In contrast, 31% of the deeper neurons had small somatic fields and 46% had bilateral fields. Ipsilateral cervical vagotomy interrupted cardiac noxious input to 8/30 (6 E, 2 I) neurons; sequential transection of the contralateral cervical vagus nerve (bilateral vagotomy) eliminated the responses to intrapericardial chemicals in 4/22 (3 E, 1 I) neurons. Spinal transection at C6–C7 segments to interrupt effects of sympathetic afferent input abolished responses to cardiac input in 10/10 (7 E, 3 I) neurons that still responded after bilateral vagotomy. Results of this study support the concept that C1–C2 superficial and deeper spinal neurons play a role in integrating cardiac noxious inputs that travel in both the cervical vagal and/or thoracic sympathetic afferent nerves.
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Takahata, M., and J. J. Wine. "Feedforward afferent excitation of peripheral inhibitors in the crayfish escape system." Journal of Neurophysiology 58, no. 6 (December 1, 1987): 1452–67. http://dx.doi.org/10.1152/jn.1987.58.6.1452.
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1. Each abdominal ganglion of the crayfish contains peripheral inhibitors of the fast flexor muscles. These flexor inhibitors (FIs), which can effectively inhibit tension development in the tailflip powerstroke muscles, are excited by a delayed central pathway from the same giant axons which trigger escape (33). The FIs also received sensory input, which increases in efficacy in the more posterior segments (4), but until now neither the origin of the input nor its central pathways had been well described. We have used intracellular recording and staining techniques to investigate the afferent input onto the two telson flexor inhibitors (F16 and F17), which receive more powerful sensory input than any of their anterior homologs (4). 2. Both F16 and F17 showed a delayed (3.7 ms) compound postsynaptic potential (PSP), which peaked at long latency when any afferent nerve in the abdomen was stimulated. The amplitude of these slow PSPs waned rapidly with repeated stimulation at 1 Hz and was increased by hyperpolarization and decreased by depolarization of the FI. The PSPs are most likely to be mediated chemically, via polysynaptic pathways. 3. When any afferent nerve from the telson was stimulated, both telson FIs showed an additional fast-rising, short-latency (1.4 ms) PSP, which preceded the slow component. This fast component was not produced by afferent nerves innervating any region other than the telson. The fast PSPs of the two FIs were similar, but in F16 the fast component was always subthreshold, whereas in F17 it often elicited an impulse at short latency. 4. The amplitude of the fast component was not affected by changing the membrane potential of the FIs, suggesting electrical transmission. In spite of its short latency, the fast component is unlikely to be mediated monosynaptically, since it was variably present even in the same animal, and occlusion was observed when any two of the four telson nerves that evoked the response were stimulated simultaneously. 5. Although occlusion was seen among responses produced by stimulating afferents from any source, the responses summated linearly with the compound excitatory postsynaptic potential evoked in FI by the lateral giant escape command axons. Thus at least two separate suprathreshold pathways converge onto the telson FIs.
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Guan, D., W. T. Phillips, and G. M. Green. "Pancreatic secretion stimulated by CCK is not mediated by capsaicin-sensitive vagal afferent pathway in awake rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 5 (May 1, 1996): G881—G886. http://dx.doi.org/10.1152/ajpgi.1996.270.5.g881.
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A capsaicin-sensitive vagal afferent pathway was reported to mediate the effect of endogenous cholecystokinin (CCK) on pancreatic secretion in anesthetized rats. Because neural blockade affects pancreatic secretion much less in awake than in anesthetized rats, the effect of capsaicin ablation of vagal afferent pathways on pancreatic secretion stimulated by endogenous CCK was examined in awake rats. During surgery, abdominal vagal trunks were exposed, and 0.1 ml of capsaicin (10 mg/ml) was applied to the vagal trunks. Ablation of the vagal afferent pathway was assessed by the ability of intraperitoneal cholecystokinin octapeptide (CCK-8) to suppress food intake and inhibit gastric emptying. Endogenous CCK release was stimulated by diversion of bile pancreatic juice from the intestine and by intraduodenal infusion of casein. Pancreatic protein and fluid secretion were significantly increased by both treatments, and the responses were unaffected by capsaicin. Intraperitoneal CCK-8 markedly inhibited food intake and gastric emptying, and both effects were significantly attenuated in capsaicin-treated rats, indicating that capsaicin treatment successfully ablated vagal afferent fibers. It is concluded that CCK-stimulated pancreatic secretion in rats is not mediated by a vagal afferent pathway.
