Relevant bibliographies by topics / Superficial dorsal horn

Academic literature on the topic 'Superficial dorsal horn'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Superficial dorsal horn.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Superficial dorsal horn"

1

Jinks, Steven L., and E. Carstens. "Superficial Dorsal Horn Neurons Identified by Intracutaneous Histamine: Chemonociceptive Responses and Modulation by Morphine." Journal of Neurophysiology 84, no. 2 (August 1, 2000): 616–27. http://dx.doi.org/10.1152/jn.2000.84.2.616.

Full text
Abstract:
We have investigated whether neurons in superficial laminae of the spinal dorsal horn respond to intracutaneous (ic) delivery of histamine and other irritant chemicals, and thus might be involved in signaling sensations of itch or chemogenic pain. Single-unit recordings were made from superficial lumbar dorsal horn neurons in pentobarbital sodium–anesthetized rats. Chemoresponsive units were identified using ic microinjection of histamine (3%, 1 μl) into the hindpaw as a search stimulus. All superficial units so identified [9 nociceptive-specific (NS), 26 wide-dynamic-range (WDR)] responded to subsequent ic histamine. A comparison group of histamine-responsive deep dorsal horn neurons ( n = 16) was similarly identified. The mean histamine-evoked discharge decayed to 50% of the maximal rate significantly more slowly for the superficial (92.2 s ± 65.5, mean ± SD) compared with deep dorsal horn neurons (28.2 s ± 11.6). In addition to responding to histamine, most superficial dorsal horn neurons were also excited by ic nicotine (22/25 units), capsaicin (21/22), topical mustard oil (5/6), noxious heat (26/30), and noxious and/or innocuous mechanical stimuli (except for 1 unit that did not have a mechanosensitive receptive field). Application of a brief noxious heat stimulus during the response to ic histamine evoked an additive response in all but two cases, followed by transient depression of firing in 11/20 units. Intrathecal (IT) administration of morphine had mixed effects on superficial dorsal horn neuronal responses to ic histamine and noxious heat. Low morphine concentrations (100 nM to 1 μM) facilitated histamine-evoked responses (to >130% of control) in 9/24 units, depressed the responses (by >70%) in 11/24, and had no effect in 4. Naloxone reversed morphine-induced effects in some but not all cases. A higher morphine concentration (10 μM) had a largely depressant, naloxone-reversible effect on histamine responses. Responses of the same superficial neurons to noxious heat were facilitated (15/25), reduced (8/25), or unaffected (2/25) by low morphine concentrations and were depressed by the higher morphine concentration. In contrast, deep dorsal horn neuronal responses to both histamine and noxious heat were primarily depressed by low concentrations of morphine in a naloxone-reversible manner. These results indicate that superficial dorsal horn neurons respond to both pruritic and algesic chemical stimuli and thus might participate in transmitting sensations of itch and/or chemogenic pain. The facilitation of superficial neuronal responses to histamine by low concentrations of morphine, coupled with inhibition of deep dorsal horn neurons, might underlie the development of pruritis that is often observed after epidural morphine.
APA, Harvard, Vancouver, ISO, and other styles
2

Zhang, Kai-Ming, Xiao-Min Wang, Angela M. Peterson, Wen-Yan Chen, and Sukhbir S. Mokha. "α2-Adrenoceptors Modulate NMDA-Evoked Responses of Neurons in Superficial and Deeper Dorsal Horn of the Medulla." Journal of Neurophysiology 80, no. 4 (October 1, 1998): 2210–14. http://dx.doi.org/10.1152/jn.1998.80.4.2210.

Full text
Abstract:
Kai-Ming Zhang, Xiao-Min Wang, Angela M. Peterson, Wen-Yan Chen, and Sukhbir S. Mokha. α2-Adrenoceptors modulate NMDA-evoked responses of neurons in the superficial and deeper dorsal horn of the medulla. J. Neurophysiol. 80: 2210–2214, 1998. Extracellular single unit recordings were made from neurons in the superficial and deeper dorsal horn of the medulla (trigeminal nucleus caudalis) in 21 male rats anesthetized with urethan. NMDA produced an antagonist-reversible excitation of 46 nociceptive as well as nonnociceptive neurons. Microiontophoretic application of a preferential α2-adrenoceptor (α2AR) agonist, (2-[2,6-dichloroaniline]-2-imidazoline) hydrochloride (clonidine), reduced the NMDA-evoked responses of 86% (6/7) of nociceptive-specific (NS) neurons, 82% (9/11) of wide dynamic range (WDR) neurons, and 67% (4/6) of low-threshold (LT) neurons in the superficial dorsal horn. In the deeper dorsal horn, clonidine inhibited the NMDA-evoked responses of 94% (16/17) of NS and WDR neurons and 60% (3/5) of LT neurons. Clonidine facilitated the NMDA-evoked responses in 14% (1/17) of NS, 9% (1/11) of WDR, and 33% (2/6) of LT neurons in the superficial dorsal horn. Idazoxan, an α2AR antagonist, reversed the inhibitory effect of clonidine in 90% (9/10) of neurons, whereas prazosin, an α1-adrenoceptor antagonist with affinity for α2BAR, and α2CAR, were ineffective. We suggest that activation of α2ARs produces a predominantly inhibitory modulation of the NMDA-evoked responses of nociceptive neurons in the medullary dorsal horn.
APA, Harvard, Vancouver, ISO, and other styles
3

Li, Jianhua, and Jere H. Mitchell. "Role of NO in modulating neuronal activity in superficial dorsal horn of spinal cord during exercise pressor reflex." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 3 (September 1, 2002): H1012—H1018. http://dx.doi.org/10.1152/ajpheart.00174.2002.

Full text
Abstract:
Static contraction of hindlimb skeletal muscle in cats induces a reflex pressor response. The superficial dorsal horn of the spinal cord is the major site of the first synapse of this reflex. In this study, static contraction of the triceps surae muscle was evoked by electrical stimulation of the tibial nerve for 2 min in anesthetized cats (stimulus parameters: two times motor threshold at 30 Hz, 0.025-ms duration). Ten stimulations were performed and 1-min rest was allowed between stimulations. Muscle contraction caused a maximal increase of 32 ± 5 mmHg in mean arterial pressure (MAP), which was obtained from the first three contractions. Activated neurons in the superficial dorsal horn were identified by c-Fos protein. Distinct c-Fos expression was present in the L6-S1 level of the superficial dorsal horn ipsilateral to the contracting leg (88 ± 14 labeled cells per section at L7), whereas only scattered c-Fos expression was observed in the contralateral superficial dorsal horn (9 ± 2 labeled cells per section, P < 0.05 compared with ipsilateral section). A few c-Fos-labeled cells were found in control animals (12 ± 5 labeled cells per section, P < 0.05 compared with stimulated cats). Furthermore, double-labeling methods demonstrated that c-Fos protein coexisted with nitric oxide (NO) synthase (NOS) positive staining in the superficial dorsal horn. Finally, an intrathecal injection of an inhibitor of NOS, N-nitro-l-arginine methyl ester (5 mM), resulted in fewer c-Fos-labeled cells (58 ± 12 labeled cells per section) and a reduced maximal MAP response (20 ± 3 mmHg, P < 0.05). These results suggest that the exercise pressor reflex induced by static contraction is mediated by activation of neurons in the superficial dorsal horn and that formation of NO in this region is involved in modulating the activated neurons and the pressor response to contraction.
APA, Harvard, Vancouver, ISO, and other styles
4

Dodd, J., and T. M. Jessell. "Cell surface glycoconjugates and carbohydrate-binding proteins: possible recognition signals in sensory neurone development." Journal of Experimental Biology 124, no. 1 (September 1, 1986): 225–38. http://dx.doi.org/10.1242/jeb.124.1.225.

Full text
Abstract:
Dorsal root ganglion (DRG) neurones transmit cutaneous sensory information from the periphery to the dorsal horn of the spinal cord. Subpopulations of DRG neurones that subserve distinct sensory modalities project to discrete regions in the dorsal horn. The formation of specific sensory connections during development may involve cell-surface interactions with spinal cord cells. Molecules that are expressed on the surface of functional subpopulations of DRG and dorsal horn neurones have therefore been identified. Distinct subsets of DRG neurones express globo- or lactoseries carbohydrate differentiation antigens. The expression of defined carbohydrate structures correlates with the embryonic lineage, peptide phenotype and the central termination site of DRG neurones. Similar or identical glycoconjugates have been implicated in cellular interactions that contribute to preimplantation embryonic development. Small-diameter DRG neurones that project to the superficial dorsal horn express N-acetyllactosamine backbone structures that are potential ligands for beta-galactoside-specific binding proteins (lectins). Two lectins have been identified that are expressed early in development in the superficial dorsal horn. These complementary molecules may contribute to the development of sensory afferent projections in the spinal cord.
APA, Harvard, Vancouver, ISO, and other styles
5