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Zhou, Shi-Yi, Yuan-Xu Lu, and Chung Owyang. "Gastric relaxation induced by hyperglycemia is mediated by vagal afferent pathways in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 5 (May 2008): G1158—G1164. http://dx.doi.org/10.1152/ajpgi.00067.2008.
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Hyperglycemia has a profound effect on gastric motility. However, little is known about the site and mechanism that sense alteration in blood glucose level. The identification of glucose-sensing neurons in the nodose ganglia led us to hypothesize that hyperglycemia acts through vagal afferent pathways to inhibit gastric motility. With the use of a glucose-clamp rat model, we showed that glucose decreased intragastric pressure in a dose-dependent manner. In contrast to intravenous infusion of glucose, intracisternal injection of glucose at 250 and 500 mg/dl had little effect on intragastric pressure. Pretreatment with hexamethonium, as well as truncal vagotomy, abolished the gastric motor responses to hyperglycemia (250 mg/dl), and perivagal and gastroduodenal applications of capsaicin significantly reduced the gastric responses to hyperglycemia. In contrast, hyperglycemia had no effect on the gastric contraction induced by electrical field stimulation or carbachol (10−5 M). To rule out involvement of serotonergic pathways, we showed that neither granisetron (5-HT3 antagonist, 0.5 g/kg) nor pharmacological depletion of 5-HT using p-chlorophenylalanine (5-HT synthesis inhibitor) affected gastric relaxation induced by hyperglycemia. Lastly, NG-nitro-l-arginine methyl ester (l-NAME) and a VIP antagonist each partially reduced gastric relaxation induced by hyperglycemia and, in combination, completely abolished gastric responses. In conclusion, hyperglycemia inhibits gastric motility through a capsaicin-sensitive vagal afferent pathway originating from the gastroduodenal mucosa. Hyperglycemia stimulates vagal afferents, which, in turn, activate vagal efferent cholinergic pathways synapsing with intragastric nitric oxide- and VIP-containing neurons to mediate gastric relaxation.
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Marshall, Andrew G., and Francis P. McGlone. "Affective Touch: The Enigmatic Spinal Pathway of the C-Tactile Afferent." Neuroscience Insights 15 (January 2020): 263310552092507. http://dx.doi.org/10.1177/2633105520925072.
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C-tactile afferents are hypothesized to form a distinct peripheral channel that encodes the affective nature of touch. Prevailing views indicate they project, as with other unmyelinated afferents, in lamina I-spinothalamic pathways that relay homeostatically relevant information from the body toward cortical regions involved in interoceptive processing. However, in a recent study, we found that spinothalamic ablation in humans, while profoundly impairing the canonical spinothalamic modalities of pain, temperature, and itch, had no effect on benchmark psychophysical affective touch metrics. These novel findings appear to indicate that perceptual judgments about the affective nature of touch pleasantness do not depend on the integrity of the lamina I-spinothalamic tract. In this commentary, we further discuss the implications of these unexpected findings. Intuitively, they suggest that signaling of emotionally relevant C-tactile mediated touch occurs in an alternative ascending pathway. However, we also argue that the deficits seen following interruption of a putative C-tactile lamina I-spinothalamic relay might be barely perceptible—a feature that would underline the importance of the C-tactile afferent in neurodevelopment.
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Xiao, Zhiying, Marc J. Rogers, Bing Shen, Jicheng Wang, Zeyad Schwen, James R. Roppolo, William C. de Groat, and Changfeng Tai. "Somatic modulation of spinal reflex bladder activity mediated by nociceptive bladder afferent nerve fibers in cats." American Journal of Physiology-Renal Physiology 307, no. 6 (September 15, 2014): F673—F679. http://dx.doi.org/10.1152/ajprenal.00308.2014.