Donovan-Rodriguez, Tansy, Anthony H. Dickenson, and Catherine E. Urch. "Gabapentin Normalizes Spinal Neuronal Responses That Correlate with Behavior in a Rat Model of Cancer-induced Bone Pain." Anesthesiology 102, no. 1 (January 1, 2005): 132–40. http://dx.doi.org/10.1097/00000542-200501000-00022.

Full text
Abstract:
Background Cancer-induced bone pain is a major clinical problem for which current treatments lack full efficacy. Gabapentin is licensed for use in neuropathic pain yet is also effective against inflammatory stimuli in animals. Methods A rat model of cancer-induced bone pain using the MRMT-1 cell line injected into the tibia was established to investigate the efficacy of acute (10, 30, 100 mg/kg) and chronic (30 mg/kg) systemic gabapentin on electrophysiological superficial dorsal horn neuronal responses to natural and noxious electrical stimuli, as well as on pain-related behavior. Results In electrophysiological studies gabapentin worked both acutely (100 mg/kg) and chronically (30 mg/kg) to normalize the hyperexcitable superficial dorsal horn neuronal response, significantly reducing electrical-evoked and mechanical-evoked but not thermal-evoked responses. The behavioral study showed that chronic gabapentin (30 mg/kg) significantly attenuated pain behavior in MRMT-1 rats, restoring responses to preoperative baseline degrees, and that this attenuation was accompanied by a reversion to normal (non-MRMT-1) wide-dynamic-range: nociceptive specific superficial dorsal horn neuronal profiles. Conclusions Pain-related behavior in this rat model of cancer-induced bone pain is strongly linked to hyperexcitability of a population of superficial dorsal horn neurones. Gabapentin normalizes the cancer-induced bone pain induced dorsal horn neuronal changes and attenuates pain behavior. It may therefore provide a novel clinical treatment for cancer-induced bone pain.
APA, Harvard, Vancouver, ISO, and other styles
6

Mizuno, Masaharu, Go Kato, and Andrew M. Strassman. "Spatial organization of activity evoked by focal stimulation within the rat spinal dorsal horn as visualized by voltage-sensitive dye imaging in the slice." Journal of Neurophysiology 122, no. 4 (October 1, 2019): 1697–707. http://dx.doi.org/10.1152/jn.00697.2018.

Full text
Abstract:
In a prior study using laser scanning photostimulation, we found a pronounced cell type-specific mediolateral asymmetry in the local synaptic connectivity in the superficial laminae of the spinal dorsal horn (Kosugi M, Kato G, Lukashov S, Pendse G, Puskar Z, Kozsurek M, Strassman AM. J Physiol 591: 1935–1949, 2013). To obtain information on dorsal horn organization that might complement findings from microelectrode studies, voltage-sensitive dye imaging was used in the present study to examine patterns of activity evoked by focal electrical stimulation, in the presence and absence of synaptic blocking agents, at different positions in transverse, parasagittal, and horizontal slices of the dorsal horn of 2- to 3-wk -old male rats. A pronounced difference in responsiveness was found between medial and lateral dorsal horn, in that medial sites in the superficial dorsal horn showed much larger synaptic responses to focal stimulation than lateral sites. This difference appeared to be a result of a difference in the intrinsic elements of the dorsal horn, rather than a difference in the inputs from the white matter, because the stimulus intensities were subthreshold for evoking synaptic responses from stimulation at sites in the white matter, although it is also possible that the greater responsiveness is due, at least in part, to activation of Aβ primary afferent fibers that pass through the medial dorsal horn. The results raise the possibility of differences between medial and dorsal horn that need to be taken into account in the interpretation of studies of dorsal horn organization. NEW & NOTEWORTHY We used voltage-sensitive dye imaging to obtain information on spatial aspects of dorsal horn organization that are difficult to examine with single-cell approaches because of the limitations of microelectrode sampling. The most noteworthy finding was a previously unreported, extreme difference between medial and lateral dorsal horn in responsiveness to focal stimulation that appears to result, at least in part, from a greater degree of excitability or local connectivity in medial dorsal horn.
APA, Harvard, Vancouver, ISO, and other styles
7

Moore, K. A., H. Baba, and C. J. Woolf. "Gabapentin — Actions on adult superficial dorsal horn neurons." Neuropharmacology 43, no. 7 (December 2002): 1077–81. http://dx.doi.org/10.1016/s0028-3908(02)00226-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Alles, Sascha R. A., Filipe Nascimento, Rafael Luján, Ana P. Luiz, Queensta Millet, M. Ali Bangash, Sonia Santana-Varela, et al. "Sensory neuron–derived NaV1.7 contributes to dorsal horn neuron excitability." Science Advances 6, no. 8 (February 2020): eaax4568. http://dx.doi.org/10.1126/sciadv.aax4568.

Full text
Abstract:
Expression of the voltage-gated sodium channel NaV1.7 in sensory neurons is required for pain sensation. We examined the role of NaV1.7 in the dorsal horn of the spinal cord using an epitope-tagged NaV1.7 knock-in mouse. Immuno–electron microscopy showed the presence of NaV1.7 in dendrites of superficial dorsal horn neurons, despite the absence of mRNA. Rhizotomy of L5 afferent nerves lowered the levels of NaV1.7 in the dorsal horn. Peripheral nervous system–specific NaV1.7 null mutant mice showed central deficits, with lamina II dorsal horn tonic firing neurons more than halved and single spiking neurons more than doubled. NaV1.7 blocker PF05089771 diminished excitability in dorsal horn neurons but had no effect on NaV1.7 null mutant mice. These data demonstrate an unsuspected functional role of primary afferent neuron-generated NaV1.7 in dorsal horn neurons and an expression pattern that would not be predicted by transcriptomic analysis.
APA, Harvard, Vancouver, ISO, and other styles
9

Hu, Hui-Juan, and Robert W. Gereau. "ERK Integrates PKA and PKC Signaling in Superficial Dorsal Horn Neurons. II. Modulation of Neuronal Excitability." Journal of Neurophysiology 90, no. 3 (September 2003): 1680–88. http://dx.doi.org/10.1152/jn.00341.2003.

Full text
Abstract:
Protein kinases belonging to the protein kinase A (PKA), protein kinase C (PKC), and extracellular signal-related kinase (ERK) families have been identified as key players in modulating nociception at the level of the spinal cord dorsal horn, yet little is known about the effects of these kinases on membrane properties of the dorsal horn neurons. PKA, PKC, and ERK exert inhibitory effects on transient potassium currents (A-type currents or IA) in mouse superficial dorsal horn neurons ( Hu et al. 2003 ). Here we aimed to determine the effects of these kinases on action potential firing and membrane properties of these neurons to evaluate the impact of the modulation of IA (and other conductances) in these neurons. We found that activating PKC and PKA has dramatic effects on action potential firing, reflecting an increase in the excitability of superficial dorsal horn neurons. In addition, we found that inhibitors of both PKC and ERK signaling decrease the excitability of dorsal horn neurons, suggesting that these kinases exert a tonic excitation of these cells. Consistent with our findings that these kinases inhibit A-type currents, we found that PKA, PKC, and ERK act to shorten the first-spike latency after depolarization induced by current injection. In addition, activation of these kinases increases spike frequency and action potential amplitude of dorsal horn neurons. Interestingly, we found that the effects of PKA and PKC activators are blocked by inhibitors of ERK signaling, suggesting that PKA and PKC may exert their actions by activation of ERKs.
APA, Harvard, Vancouver, ISO, and other styles
10

Jennings, Ernie. "Differential Afferent Input To Superficial and Deep Dorsal Horn." NeuroReport 13, no. 7 (May 2002): 929–30. http://dx.doi.org/10.1097/00001756-200205240-00004.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Superficial dorsal horn"

1

Suthamnatpong, Ornsiri. "Organisational aspects of the superficial dorsal horn of the lumbar spinal cord." Thesis, University of Liverpool, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263765.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Coull, Jeffrey A. M. "Plasticity of local inhibition in the superficial dorsal horn and its contribution to neuropathic pain." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85145.