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The goal of the present study was to determine if supraspinal pathways are necessary for inhibition of bladder reflex activity induced by activation of somatic afferents in the pudendal or tibial nerve. Cats anesthetized with α-chloralose were studied after acute spinal cord transection at the thoracic T9/T10 level. Dilute (0.25%) acetic acid was used to irritate the bladder, activate nociceptive afferent C-fibers, and trigger spinal reflex bladder contractions (amplitude: 19.3 ± 2.9 cmH2O). Hexamethonium (a ganglionic blocker, intravenously) significantly ( P < 0.01) reduced the amplitude of the reflex bladder contractions to 8.5 ± 1.9 cmH2O. Injection of lidocaine (2%, 1–2 ml) into the sacral spinal cord or transection of the sacral spinal roots and spinal cord further reduced the contraction amplitude to 4.2 ± 1.3 cmH2O. Pudendal nerve stimulation (PNS) at frequencies of 0.5–5 Hz and 40 Hz but not at 10–20 Hz inhibited reflex bladder contractions, whereas tibial nerve stimulation (TNS) failed to inhibit bladder contractions at all tested frequencies (0.5–40 Hz). These results indicate that PNS inhibition of nociceptive afferent C-fiber-mediated spinal reflex bladder contractions can occur at the spinal level in the absence of supraspinal pathways, but TNS inhibition requires supraspinal pathways. In addition, this study shows, for the first time, that after acute spinal cord transection reflex bladder contractions can be triggered by activating nociceptive bladder afferent C-fibers using acetic acid irritation. Understanding the sites of action for PNS or TNS inhibition is important for the clinical application of pudendal or tibial neuromodulation to treat bladder dysfunctions.
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Jammes, Y. "Tonic sensory pathways of the respiratory system." European Respiratory Journal 1, no. 2 (February 1, 1988): 176–83. http://dx.doi.org/10.1183/09031936.93.01020176.
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Both respiratory centres and the preganglionic vagal motoneurones, which control respiratory (striated) and airway (smooth) muscles respectively, receive information on the lungs, the circulation and the skeletal and respiratory muscles. Each of these nervous pathways has two components: one is phasic, i.e. in phase with biological rhythms, and comes from mechanoreceptors connected to large myelinated fibres; the second has a tonic low frequency firing rate and corresponds to the spontaneous activity of polymodal receptors connected to thin sensory fibres, which act mostly as sensors of changes in extracellular fluid composition (O2 and/or CO2 partial pressure, pH, release of algesic agents etc...). Some of them also detect large mechanical disturbances or local temperature changes. The influence of tonic background sensory activity is well known in animals concerning the role played by arterial chemoreceptors in the control of ventilation and of thin vagal afferents from the lungs (bronchopulmonary C-fibres and irritant receptors) in reflex facilitation of the bronchoconstrictor vagal tone. Moreover, the stimulation of thin sensory fibres in particular circumstances is responsible for hyperventilation (arterial chemoreceptors and muscle afferents), increased airway tone (arterial chemoreceptors and mostly thin vagal afferent fibres) or bronchodilation (muscle afferents). These peripheral inputs project centrally on different structures and also on brain stem neurones, which integrate simultaneously chemosensory, vagal and muscle information. This results in complex interactions between the different sensory pathways.
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Ciriello, John, and Monica M. Caverson. "Central Organization of Afferent Renal Nerve Pathways." Clinical and Experimental Hypertension. Part A: Theory and Practice 9, sup1 (January 1987): 33–46. http://dx.doi.org/10.3109/10641968709160162.
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Turner, Richard D., and Surinder S. Birring. "Chronic cough: ATP, afferent pathways and hypersensitivity." European Respiratory Journal 54, no. 1 (June 4, 2019): 1900889. http://dx.doi.org/10.1183/13993003.00889-2019.
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Derbyshire, Stuart W. G. "Visceral Afferent Pathways and Functional Brain Imaging." Scientific World JOURNAL 3 (2003): 1065–80. http://dx.doi.org/10.1100/tsw.2003.93.