Full text
Abstract:
Neurons found in the superficial dorsal horn (SDH), particularly in the first lamina, are critical for mediating transmission of pain-related information to the brain, and thus influence pain perception. Excitability control of these neurons derives largely from a network of inhibitory interneurons that render dynamic inhibition via the GABA (gamma-aminobutyric acid) and glycine neurotransmitter systems. However, the processes that contribute to the regulation of these systems under normal and pathophysiological conditions have not been well elucidated. To shed light on these issues, our studies employed a variety of techniques to examine mechanisms of plasticity of intrinsic inhibition in the SDH. We began this survey by examining the organization of GABA- and glycine-mediated inhibition in SDH neurons from developmentally immature rats; this study was undertaken to understand the early arrangements of local inhibition in the pain pathway, a critical study for a system that is phylogenetically primitive. We found that in slices taken from neonates, corelease of GABA and glycine from terminals coactivated postsynaptic GABA A and glycine receptors (GABAARs and GlyRs) on lamina I and II neurons. In contrast, at all ages older than three weeks, quantal release of GABA and glycine never coactivated GABAA and glycine receptors at synapses. Because neurobiological processes will often revert to a developmental state when subjected to insult, we next assessed whether lamina I neuronal inhibitory synapses would assume an immature-like configuration after nerve injury. We found that GABAARs and GlyRs did indeed comediate quantal postsynaptic events in adult lamina I neurons after peripheral nerve injury (PNI); moreover, we revealed a shift in neuronal anion gradient that translated to GABAAR/GlyR-mediated postsynaptic currents that were depolarizing. This shift was caused by the downregulation of the anion cotransporter KCC2, and was shown to direc
APA, Harvard, Vancouver, ISO, and other styles
3

Stewart, Anika Louise. "Which neurones in the superficial dorsal horn of the rat spinal cord mediate acute itch?" Thesis, University of Liverpool, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.425704.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Bailey, Andrea Lee. "A behavioural and morphological analysis of compromised primary afferent C-fibre input to the superficial dorsal horn of the rat spinal cord." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66754.

Full text
Abstract:
Neuropathic pain is caused by direct or indirect damage of the central nervous system or of primary afferent fibres (PAF). Small diameter C-fibres (C-PAF) are of great interest as they are responsible for the transduction of pain-related signals arising from the periphery. The adult C-fibre neuronal populations can be distinguished by their neuropeptide expression profile. The peptidergic population expresses neuropeptides such as substance P (sP) and calcitonin gene-related peptide (CGRP). The non-peptidergic C-fibres express the cell surface glycoproteins binding the plant lectin IB4 and lack neuropeptides. Non-peptidergic afferents are known to play a role in nociceptive transmission; however our understanding of the nature of this information and how it is processed by these afferents in the spinal cord is limited. In this thesis, we focused on examining the morphological, neurochemical and behavioural consequences of compromised C-PAF input to the superficial dorsal horn. Our approach was two-fold: a) to study the effects of a constriction injury of the sciatic nerve; b to study the effects of selectively ablating the IB4-binding sub-population of C-PAFs by means of an intra-sciatic injection of IB4-Saporin. In the peripheral nerve lesion study we examined the time-related effects of a constriction neuropathy on the peptidergic and non-peptidergic C-PAFs using neurochemical markers for each neuronal population. We observed a transient loss of IB4-binding in lamina II, resultant from the degeneration of CIa synaptic glomeruli. Paw withdrawal latencies to noxious heat stimuli were significantly reduced in neuropathic animals throughout the 3 week time course. Sensitivity to cold stimuli was also significantly altered in neuropathic animals. Paw withdrawal thresholds to innocuous and noxious mechanical stimulation were significantly reduced in neuropathic animals. We did not detect any change in the de
La douleur neuropathique est causée par des lésions des fibres afférentes primaires. Les fibres nerveuses de type C (non-myélinisées) sont d'un intérêt particulier, étant responsables de la transmission des influx douloureux provenant de la périphérie. La population de fibres nerveuses C est hétérogène: a) la population peptidergique contient des neuropeptides comme la substance P (sP) et le peptide lié au gène de la calcitonine (CGRP); b) la population non-peptidergique a la capacité de se lier à la lectine IB4. Notre compréhension de la nature de l'information nociceptive et des mécanismes impliqués dans le traitement de celle-ci par ces fibres afférentes non-peptidergiques dans la moelle épinière restent limités. Dans cette thèse, nous avons étudié les conséquences morphologiques, neurochimiques et comportementales des lésions des fibres afférentes primaires de type C (C-PAFs) dans la corne dorsale superficielle. Cet effort fut mené de deux façons: soit par des lésions produites par constriction du nerf sciatique, soit par suppression sélective de la sous-population de C-PAFs se liant à IB4. L'observation des terminaisons des PAFs se liant à IB4 dans la couche II révélait la perte passagère du marquage d'IB4 résultant de la dégénérescence des glomérules synaptiques CIa. Des tests mesurant les temps de retrait de patte en réponse à des stimulations mécaniques, thermiques chaudes et froides appliquées à la périphérie furent effectués chez ces animaux. Spécifiquement, les seuils de retrait étaient plus faibles lors des tests de nociception thermique effectués au cours des trois semaines d'étude. La réactivité aux stimulations froides était également significativement altérée chez les animaux neuropathiques. Les seuils de retraits de patte vis-à-vis les stimulations mécaniques étaient significativement réduits chez les animaux neuropathique
APA, Harvard, Vancouver, ISO, and other styles
5

Gerke, Michelle Barbara. "Characterisation of the expression of cell-surface carbohydrates by primary sensory neurones and their applications in the study of pain." Thesis, Queensland University of Technology, 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Ford, Neil C. "The role of voltage-independent cation channels in shaping spinal nociceptive circuit output and pain sensitivity in developing rodents." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1530798481340688.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Farrell, Kristen Elise. "Investigation of visceral sensory processing mechanisms in the superficial dorsal horn of the spinal cord." Thesis, 2017. http://hdl.handle.net/1959.13/1335508.

Full text
Abstract:
Research Doctorate - Doctor of Philosophy (PhD)
Pain is the most common symptom of inflammatory diseases of viscera or the gastrointestinal tract. Importantly, pain occurs during active disease and often persists during clinical remission. The specific functional mechanisms underlying the development and maintenance of visceral pain are not known. To date, functional studies have focussed on the peripheral nervous system, using gut-nerve preparations, in animal models of visceral hypersensitivity. Clinical studies, however, suggest changes in the central nervous system CNS contribute to altered sensory perception in visceral inflammation. This thesis first explored the central mechanisms underlying visceral hypersensitivity in animal models of visceral inflammation. I completed a systematic review and found extensive evidence for CNS plasticity, particularly within the spinal cord dorsal horn (DH), in animal models of visceral inflammation. I also found no studies had examined the functional properties of DH neurons during visceral inflammation even though these properties are critical determinants of neuron output and altered signaling to the brain. Next, to study the functional properties of neurons that received colonic inputs, I developed an in vivo preparation that permitted wholecell electrophysiological recording from DH neurons in intact adult mice. I showed that in naïve animals, neurons with colonic inputs responded to visceral stimulation with predominately subthreshold synaptic activity. Their membrane and synaptic properties also differed from neurons lacking colonic inputs. I next repeated these experiments in a mouse model of mild colitis. During colitis the responses of DH neurons to visceral and cutaneous stimulation and their synaptic properties were altered in a manner that would make DH neurons more excitable. Conversely, several measures of intrinsic excitability were decreased following colitis. These data suggest visceral inflammation has complex effects on the functional properties of DH neurons and likely reflects the crucial role the spinal cord plays in modulating sensory inputs from the viscera.
APA, Harvard, Vancouver, ISO, and other styles
8

Wrigley, Paul John. "Cold thermal processing in the spinal cord." 2006. http://hdl.handle.net/2123/1619.