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The application of functional imaging to study painful sensations has generated considerable interest regarding insight into brain dysfunction that may be responsible for functional pain such as that suffered in patients with irritable bowel syndrome (IBS). This review provides a brief introduction to the development of brain science as it relates to pain processing and a snapshot of recent functional imaging results with somatic and visceral pain. Particular emphasis is placed on current hypotheses regarding dysfunction of the brain-gut axis in IBS patients. There are clear and interpretable differences in brain activation following somatic as compared with visceral noxious sensation. Noxious visceral distension, particularly of the lower gastrointestinal tract, activates regions associated with unpleasant affect and autonomic responses. Noxious somatic sensation, in contrast, activates regions associated with cognition and skeletomotor responses. Differences between IBS patients and control subjects, however, were far less clear and interpretable. While this is in part due to the newness of this field, it also reflects weaknesses inherent within the current understanding of IBS. Future use of functional imaging to examine IBS and other functional disorders will be more likely to succeed by describing clear theoretical and clinical endpoints.
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Imig, J. D., and L. G. Navar. "Afferent arteriolar response to arachidonic acid: involvement of metabolic pathways." American Journal of Physiology-Renal Physiology 271, no. 1 (July 1, 1996): F87—F93. http://dx.doi.org/10.1152/ajprenal.1996.271.1.f87.
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Arachidonic acid (AA) metabolites have been implicated in the control of renal hemodynamics, but the nature of the metabolites produced by renal cells when AA is released has remained uncertain. Experiments were performed using the in vitro perfused juxtamedullary nephron preparation to examine the effects of perfusion and superfusion of AA on the renal microvasculature. Extraluminal exposure of the vessels by superfusion with solutions containing 0.1, 1.0, and 10 microM AA decreased afferent arteriolar diameter by 8 +/- 2, 16 +/- 3, and 20 +/- 3%, respectively. The same doses of AA added to the perfusate produced a similar afferent arteriolar vasoconstriction. Inhibition of the major enzymatic pathways unmasked differential responses of AA that were dependent on the direction from which the vasculature was exposed to AA. 17-Octadecynoic acid (1 microM), an inhibitor of the cytochrome P-450 pathway, eliminated the vasoconstrictor response to superfused AA but had little effect on the response to perfused AA. Lipoxygenase inhibition with baicalein (0.5 microM) did not alter the afferent arteriolar vasoconstriction during superfusion with AA but did attenuate the vasoconstrictor response to perfused AA by 34%. Cyclooxygenase inhibition with 10 microM indomethacin reduced the afferent arteriolar response to superfusion with 10 microM AA by 46%, but the responses to perfusion with AA were reversed, leading to the unmasking of a 17% afferent arteriolar dilation. The AA-induced vasorelaxation observed during cyclooxygenase inhibition was prevented by the subsequent addition of a P-450 inhibitor. Additionally, after endothelial removal with 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate (CHAPS), the vasodilatory response reverted to a vasoconstriction. The results of this study demonstrate that in the rat, AA metabolites exert predominant actions on afferent arterioles, but differential responses are mediated via different enzymatic pathways depending on the origin of AA. Increased AA availability of intraluminal origin leads to production of cyclooxygenase-derived vasoconstrictor metabolites and also to endothelial-derived cytochrome P-450 vasodilatory metabolites. In contrast, increased AA availability of interstitial origin leads to production of vasoconstrictor cytochrome P-450 metabolites.
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Owyang, C. "Physiological mechanisms of cholecystokinin action on pancreatic secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 271, no. 1 (July 1, 1996): G1—G7. http://dx.doi.org/10.1152/ajpgi.1996.271.1.g1.
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Recent experimental studies in animals and humans provide strong evidence that cholecystokinin (CCK) acts via cholinergic pathways to mediate pancreatic enzyme secretion. These studies indicate that the sites of CCK's action to stimulate pancreatic secretion are dose dependent. Doses of CCK that produce physiological plasma CCK levels act via stimulation of the vagal afferent pathway originating from the gastroduodenal mucosa, whereas doses that produce supraphysiological CCK levels act to stimulate intrapancreatic neurons and pancreatic acini. These CCK-sensitive fibers are also responsive to a wide range of chemical and osmotic stimuli. In this manner, gastrointestinal afferents responding to hormones such as CCK and the ever-changing chemical and physical luminal environment provide sensory information to the central nervous system, which in turn stimulates pancreatic secretion via a vagal cholinergic pathway.
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Kubin, Leszek, George F. Alheid, Edward J. Zuperku, and Donald R. McCrimmon. "Central pathways of pulmonary and lower airway vagal afferents." Journal of Applied Physiology 101, no. 2 (August 2006): 618–27. http://dx.doi.org/10.1152/japplphysiol.00252.2006.