Full text
Abstract:
Doctor of Philosophy(PhD)
Two recently identified transient receptor potential (TRP) channels, TRPM8 and TRPA1, have been proposed to play an important role in mammalian cool and cold peripheral sensory transduction. When expressed in cell-lines the cloned TRPM8 and TRPA1 receptors have distinct pharmacological and temperature response characteristics. Although these receptors are also transported to the central terminals of primary afferents, little is known about their centrally mediated actions. In this thesis, I use an in vitro electrophysiological approach to investigate the dorsal horn processing of cool afferent modalities and the role of TRP ion channels. The results of this thesis provide further information on thermal processing, indicate direction for further research and suggest possible therapeutic targets for the management of abnormal cold sensory processing. Initial experiments demonstrate that the cooling agents and known TRPM8 and TRPA1 agonists, menthol and icilin, inhibit primary afferent evoked excitatory postsynaptic currents (EPSCs) in rat spinal cord dorsal horn neurons. In addition, temperature reduction, menthol and icilin increase the frequency of miniature EPSCs without affecting amplitude distribution or kinetics. Little or no direct postsynaptic effect on dorsal horn neurons, GABAergic or glycinergic transmission was found. In combination, these observations demonstrate that temperature reduction, menthol and icilin act presynaptically to increase the probability of glutamate release from primary afferent fibres. Further examination of the changes in glutamatergic synaptic transmission induced by temperature reduction, menthol and icilin reveals a subset of neurons sensitive to innocuous cool (< 29 oC) and low concentrations of icilin (3-10 µM) which closely match the temperature activation and pharmacological profile of TRPM8. In addition, the majority of lamina I and II neurons displayed characteristics partly consistent with TRPA1-activation, including a concentration-dependent response to icilin and blockade by ruthenium red. The present experiments did not allow thermal characterisation of these TRPA1-like responses. Together these observations indicate that the effects of menthol and icilin on glutamatergic synaptic transmission in the superficial dorsal horn are mediated by TRPM8 and possibly by TRPA1. Examination of the anatomical location of neurons activated by temperature reduction, menthol, icilin and capsaicin allowed the central termination pattern of thermoreceptive primary afferent fibres with specific TRP-like response characteristics to be determined. TRPM8-like presynaptic activation was confined to a subpopulation of neurons located in lamina I and outer lamina II, while the majority of neurons throughout laminae I and II received inputs sensitive to menthol, high concentrations of icilin and capsaicin. These findings suggest that innocuous cool sensation projects to a specific subpopulation of superficial dorsal horn neurons unlike other modalities (mediated by TRPV1, possibly TRPA1 and other receptors), which non-selectively engage circuits within the entire superficial dorsal horn. No morphological specificity was identified for recovered neurons after electrophysiological characterisation. Finally, mu-opioids were shown to inhibit basal glutamatergic synaptic transmission as well as menthol- and icilin-induced transmission in the superficial dorsal horn. Of particular interest, delta-opioids selectively inhibited icilin-induced synaptic transmission within the same location. The selective effect of delta-opioids suggests a possible role in modulating receptors activated by icilin (TRPM8 and TRPA1). Overall, this thesis provides further evidence that TRPM8 is responsible for the transduction of innocuous cold sensation in mammals and is a potential therapeutic target in humans with cold hyperaesthesia secondary to abnormal thermal processing. The use of delta-opioid agonists warrants further investigation in cold hypersensitivity states and potentially other forms of pain.
APA, Harvard, Vancouver, ISO, and other styles

Books on the topic "Superficial dorsal horn"

1

Cervero, F., G. J. Bennett, and P. M. Headley, eds. Processing of Sensory Information in the Superficial Dorsal Horn of the Spinal Cord. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0825-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Fernando, Cervero, Bennett G. J, Headley P. M, and North Atlantic Treaty Organization. Scientific Affairs Division., eds. Processing of sensory information in the superficial dorsal horn of the spinal cord. New York: Plenum Press, 1989.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Bennett, G. J., F. Cervero, and P. M. Headley. Processing of Sensory Information in the Superficial Dorsal Horn of the Spinal Cord. Springer, 2013.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Bennett, G. J., F. Cervero, and P. M. Headley. Processing of Sensory Information in the Superficial Dorsal Horn of the Spinal Cord. Springer London, Limited, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Donaghy, Michael. The clinical approach. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0030.