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Lung sensory receptors with afferent fibers coursing in the vagus nerves are broadly divided into three groups: slowly (SAR) and rapidly (RAR) adapting stretch receptors and bronchopulmonary C fibers. Central terminations of each group are found in largely nonoverlapping regions of the caudal half of the nucleus of the solitary tract (NTS). Second order neurons in the pathways from these receptors innervate neurons located in respiratory-related regions of the medulla, pons, and spinal cord. The relative ease of selective activation of SARs, and to a lesser extent RARs, has allowed for more complete physiological and morphological characterization of the second and higher order neurons in these pathways than for C fibers. A subset of NTS neurons receiving afferent input from SARs (termed pump or P-cells) mediates the Breuer-Hering reflex and inhibits neurons receiving afferent input from RARs. P-cells and second order neurons in the RAR pathway also provide inputs to regions of the ventrolateral medulla involved in control of respiratory motor pattern, i.e., regions containing a predominance of bulbospinal premotor neurons, as well as regions containing respiratory rhythm-generating neurons. Axon collaterals from both P-cells and RAR interneurons, and likely from NTS interneurons in the C-fiber pathway, project to the parabrachial pontine region where they may contribute to plasticity in respiratory control and integration of respiratory control with other systems, including those that provide for voluntary control of breathing, sleep-wake behavior, and emotions.
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Sengupta, Jyoti N., Bidyut K. Medda, and Reza Shaker. "Effect of GABAB receptor agonist on distension-sensitive pelvic nerve afferent fibers innervating rat colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 283, no. 6 (December 1, 2002): G1343—G1351. http://dx.doi.org/10.1152/ajpgi.00124.2002.
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Spinal afferents innervating the gastrointestinal tract are the major pathways for visceral nociception. Many centrally acting analgesic drugs attenuate responses of visceral primary afferent fibers by acting at the peripheral site. γ-Amino butyric acid (GABA), a major inhibitory neurotransmitter, acts via metobotropic GABAB and ionotropic GABAA/GABAC receptors. The aim of this study was to test the peripheral effect of selective GABABreceptor agonist baclofen on responses of the pelvic nerve afferent fibers innervating the colon of the rat. Distension-sensitive pelvic nerve afferent fibers were recorded from the S1 sacral dorsal root in anesthetized rats. The effect of baclofen (1–300 μmol/kg) was tested on responses of these fibers to colorectal distension (CRD; 60 mmHg, 30 s). A total of 21 pelvic nerve afferent fibers was recorded. Mechanosensitive properties of four fibers were also recorded before and after bilateral transections of T12-S3 ventral roots (VR). Effect of baclofen was tested on 15 fibers (7 in intact rats, 4 in rats with transected VR, and 4 in rats pretreated with CGP 54626). In nine fibers (5/7 in intact and 4/4 in VR transected rats), baclofen produced dose-dependent inhibition of response to CRD. Pretreatment with selective GABAB receptor antagonist CGP 54626 (1 μmol/kg) reversed the inhibitory effect of baclofen. Results suggest a peripheral role of GABAB receptors in the inhibition of mechanotransduction property of distension-sensitive pelvic nerve afferent fibers.
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Kang, Y. M., K. Lamb, G. F. Gebhart, and K. Bielefeldt. "Experimentally induced ulcers and gastric sensory-motor function in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 288, no. 2 (February 2005): G284—G291. http://dx.doi.org/10.1152/ajpgi.00250.2004.
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Prior studies have demonstrated that inflammation can sensitize visceral afferent neurons, contributing to the development of hyperalgesia. We hypothesized that both afferent and efferent pathways are affected, resulting in changes in motor and sensory function. Kissing ulcers (KU) were induced in the distal stomach by injecting 60% acetic acid for 45 s into a clamped area of the stomach. In controls, saline was injected into the stomach. A balloon catheter was surgically placed into the stomach, and electromyographic responses to gastric distension were recorded from the acromiotrapezius muscle at various times after ulcer induction. The accommodation reflex was assessed by slowly infusing saline into the distally occluded stomach. Gastric pressure changes in response to vagal stimulation were measured in anesthetized rats. Contractile function of circular muscle strips was examined in vitro using force-displacement transducers. KU caused gastric hypersensitivity that persisted for at least 14 days. Fluid distension of the stomach led to a rapid pressure increase in KU but not in control animals, consistent with an impaired accommodation reflex. Gastric ulcers enhanced the contractile response to vagal stimulation, whereas the effect of cholinergic stimulation on smooth muscle in vitro was not changed. These data suggest that inflammation directly alters gastric sensory and motor function. Increased activation of afferents will trigger vagovagal reflexes, thereby further changing motility and indirectly activating sensory neurons. Thus afferent and efferent pathways both contribute to the development of dyspeptic symptoms.
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Moncrief, Karli, Shereen Hamza, and Susan Kaufman. "Splenic reflex modulation of central cardiovascular regulatory pathways." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 1 (July 2007): R234—R242. http://dx.doi.org/10.1152/ajpregu.00562.2006.
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The splenorenal reflex induces changes in mean arterial pressure (MAP) and renal function. We hypothesized that, in addition to spinal pathways previously identified, these effects are also mediated through central pathways. We investigated the effect of elevated splenic venous pressure on central neural activation in intact, renal-denervated, and renal + splenic-denervated rats. Fos-labeled neurons were quantified in the nucleus of the tractus solitarius (NTS), paraventricular nucleus (PVN), supraoptic nucleus (SON), and subfornical organ (SFO) after 1-h partial splenic vein occlusion (SVO) in conscious rats bearing balloon occluders around the splenic vein, telemetric pressure transducers in the gastric vein (splenic venous pressure), and abdominal aorta catheters (MAP). SVO stimulated Fos expression in the PVN and SON, but not NTS or SFO of intact rats. Renal denervation abolished this response in the parvocellular PVN, while renal + splenic denervation abolished activation in the magnocellular PVN and the SON. In renal-denervated animals, SVO depressed Fos expression in the NTS and increased expression in the SFO, responses that were abolished by renal + splenic denervation. In intact rats, SVO also induced a fall in right atrial pressure, an increase in renal afferent nerve activity, and an increase in MAP. We conclude that elevated splenic venous pressure does induce hypothalamic activation and that this is mediated through both splenic and renal afferent nerves. However, in the absence of renal afferent input, SVO depressed NTS activation, probably as a result of the accompanying fall in cardiac preload and reduced afferent signaling from the cardiopulmonary receptors.
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Raybould, Helen E., Jorg Glatzle, Carla Robin, James H. Meyer, Thomas Phan, Helen Wong, and Catia Sternini. "Expression of 5-HT3 receptors by extrinsic duodenal afferents contribute to intestinal inhibition of gastric emptying." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 3 (March 1, 2003): G367—G372. http://dx.doi.org/10.1152/ajpgi.00292.2001.
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Intestinal perfusion with carbohydrates inhibits gastric emptying via vagal and spinal capsaicin-sensitive afferent pathways. The aim of the present study was to determine the role of 1) 5-hydroxytryptamine (5-HT)3receptors (5-HT3R) in mediating glucose-induced inhibition of gastric emptying and 2) 5-HT3R expression in vagal and spinal afferents in innervating the duodenum. In awake rats fitted with gastric and duodenal cannulas, perfusion of the duodenum with glucose (50 and 100 mg) inhibited gastric emptying. Intestinal perfusion of mannitol inhibited gastric emptying only at the highest concentration (990 mosm/kgH2O). Pretreatment with the 5-HT3R antagonist tropisetron abolished both glucose- and mannitol-induced inhibition of gastric emptying. Retrograde labeling of visceral afferents by injection of dextran-conjugated Texas Red into the duodenal wall was used to identify extrinsic primary afferents. Immunoreactivity for 5-HT3R, visualized with an antibody directed to the COOH terminus of the rat 5-HT3R, was found in >80% of duodenal vagal and spinal afferents. These results show that duodenal extrinsic afferents express 5-HT3R and that the receptor mediates specific glucose-induced inhibition of gastric emptying. These findings support the hypothesis that enterochromaffin cells in the intestinal mucosa release 5-HT in response to glucose, which activates 5-HT3R on afferent nerve terminals to evoke reflex changes in gastric motility. The primary glucose sensors of the intestine may be mucosal enterochromaffin cells.