Full text
Abstract:
This chapter describes the appropriate clinical approach to take when presented with a patient reporting a neurological symptom. Just under 10 per cent of the population consult their general practitioner about a neurological symptom each year in the United Kingdom. About 10 per cent of these are referred for a specialist opinion, usually to a neurologist. Nine conditions account for roughly 75 per cent of general neurological referrals and are diagnosed initially on purely clinical grounds, with the other 25 per cent representing the full range of other, potentially very rare, neurological disorders.This chapter underlines the importance of a thorough and informative history to achieve successful diagnosis. Crucial facets for a good history include information on the time course of symptom development, whether symptoms are negative or positive, previous neurological history (both personal and familial), as well as other potentially contributory general medical disorders. The general neurological examination is also described, as are specific examination manoeuvres that may be added to the general neurological examination in specific clinical circumstances.Reflexes play an important role in diagnostic neurology because they reflect the integrity of, or alterations in, the neural structures responsible for their arc. Loss of a reflex may be due to interruption of the afferent path by a lesion involving the first sensory neurone in the peripheral nerves, plexuses, spinal nerves, or dorsal roots, by damage to the central paths of the arc in the brainstem or spinal cord, by lesions of the lower motor neurone at any point between the anterior horn cells and the muscles, of the muscles themselves, or by the neural depression produced by neural shock. In clinical practice, the most useful and oft-elicited reflexes are the tendon reflexes of the limbs, the jaw jerk, the plantar response, the superficial abdominal reflexes, the pupil-light response, and in infants, the Moro reflex. The place of these particular reflexes in the routine neurological examination is outlined, and the elicitation and significance of these reflexes and of a wide variety of others which are used occasionally are described.Examinations that allow localization lesions that are responsible for muscle weaknesses and the assessment of somatosensory abnormalities are described, as are neurological disorders that result in identifiable gait disorders. The clinical signs and examinations relevant to autonomic disorders are also discussed.Intensive care may be required for patients critically ill either as a result of primary neurological disease, or in those in whom a neurological disorder is a component of, or secondary to, a general medical disorder. Indications for admission to neurological intensive care have been defined (Howard et al. 2003): impaired consciousness, bulbar muscle failure, severe ventilatory respiratory failure, uncontrolled seizures, severely raised intracranial pressure, some monitoring and interventional treatments, and unforeseen general medical complications. Naturally specific treatments indicated for the particular diagnosis should be instituted along with general intensive care measures.Finally, the discussion of diagnoses of chronic or terminal conditions with patients is discussed, with particular focus on the best way to present the diagnosis to the patient.
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Superficial dorsal horn"

1

Cervero, Fernando. "The Superficial Dorsal Horn." In Processing of Sensory Information in the Superficial Dorsal Horn of the Spinal Cord, 1–9. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0825-6_1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Collins, J. G. "What Modulates Tonic Modulation of Spinal Dorsal Horn Neurons?" In Processing of Sensory Information in the Superficial Dorsal Horn of the Spinal Cord, 489–98. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0825-6_49.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Willis, William D. "Projections of the Superficial Dorsal Horn to the Midbrain and Thalamus." In Processing of Sensory Information in the Superficial Dorsal Horn of the Spinal Cord, 217–37. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0825-6_24.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Drdla, Ruth, and Jürgen Sandkühler. "Long-Term Potentiation in Superficial Spinal Dorsal Horn: A Pain Amplifier." In Synaptic Plasticity in Pain, 201–18. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0226-9_9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Sugiura, Y., N. Terui, Y. Hosoya, and K. Kohno. "Distribution of Unmyelinated Primary Afferent Fibers in the Dorsal Horn." In Processing of Sensory Information in the Superficial Dorsal Horn of the Spinal Cord, 15–27. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0825-6_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Duggan, A. W., C. R. Morton, I. A. Hendry, and W. D. Hutchison. "Peripheral Stimuli Releasing Neuropeptides in the Dorsal Horn of the Cat." In Processing of Sensory Information in the Superficial Dorsal Horn of the Spinal Cord, 347–63. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0825-6_35.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Hope, P. J., N. El-Yassir, S. M. Fleetwood-Walker, and R. Mitchell. "Opioid and Serotonergic Effects on Lamina I and Deeper Dorsal Horn Neurones." In Processing of Sensory Information in the Superficial Dorsal Horn of the Spinal Cord, 399–402. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0825-6_39.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Ness, T. J., and G. F. Gebhart. "Superficial Dorsal Horn Neurons in the Rat Responsive to Visceral and Cutaneous Inputs." In Processing of Sensory Information in the Superficial Dorsal Horn of the Spinal Cord, 159–62. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0825-6_18.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Leah, J. D., T. Herdegen, and M. Zimmermann. "Physiological and Pharmacological Induction of C-FOS Protein Immunoreactivity in Superficial Dorsal Horn Neurones." In Processing of Sensory Information in the Superficial Dorsal Horn of the Spinal Cord, 307–10. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0825-6_30.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Perl, Edward R., and Stephen P. Schneider. "Glutamate and Other Putative Mediators of Fast Synaptic Action in the Superficial Dorsal Horn." In Processing of Sensory Information in the Superficial Dorsal Horn of the Spinal Cord, 331–45. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0825-6_34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Superficial dorsal horn' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography