Journal articles on the topic 'Superficial dorsal horn'
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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Nastrom, J., S. P. Schneider, and E. R. Perl. "Differential L-glutamate responsiveness among superficial dorsal horn neurons." Journal of Neurophysiology 72, no. 6 (December 1, 1994): 2956–65. http://dx.doi.org/10.1152/jn.1994.72.6.2956.
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1. Intracellular recordings were made from 128 superficial dorsal horn (laminae I and II) neurons in slice preparations of the lumbosacral spinal cord obtained from young hamsters. Stimulation of the segmental dorsal root evoked postsynaptic potentials in all neurons. The average transmembrane resting potential was -61 +/- 1 mV (mean +/- SE; n = 123). The mean action potential amplitude was 75 +/- 1 mV (n = 105) with a duration at half peak of 1.1 +/- 0.1 ms (n = 102). The mean input resistance of these neurons was 72 +/- 4 M omega (n = 125). These values are comparable to those reported in other studies on neurons of this region using penetrating microelectrodes. 2. Bath application of N-methyl-D-aspartate (NMDA; 50 microM) depolarized 67 of 71 (94%) of the tested neurons. Superfusion with the non-NMDA amino acid agonists DL-alpha-amino-3-hydroxy-5-methyl-4- isoxazole propionic acid (AMPA; 20 microM) and kainate (KA; 50 microM) depolarized all tested neurons by > 10 mV. On the other hand, only 13 of 67 (19%) tested neurons were depolarized > 4 mV by superfusion solutions containing 3 mM L-glutamate (Glu). L-Aspartate at 3 mM depolarized three out of seven neurons by > 4 mV and appeared to be equally as effective as Glu. 3. The non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM) substantially attenuated the AMPA- and KA-induced depolarizations and partially attenuated the NMDA-induced depolarizations. The NMDA antagonist 3 [(+/-)-2-carboxypiperazin-4-yl]-propyl-1-phosphonic acid (CPP; 50 microM) reversibly blocked the NMDA-induced depolarization in all tested neurons. Glu-induced depolarization was unaffected by CNQX but was attenuated by CPP in three of three tested neurons. These observations indicate that some of the Glu-induced depolarization was mediated by NMDA receptors. 4. CNQX reversibly attenuated excitatory postsynaptic potentials (EPSPs) produced by primary afferent activity in A delta- and C-fibers whereas CPP suppressed only the late EPSP components. Therefore in the neurons sampled, synaptic responses evoked from primary afferent fibers appear to be mediated by both non-NMDA and NMDA receptors. 5. The glutamate uptake inhibitors, L-trans-pyrrolidine-2,4-dicarboxylate (L-trans PDC; 50 microM; n = 6) and threo-3-hydroxy-D-aspartate (1 mM; n = 1) did not have a consistent effect upon Glu action background discharge, RN or Vm in Glu-unresponsive neurons.(ABSTRACT TRUNCATED AT 400 WORDS)
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Kawasaki, Yasuhiko, Terumasa Nakatsuka, Mika Sasaki, Fumimasa Amaya, and Tatsuro Kohno. "Role of D-serine in superficial dorsal horn neuron." PAIN RESEARCH 26, no. 1 (2011): 19–28. http://dx.doi.org/10.11154/pain.26.19.
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Hu, Hui-Juan, Kathi S. Glauner, and Robert W. Gereau. "ERK Integrates PKA and PKC Signaling in Superficial Dorsal Horn Neurons. I. Modulation of A-Type K+ Currents." Journal of Neurophysiology 90, no. 3 (September 2003): 1671–79. http://dx.doi.org/10.1152/jn.00340.2003.
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The transient outward potassium currents (also known as A-type currents or IA) are important determinants of neuronal excitability. In the brain, IA is modulated by protein kinase C (PKC), protein kinase A (PKA), and extracellular signal-related kinase (ERK), three kinases that have been shown to be critical modulators of nociception. We wanted to determine the effects of these kinases on IA in superficial dorsal horn neurons. Using whole cell recordings from cultured mouse spinal cord superficial dorsal horn neurons, we found that PKC and PKA both inhibit IA in these cells, and that PKC has a tonic inhibitory action on IA. Further, we provide evidence supporting the hypothesis that PKC and PKA do not modulate IA directly, but rather act as upstream activators of ERKs, which modulate IA. These results suggest that ERKs serve as signal integrators in modulation of IA in dorsal horn neurons and that modulation of A-type potassium currents may underlie aspects of central sensitization mediated by PKC, PKA, and ERKs.
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Dubuisson, David. "Effect of dorsal-column stimulation on gelatinosa and marginal neurons of cat spinal cord." Journal of Neurosurgery 70, no. 2 (February 1989): 257–65. http://dx.doi.org/10.3171/jns.1989.70.2.0257.
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✓ Single neuronal units with physiological characteristics of superficial dorsal-horn neurons were recorded extracellularly in laminae 1, 2, and 3 of cat spinal cord. When focal electrical stimulation was applied to the ipsilateral dorsal column, most of the units were excited transsynaptically at various latencies consistent with an effect mediated by large myelinated axons. Units recorded in laminae 2 and 3 had earlier latencies of activation than units in lamina 1. Units with cutaneous receptive fields only for noxious stimuli were activated at significantly longer latencies than units responsive to innocuous stimuli. The time course of these effects was consistent with the concept that many cells in laminae 1 to 3 receive direct excitatory synaptic input from collaterals of dorsal-column fibers, and some lamina 1 cells receive excitatory synaptic input from lamina 2 neurons. Previous reports have emphasized the inhibitory action of dorsal-column stimulation on nociceptive responses of cells in laminae 4 and 5 of the dorsal-horn, particularly those of the spinocervical tract in cats and the spinothalamic tract in primates. The present study suggests that some of this inhibition might be sustained by a network of interneurons in or near the substantia gelatinosa and marginal layer. The therapeutic efficiency of dorsal-column stimulation for pain relief in humans may depend in part on the activation of neurons in the superficial layers of the dorsal horn.
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Mason, Peggy. "Placing pain on the sensory map: Classic papers by Ed Perl and colleagues." Journal of Neurophysiology 97, no. 3 (March 2007): 1871–73. http://dx.doi.org/10.1152/jn.01327.2006.
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This essay looks at two papers published by Ed Perl and co-workers that identified specifically nociceptive neurons in the periphery and superficial dorsal horn. Bessou P and Perl ER. Response of cutaneous sensory units with unmyelinated fibers to noxious stimuli. J Neurophysiol 32: 1025–1043 1969. Christensen BN and Perl ER. Spinal neurons specifically excited by noxious or thermal stimuli: marginal zone of the dorsal horn. J Neurophysiol 33: 293–307 1970.
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Almeida, Armando, Isaura Tavares, and Deolinda Lima. "Projection sites of superficial or deep dorsal horn in the dorsal reticular nucleus." NeuroReport 6, no. 9 (June 1995): 1245–48. http://dx.doi.org/10.1097/00001756-199506090-00004.
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Sequeira, Sandra, and Jacques Näsström. "Low-Affinity Kainate Receptors and Long-Lasting Depression of NMDA-Receptor–Mediated Currents in Rat Superficial Dorsal Horn." Journal of Neurophysiology 80, no. 2 (August 1, 1998): 895–902. http://dx.doi.org/10.1152/jn.1998.80.2.895.
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Sequeira, Sandra and Jacques Näsström. Low-affinity kainate receptors and long-lasting depression of NMDA-receptor–mediated currents in rat superficial dorsal horn. J. Neurophysiol. 80: 895–902, 1998. In an in vitro spinal cord slice preparation whole cell electrophysiological recordings of rat superficial dorsal horn neurons responding differentially to glutamate (Glu) and N-methyl-d-aspartate (NMDA) were investigated systematically for the role of kainate (KA) receptors in modulating their activity. In these neurons, coapplication of Glu and NMDA, as well as application of Glu immediately before NMDA, induced long- and short-lasting depressions of NMDA-induced currents as well as depression of NMDA-receptor–mediated excitatory postsynaptic currents. KA applied before NMDA mimicked Glu-induced attenuating effects. Furthermore, the low-affinity KA receptor antagonist 5-nitro-6,7,8,9- tetrahydrobenzo[G]indole-2,3-dione-3-oxime potentiated Glu-induced NMDA-receptor–mediated currents in neurons responding differentially to Glu and NMDA. These results provide evidence for a novel mechanism, which may relate to classical long-term depression, involving low-affinity KA receptors in long-lasting modulation of NMDA-receptor–mediated currents. This implies a physiological role of KA receptors in long-term modulation of sensory transmission in the superficial dorsal horn of rat spinal cord.
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Akiyama, T., M. Nagamine, A. Davoodi, M. Ivanov, M. Iodi Carstens, and E. Carstens. "Innocuous warming enhances peripheral serotonergic itch signaling and evokes enhanced responses in serotonin-responsive dorsal horn neurons in the mouse." Journal of Neurophysiology 117, no. 1 (January 1, 2017): 251–59. http://dx.doi.org/10.1152/jn.00703.2016.
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Itch is often triggered by warming the skin in patients with itchy dermatitis, but the underlying mechanism is largely unknown. We presently investigated if warming the skin enhances histamine- or serotonin (5-HT)-evoked itch behavior or responses of sensory dorsal root ganglion (DRG) cells, and if responses of superficial dorsal horn neurons to innocuous warming are enhanced by these pruritogens. In a temperature-controlled environmental chamber, mice exhibited greater scratching following intradermal injection of 5-HT, but not histamine, SLIGRL, or BAM8-22, when the skin surface temperature was above 36°C. Calcium imaging of DRG cells in a temperature-controlled bath revealed that responses to 5-HT, but not histamine, were significantly greater at a bath temperature of 35°C vs. lower temperatures. Single-unit recordings revealed a subpopulation of superficial dorsal horn neurons responsive to intradermal injection of 5-HT. Of these, 58% responded to innocuous skin warming (37°C) prior to intradermal injection of 5-HT, while 100% responded to warming following intradermal injection of 5-HT. Warming-evoked responses were superimposed on the 5-HT-evoked elevation in firing and were significantly larger compared with responses pre-5-HT, as long as 30 min after the intradermal injection of 5-HT. Five-HT-insensitive units, and units that either did or did not respond to intradermal histamine, did not exhibit any increase in the incidence of warmth sensitivity or in the mean response to warming following intradermal injection of the pruritogen. The results suggest that 5-HT-evoked responses of pruriceptors are enhanced during skin warming, leading to increased firing of 5-HT-sensitive dorsal horn neurons that signal nonhistaminergic itch. NEW & NOTEWORTHY Skin warming often exacerbates itch in patients with itchy dermatitis. We demonstrate that warming the skin enhanced serotonin-evoked, but not histamine-evoked, itch behavior and responses of sensory dorsal root ganglion cells. Moreover, serotonin, but not histamine, enhanced responses of superficial dorsal horn neurons to innocuous warming. The results suggest that skin warming selectively enhances the responses of serotonin-sensitive pruriceptors, leading to increased firing of serotonin-sensitive dorsal horn neurons that signal nonhistaminergic itch.
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Li, Ping, Amelita A. Calejesan, and Min Zhuo. "ATP P2× Receptors and Sensory Synaptic Transmission Between Primary Afferent Fibers and Spinal Dorsal Horn Neurons in Rats." Journal of Neurophysiology 80, no. 6 (December 1, 1998): 3356–60. http://dx.doi.org/10.1152/jn.1998.80.6.3356.
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Li, Ping, Amelita A. Calean, and Min Zhuo. ATP P2× receptors and sensory synaptic transmission between primary afferent fibers and spinal dorsal horn neurons in rats. J. Neurophysiol. 80: 3356–3360, 1998. Glutamate is a major fast transmitter between primary afferent fibers and dorsal horn neurons in the spinal cord. Recent evidence indicates that ATP acts as another fast transmitter at the rat cervical spinal cord and is proposed to serve as a transmitter for nociception and pain. Sensory synaptic transmission between dorsal root afferent fibers and neurons in the superficial dorsal horn of the lumbar spinal cord were examined by whole cell patch-clamp recording techniques. Experiments were designed to test if ATP could serve as a transmitter at the lumbar spinal cord. Monosynaptic excitatory postsynaptic currents (EPSCs) were completely abolished after the blockade of both glutamatergic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate and N-methyl-d-aspartate receptors. No residual current was detected, indicating that glutamate but not ATP is a fast transmitter at the dorsal horn of the lumbar spinal cord. Pyridoxal-phosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS), a selective P2× receptor antagonist, produced an inhibitory modulatory effect on fast EPSCs and altered responses to paired-pulse stimulation, suggesting the involvement of a presynaptic mechanism. Intrathecal administration of PPADS did not produce any antinociceptive effect in two different types of behavioral nociceptive tests. The present results suggest that ATP P2×2 receptors modulate excitatory synaptic transmission in the superficial dorsal horn of the lumbar spinal cord by a presynaptic mechanism, and such a mechanism does not play an important role in behavioral responses to noxious heating. The involvement of other P2× subtype receptors, which is are less sensitive to PPADS, in acute nociceptive modulation and persistent pain remains to be investigated.
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Baccei, Mark L., and Maria Fitzgerald. "Intrinsic firing properties of developing rat superficial dorsal horn neurons." NeuroReport 16, no. 12 (August 2005): 1325–28. http://dx.doi.org/10.1097/01.wnr.0000175612.08560.10.
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Jeong, Hyo-Jin, Robert J. Vandenberg, and Christopher W. Vaughan. "N-arachidonyl-glycine modulates synaptic transmission in superficial dorsal horn." British Journal of Pharmacology 161, no. 4 (June 22, 2010): 925–35. http://dx.doi.org/10.1111/j.1476-5381.2010.00935.x.
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Ding, Jin-Dong, and Richard J. Weinberg. "Localization of soluble guanylyl cyclase in the superficial dorsal horn." Journal of Comparative Neurology 495, no. 6 (2006): 668–78. http://dx.doi.org/10.1002/cne.20901.
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Wall, Patrick D., and Malcolm Lidierth. "Five Sources of a Dorsal Root Potential: Their Interactions and Origins in the Superficial Dorsal Horn." Journal of Neurophysiology 78, no. 2 (August 1, 1997): 860–71. http://dx.doi.org/10.1152/jn.1997.78.2.860.
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Wall, Patrick D. and Malcolm Lidierth. Five sources of a dorsal root potential: their interactions and origins in the superficial dorsal horn. J. Neurophysiol. 78: 860–871, 1997. The dorsal root potential (DRP) was measured on the lumbar dorsal roots of urethan anesthetized rats and evoked by stimulation of five separate inputs. In some experiments, the dorsal cord potential was recorded simultaneously. Stimulation of the L3 dorsal root produced a DRP on the L2 dorsal root containing the six components observed in the cat including the prolonged negative wave (DRP V of Lloyd 1952 ). A single shock to the myelinated fibers in the sural nerve produced a DRP on the L6 dorsal root after the arrival in the cord of the afferent volley. The shape of this DRP was similar to that produced by dorsal root stimulation. Repetitive stimulation of the myelinated fibers in the gastrocnemius nerve also produced a prolonged negative DRP on the L6 dorsal root. When a single stimulus (<5 μA; 200 μs) was applied through a microelectrode to the superficial Lissauer Tract (LT) at the border of the L2 and L3 spinal segments, a characteristic prolonged negative DRP (LT-DRP) began on the L2 dorsal root after some 15 ms. Stimulation of the LT evoked DRPs bilaterally. Recordings on nearby dorsal roots showed this DRP to be unaccompanied by stimulation of afferent fibers in those roots. The LT-DRP was unaffected by neonatal capsaicin treatment that destroyed most unmyelinated fibers. Measurements of myelinated fiber terminal excitability to microstimulation showed that the LT-DRP was accompanied by primary afferent depolarization. Repetitive stimulation through a microelectrode in sensorimotor cortex provoked a prolonged and delayed negative DRP (recorded L2–L4). Stimulation in the cortical arm area and recording on cervical dorsal roots showed that the DRP was evoked more from motor areas than sensory areas of cortex. Interactions were observed between the LT-DRP and that evoked from the sural or gastrocnemius nerves or motor cortex. The LT-DRP was inhibited by preceding stimulation of the other three sources but LT stimulation did not inhibit DRPs evoked from sural or gastrocnemius nerves on the L6 dorsal root or from motor cortex on the L3 root. However, LT stimulation did inhibit the DRP evoked by a subsequent Lissaeur tract stimulus. Recordings were made from superficial dorsal horn neurons. Covergence of input from LT sural, and gastrocnemius nerves and cortex was observed. Spike-triggered averaging was used to examine the relationship between the ongoing discharge of superficial dorsal horn neurons and the spontaneous DRP. The discharge of 81% of LT responsive cells was correlated with the DRP.
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Nie, Hui, Haijun Zhang, and Han-Rong Weng. "Bidirectional Neuron–Glia Interactions Triggered by Deficiency of Glutamate Uptake at Spinal Sensory Synapses." Journal of Neurophysiology 104, no. 2 (August 2010): 713–25. http://dx.doi.org/10.1152/jn.00282.2010.
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Bidirectional interactions between neurons and glial cells are crucial to the genesis of pathological pain. The mechanisms regulating these interactions and the role of this process in relaying synaptic input in the spinal dorsal horn remain to be established. We studied the role of glutamate transporters in the regulation of such interactions. On pharmacological blockade of glutamate transporters, slow inward currents (SICs) appeared spontaneously and/or were evoked by peripheral synaptic input in the spinal superficial dorsal horn neurons, including the spinothalamic tract neurons. We showed that the SICs were induced by the release of glutamate from glial cells. On inhibition of glutamate uptake, the stimulation-induced, synaptically released glutamate activated glial cells and caused glial cells to release glutamate. Glial-derived glutamate acted on extrasynaptic N-methyl-d-aspartate (NMDA) receptors mainly composed of NR2B receptors and generated SICs, which led to depolarization and action potential generation in superficial spinal dorsal horn neurons. Thus glutamate transporters regulate glutamatergic neuron–glia interactions at spinal sensory synapses. When glutamate uptake is impaired, glial cells function like excitatory interneurons—they are activated by peripheral synaptic input and release glutamate to activate postsynaptic neurons in spinal pain pathways.
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Allen, Brian J., Jun Li, Patrick M. Menning, Scott D. Rogers, Joseph Ghilardi, Patrick W. Mantyh, and Donald A. Simone. "Primary Afferent Fibers That Contribute to Increased Substance P Receptor Internalization in the Spinal Cord After Injury." Journal of Neurophysiology 81, no. 3 (March 1, 1999): 1379–90. http://dx.doi.org/10.1152/jn.1999.81.3.1379.
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Primary afferent fibers that contribute to increased substance P receptor internalization in the spinal cord after injury. Upon noxious stimulation, substance P (SP) is released from primary afferent fibers into the spinal cord where it interacts with the SP receptor (SPR). The SPR is located throughout the dorsal horn and undergoes endocytosis after agonist binding, which provides a spatial image of SPR-containing neurons that undergo agonist interaction. Under normal conditions, SPR internalization occurs only in SPR+ cell bodies and dendrites in the superficial dorsal horn after noxious stimulation. After nerve transection and inflammation, SPR immunoreactivity increases, and both noxious as well as nonnoxious stimulation produces SPR internalization in the superficial and deep dorsal horn. We investigated the primary afferent fibers that contribute to enhanced SPR internalization in the spinal cord after nerve transection and inflammation. Internalization evoked by electrical stimulation of the sciatic nerve was examined in untreated animals, at 14 days after sciatic nerve transection or sham surgery and at 3 days after hindpaw inflammation. Electrical stimulation was delivered at intensities to excite Aβ fibers only, Aβ and Aδ fibers or A and C fibers as determined by the compound action potential recorded from the tibial nerve. Electrical stimuli were delivered at a constant rate of 10 Hz for a duration of 5 min. Transection of the sciatic nerve and inflammation produced a 33.7 and 32.5% increase in SPR and immunoreactivity in lamina I, respectively. Under normal conditions, stimulation of Aδ or C fibers evoked internalization that was confined to the superficial dorsal horn. After transection or inflammation, there was a 20–24% increase in the proportion of SPR+ lamina I neurons that exhibited internalization evoked by stimulation of Aδ fibers. The proportion of lamina I SPR+ neurons that exhibited internalization after stimulation of C-fibers was not altered by transection or inflammation because this was nearly maximal under normal conditions. Moreover, electrical stimulation sufficient to excite C fibers evoked SPR internalization in 22% of SPR+ lamina III neurons after nerve transection and in 32–36% of SPR+ neurons in lamina III and IV after inflammation. Stimulation of Aβ fibers alone never evoked internalization in the superficial or deep dorsal horn. These results indicate that activation of small-caliber afferent fibers contributes to the enhanced SPR internalization in the spinal cord after nerve transection and inflammation and suggest that recruitment of neurons that possess the SPR contributes to hyperalgesia.
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Boakye, Paul A., Vladimir Rancic, Kerri H. Whitlock, Danielle Simmons, Frank M. Longo, Klaus Ballanyi, and Peter A. Smith. "Receptor dependence of BDNF actions in superficial dorsal horn: relation to central sensitization and actions of macrophage colony stimulating factor 1." Journal of Neurophysiology 121, no. 6 (June 1, 2019): 2308–22. http://dx.doi.org/10.1152/jn.00839.2018.
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Peripheral nerve injury elicits an enduring increase in the excitability of the spinal dorsal horn. This change, which contributes to the development of neuropathic pain, is a consequence of release and prolonged exposure of dorsal horn neurons to various neurotrophins and cytokines. We have shown in rats that nerve injury increases excitatory synaptic drive to excitatory neurons but decreases drive to inhibitory neurons. Both effects, which contribute to an increase in dorsal horn excitability, appear to be mediated by microglia-derived BDNF. We have used multiphoton Ca2+ imaging and whole cell recording of spontaneous excitatory postsynaptic currents in defined-medium organotypic cultures of GAD67-GFP+ mice spinal cord to determine the receptor dependence of these opposing actions of BDNF. In mice, as in rats, BDNF enhances excitatory transmission onto excitatory neurons. This is mediated via presynaptic TrkB and p75 neurotrophin receptors and exclusively by postsynaptic TrkB. By contrast with findings from rats, in mice BDNF does not decrease excitation of inhibitory neurons. The cytokine macrophage colony-stimulating factor 1 (CSF-1) has also been implicated in the onset of neuropathic pain. Nerve injury provokes its de novo synthesis in primary afferents, its release in spinal cord, and activation of microglia. We now show that CSF-1 increases excitatory drive to excitatory neurons via a BDNF-dependent mechanism and decreases excitatory drive to inhibitory neurons via BDNF-independent processes. Our findings complete missing steps in the cascade of events whereby peripheral nerve injury instigates increased dorsal horn excitability in the context of central sensitization and the onset of neuropathic pain. NEW & NOTEWORTHY Nerve injury provokes synthesis of macrophage colony-stimulating factor 1 (CSF-1) in primary afferents and its release in the dorsal horn. We show that CSF-1 increases excitatory drive to excitatory dorsal horn neurons via BDNF activation of postsynaptic TrkB and presynaptic TrkB and p75 neurotrophin receptors. CSF-1 decreases excitatory drive to inhibitory neurons via a BDNF-independent processes. This completes missing steps in understanding how peripheral injury instigates central sensitization and the onset of neuropathic pain.
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Nieto-Rostro, Manuela, Krishma Ramgoolam, Wendy S. Pratt, Akos Kulik, and Annette C. Dolphin. "Ablation of α2δ-1 inhibits cell-surface trafficking of endogenous N-type calcium channels in the pain pathway in vivo." Proceedings of the National Academy of Sciences 115, no. 51 (November 28, 2018): E12043—E12052. http://dx.doi.org/10.1073/pnas.1811212115.
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The auxiliary α2δ calcium channel subunits play key roles in voltage-gated calcium channel function. Independent of this, α2δ-1 has also been suggested to be important for synaptogenesis. Using an epitope-tagged knockin mouse strategy, we examined the effect of α2δ-1 on CaV2.2 localization in the pain pathway in vivo, where CaV2.2 is important for nociceptive transmission and α2δ-1 plays a critical role in neuropathic pain. We find CaV2.2 is preferentially expressed on the plasma membrane of calcitonin gene-related peptide-positive small nociceptors. This is paralleled by strong presynaptic expression of CaV2.2 in the superficial spinal cord dorsal horn. EM-immunogold localization shows CaV2.2 predominantly in active zones of glomerular primary afferent terminals. Genetic ablation of α2δ-1 abolishes CaV2.2 cell-surface expression in dorsal root ganglion neurons and dramatically reduces dorsal horn expression. There was no effect of α2δ-1 knockout on other dorsal horn pre- and postsynaptic markers, indicating the primary afferent pathways are not otherwise affected by α2δ-1 ablation.
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Laird, J. M., and F. Cervero. "Tonic descending influences on receptive-field properties of nociceptive dorsal horn neurons in sacral spinal cord of rat." Journal of Neurophysiology 63, no. 5 (May 1, 1990): 1022–32. http://dx.doi.org/10.1152/jn.1990.63.5.1022.
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1. Single-unit electrical activity has been recorded from 34 dorsal horn neurons in the sacral segments (S1-2) of the spinal cord in halothane-anesthetized rats. All of the neurons had cutaneous receptive fields (RFs) on the rat's tail. The neurons were classified according to their responses to both innocuous and noxious mechanical stimulation of their RFs. Twenty-five cells were driven by both innocuous and noxious skin stimulation (multireceptive or class 2), and 9 neurons were driven only by noxious skin stimulation (nocireceptive or class 3). 2. The RF size, mechanical threshold, and afferent input properties of these neurons were determined in the intact anesthetized and spinalized states. Reversible spinalization was achieved by cooling the cervical spinal cord to 4 degrees C. 3. The class 2 neurons had a mean RF size of 919.8 +/- 112.0 (SE) mm2 in the intact animal. Fourteen of the 25 class 2 cells had larger RFs in the spinal state (mean increase = 330.0 mm2, SE = 79.2) and so were under tonic descending inhibition. Five neurons, all with C-fiber input, had smaller RFs (mean decrease = 247.6 mm2, SE = 136.6) and higher mechanical thresholds in the spinal state and so were under tonic descending excitation. Six neurons were unaffected by spinalization. 4. Five class 3 neurons recorded in the superficial dorsal horn had small RFs in the intact animal (mean = 201.0 mm2, SE = 48.8) and showed little or no change in RF size on spinalization (mean increase = 33.4 mm2, SE = 16.7), but their mechanical thresholds did decrease, indicating weak tonic descending inhibition. In contrast, four class 3 neurons recorded in the deep dorsal horn had larger RFs in the intact animal (mean = 566.8 mm2, SE = 156.8), and were under strong tonic descending inhibition, because they had much larger RFs (mean increase = 461.0 mm2, SE = 68.3), lower mechanical thresholds, and stronger C-fiber afferent input in the spinal state. 5. We conclude that the majority of nociceptive dorsal horn neurons are subject to a net tonic descending control of their RF properties. The class 2 neurons in the deep dorsal horn appear to be a heterogeneous population, some cells being under tonic descending excitation and others under tonic descending inhibition. Class 3 cells can be separated into those located in the superficial dorsal horn, whose RF properties show very little change on spinalization, and those in the deep dorsal horn, whose RF properties change markedly on spinalization.(ABSTRACT TRUNCATED AT 400 WORDS)
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Furutani, Kenta, Miho Ikoma, Hideaki Ishii, Hiroshi Baba, and Tatsuro Kohno. "Bupivacaine Inhibits Glutamatergic Transmission in Spinal Dorsal Horn Neurons." Anesthesiology 112, no. 1 (January 1, 2010): 138–43. http://dx.doi.org/10.1097/01.anes.0000365964.97138.9a.
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Background The local anesthetic bupivacaine is thought not only to block sodium channels but also to interact with various receptors. Here, the authors focus on excitatory glutamatergic transmission in the superficial dorsal horn of the spinal cord with respect to its importance for nociceptive processing. Methods The effects of bupivacaine on the response to exogenous administration of N-methyl-D-aspartate (NMDA) receptor agonists were examined in lamina II neurons of adult rat spinal cord slices using the whole-cell patch-clamp technique. Results Bupivacaine (0.5, 2 mm) dose-dependently reduced the peak amplitudes of exogenous NMDA-induced currents. However, this inhibitory effect of bupivacaine (2 mm) was not blocked by the presence of tetrodotoxin, a sodium channel blocker, or La(3+), a voltage-gated Ca+ channel blocker, and was unaffected by changes in pH conditions. Moreover, intrapipette guanosine-5'-O-(2-thiodiphosphate) (1 mm), a G-protein inhibitor, did not block the reduction of NMDA current amplitudes by bupivacaine. Similarly, lidocaine, ropivacaine, and mepivacaine also reduced the amplitudes of NMDA-induced currents. Conclusions These findings raise the possibility that the antinociceptive effect of bupivacaine may be due to direct modulation of NMDA receptors in the superficial dorsal horn. In addition to voltage-gated sodium channels, glutamate NMDA receptors are also important for analgesia induced by local anesthetics.
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Graham, B. A., M. A. Tadros, P. R. Schofield, and R. J. Callister. "Probing glycine receptor stoichiometry in superficial dorsal horn neurones using thespasmodicmouse." Journal of Physiology 589, no. 10 (May 13, 2011): 2459–74. http://dx.doi.org/10.1113/jphysiol.2011.206326.
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Graham, B. A., A. M. Brichta, P. R. Schofield, and R. J. Callister. "Altered potassium channel function in the superficial dorsal horn of thespasticmouse." Journal of Physiology 584, no. 1 (September 28, 2007): 121–36. http://dx.doi.org/10.1113/jphysiol.2007.138198.
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Largent-Milnes, Tally M., Deborah M. Hegarty, Sue A. Aicher, and Michael C. Andresen. "Physiological temperatures drive glutamate release onto trigeminal superficial dorsal horn neurons." Journal of Neurophysiology 111, no. 11 (June 1, 2014): 2222–31. http://dx.doi.org/10.1152/jn.00912.2013.
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Trigeminal sensory afferent fibers terminating in nucleus caudalis (Vc) relay sensory information from craniofacial regions to the brain and are known to express transient receptor potential (TRP) ion channels. TRP channels are activated by H+, thermal, and chemical stimuli. The present study investigated the relationships among the spontaneous release of glutamate, temperature, and TRPV1 localization at synapses in the Vc. Spontaneous excitatory postsynaptic currents (sEPSCs) were recorded from Vc neurons ( n = 151) in horizontal brain-stem slices obtained from Sprague-Dawley rats. Neurons had basal sEPSC rates that fell into two distinct frequency categories: High (≥10 Hz) or Low (<10 Hz) at 35°C. Of all recorded neurons, those with High basal release rates (67%) at near-physiological temperatures greatly reduced their sEPSC rate when cooled to 30°C without amplitude changes. Such responses persisted during blockade of action potentials indicating that the High rate of glutamate release arises from presynaptic thermal mechanisms. Neurons with Low basal frequencies (33%) showed minor thermal changes in sEPSC rate that were abolished after addition of TTX, suggesting these responses were indirect and required local circuits. Activation of TRPV1 with capsaicin (100 nM) increased miniature EPSC (mEPSC) frequency in 70% of neurons, but half of these neurons had Low basal mEPSC rates and no temperature sensitivity. Our evidence indicates that normal temperatures (35–37°C) drive spontaneous excitatory synaptic activity within superficial Vc by a mechanism independent of presynaptic action potentials. Thus thermally sensitive inputs on superficial Vc neurons may tonically activate these neurons without afferent stimulation.
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Feng, Xiao-Jin, Long-Xian Ma, Cui Jiao, Hai-Xia Kuang, Fei Zeng, Xue-Ying Zhou, Xiao-E. Cheng, et al. "Nerve injury elevates functional Cav3.2 channels in superficial spinal dorsal horn." Molecular Pain 15 (January 2019): 174480691983656. http://dx.doi.org/10.1177/1744806919836569.
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Rojas-Piloni, Gerardo, Anthony H. Dickenson, and Miguel Condés-Lara. "Superficial dorsal horn neurons with double spike activity in the rat." Neuroscience Letters 419, no. 2 (May 2007): 147–52. http://dx.doi.org/10.1016/j.neulet.2007.04.032.
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Kaimoto, Taeko, Emiko Senba, Hiroshi Yamasaki, and Masaya Tohyama. "Galanin-containing neurons in the superficial dorsal horn: An immunocytochemical study." Neuroscience Research Supplements 14 (January 1991): S153. http://dx.doi.org/10.1016/s0921-8696(06)80448-2.
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Mantyh, Patrick W., and Stephen P. Hunt. "Setting the tone: superficial dorsal horn projection neurons regulate pain sensitivity." Trends in Neurosciences 27, no. 10 (October 2004): 582–84. http://dx.doi.org/10.1016/j.tins.2004.07.007.
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Jennings, E. A., C. W. Vaughan, and M. J. Christie. "Cannabinoid actions on rat superficial medullary dorsal horn neurons in vitro." Journal of Physiology 534, no. 3 (August 2001): 805–12. http://dx.doi.org/10.1111/j.1469-7793.2001.00805.x.
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Jia, Hongge, Aldo Rustioni, and Juli G. Valtschanoff. "Metabotropic glutamate receptors in superficial laminae of the rat dorsal horn." Journal of Comparative Neurology 410, no. 4 (August 9, 1999): 627–42. http://dx.doi.org/10.1002/(sici)1096-9861(19990809)410:4<627::aid-cne9>3.0.co;2-8.
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Li, Jie, Elizabeth Kritzer, Neil C. Ford, Shahriar Arbabi, and Mark L. Baccei. "Connectivity of pacemaker neurons in the neonatal rat superficial dorsal horn." Journal of Comparative Neurology 523, no. 7 (February 17, 2015): 1038–53. http://dx.doi.org/10.1002/cne.23706.
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Furuse, Shingo, Tomoyuki Kawamata, Jun Yamamoto, Yukitoshi Niiyama, Keiichi Omote, Masahiko Watanabe, and Akiyoshi Namiki. "Reduction of Bone Cancer Pain by Activation of Spinal Cannabinoid Receptor 1 and Its Expression in the Superficial Dorsal Horn of the Spinal Cord in a Murine Model of Bone Cancer Pain." Anesthesiology 111, no. 1 (July 1, 2009): 173–86. http://dx.doi.org/10.1097/aln.0b013e3181a51e0d.
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Background Bone cancer pain has a strong impact on the quality of life of patients, but it is difficult to treat. Therefore, development of a novel strategy for the treatment of bone cancer pain is needed for improvement of patient quality of life. This study examined whether selective spinal cannabinoid receptor 1 (CB1) activation alleviates bone cancer pain and also examined the spinal expression of CB1. Methods A bone cancer pain model was made by implantation of sarcoma cells into the intramedullary space of the mouse femur. In behavioral experiments, the authors examined the effects of activation of spinal CB1 and inhibition of metabolism of endocannabinoid on bone cancer-related pain behaviors. Immunohistochemical experiments examined the distribution and localization of CB1 in the superficial dorsal horn of the spinal cord using specific antibodies. Results Spinal CB1 activation by exogenous administration of a CB1 agonist arachidonyl-2-chloroethylamide reduced bone cancer-related pain behaviors, including behaviors related to spontaneous pain and movement-evoked pain. In immunohistochemical experiments, although mu-opioid receptor 1 expression was reduced in the superficial dorsal horn ipsilateral to the site of implantation of sarcoma cells, CB1 expression was preserved. In addition, CB1 was mainly expressed in the axon terminals, but not in the dendritic process in the superficial dorsal horn. Conclusion Spinal CB1 activation reduced bone cancer-related pain behavior. Presynaptic inhibition may contribute to the analgesic effects of spinal CB1 activation. These findings may lead to novel strategies for the treatment of bone cancer pain.
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Pancaro, Carlo, Weiya Ma, Michelle Vincler, Frederic Duflo, and James C. Eisenach. "Clonidine-induced Neuronal Activation in the Spinal Cord Is Altered after Peripheral Nerve Injury." Anesthesiology 98, no. 3 (March 1, 2003): 748–53. http://dx.doi.org/10.1097/00000542-200303000-00026.
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Background Alpha 2 adrenoceptor agonists produce antinociception in normal animals and alleviate mechanical allodynia in animals with nerve injury, although their mechanism of action may differ in these situations. The purpose of this study was to examine the location and number of cells in the spinal cord activated by intrathecal clonidine in these two circumstances and to test whether one class of interneurons, cholinergic, express alpha 2 adrenoceptors. Methods Intrathecal saline or clonidine, 10 and 30 microg, was injected in normal rats or those with mechanical allodynia following partial sciatic nerve section. Two hours later, animals were anesthetized and pericardially perfused. The number of cells in superficial and deep dorsal horn laminae at the L4-L5 level immunostained for phosphorylated cAMP response element binding protein (pCREB) were quantified. In separate studies, the authors colocalized alpha2C adrenoceptors with cholinergic neurons. Results Intrathecal clonidine increased pCREB immunoreactive cells in both superficial and deep laminae by 50-100% in normal animals. The number of pCREB immunoreactive cells increased in nerve-injured compared to normal rats. Intrathecal clonidine decreased pCREB immunoreactive cells in the deep dorsal horn of injured animals. Alpha2C adrenoceptors colocalized with cholinergic neurons in both superficial and deep dorsal horn. Discussion Previous studies suggest a shift in alpha 2 adrenoceptor subtype and the involvement of cholinergic interneurons in antinociception in the spinal cord after nerve injury. The current results suggest that intrathecal clonidine, by direct or indirect methods, increases neuronal activation in normal animals, presumably leading to net inhibition of pain signaling, whereas it reduces the increase in neuronal activity induced by nerve injury.
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Nicholson, R., A. K. Dixon, D. Spanswick, and K. Lee. "Noradrenergic receptor mRNA expression in adult rat superficial dorsal horn and dorsal root ganglion neurons." Neuroscience Letters 380, no. 3 (June 2005): 316–21. http://dx.doi.org/10.1016/j.neulet.2005.01.079.
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Runyan, Stephen A., Roland Roy, Hui Zhong, and Patricia E. Phelps. "L1 CAM expression in the superficial dorsal horn is derived from the dorsal root ganglion." Journal of Comparative Neurology 485, no. 4 (May 16, 2005): 267–79. http://dx.doi.org/10.1002/cne.20479.
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Renehan, W. E., M. F. Jacquin, R. D. Mooney, and R. W. Rhoades. "Structure-function relationships in rat medullary and cervical dorsal horns. II. Medullary dorsal horn cells." Journal of Neurophysiology 55, no. 6 (June 1, 1986): 1187–201. http://dx.doi.org/10.1152/jn.1986.55.6.1187.
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In Nembutal-anesthetized rats, 31 physiologically identified medullary dorsal horn (MDH) cells were labeled with horseradish peroxidase (HRP). Ten responded only to deflection of one or more vibrissae. Six cells were activated by guard hair movement only, six by deflection of guard hairs or vibrissa(e), and seven by pinch of facial skin with serrated forceps. Different classes of low-threshold cells could not be distinguished on the basis of their somadendritic morphologies or laminar distribution. Neurons activated by multiple vibrissae were unique, however, in that one sent its axon into the medial lemniscus, and three projected into the trigeminal spinal tract. None of the guard hair-only or vibrissae-plus-guard hair neurons had such projections. Cells that responded best to noxious stimulation were located mainly in laminae I, II, and deep V, while neurons activated by vibrissa(e) and/or guard hair deflection were located in layers III, IV, and superficial V. Low-threshold neurons generally had fairly thick dendrites with few spines, whereas high-threshold cells tended to have thinner dendrites with numerous spines. Moreover, the dendritic arbors of low-threshold cells were, for the most part, denser than those of the noxious cells. Neurons with mandibular receptive fields were located in the dorsomedial portion of the MDH; cells with ophthalmic fields were found in the ventrolateral MDH, and maxillary cells were interposed. Cells sensitive to deflection of dorsal mystacial vibrissae and/or guard hairs were located ventral to those activated by more ventral hairs. Neurons with rostral receptive fields were found in the rostral MDH, while cells activated by hairs of the caudal mystacial pad, periauricular, and periorbital regions were located in the caudal MDH. Receptive-field types were encountered that have not been reported for trigeminal primary afferent neurons: multiple vibrissae; vibrissae plus guard hairs; and wide dynamic range. The latter two can be explained by the convergence of different primary afferent types onto individual neurons. Our failure to find a significant relationship between dendritic area (in the transverse plane) and the number of vibrissae suggests that primary afferent convergence may not be responsible for the synthesis of the multiple vibrissae receptive field. Excitatory connections between MDH neurons may, therefore, account for multiple vibrissae receptive fields in the MDH.
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Bardoni, Rita. "Excitatory Synaptic Transmission in Neonatal Dorsal Horn: NMDA and ATP Receptors." Physiology 16, no. 2 (April 2001): 95–100. http://dx.doi.org/10.1152/physiologyonline.2001.16.2.95.
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Postnatal development sees a strong synaptogenesis in rat superficial dorsal horn. My studies show that synapses mediated by two excitatory neurotransmitters, glutamate and ATP, are functional since the very first postnatal days. Using an electrophysiological approach, the functional properties of two receptors activated by these neurotransmitters, glutamatergic NMDA and ATP ionotropic receptors, are described.
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Leng, Yu-Fang, Xiang-Mei Gao, Shu-Xiu Wang, and Yan-Hong Xing. "Effects of Tetramethylpyrazine on Neuronal Apoptosis in the Superficial Dorsal Horn in a Rat Model of Neuropathic Pain." American Journal of Chinese Medicine 40, no. 06 (January 2012): 1229–39. http://dx.doi.org/10.1142/s0192415x12500917.
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The Bennett and Xie (1988) model of chronic constriction injury (CCI) investigated the effects of tetramethylpyrazine (TMP) on neuropathic pain-associated behaviors and neuronal apoptosis in the spinal dorsal horn. Fifty-four male rats were randomly divided into sham (group S), CCI (group C) and TMP groups (group T). Each group was divided into subgroups (n = 6 in each group) according the time of sacrifice: 3 d, 7 d and 14 d. Rat sciatic nerves were unligated (group S), or the right sciatic nerve was loosely ligated (groups C and T) to produce CCI. Mechanical withdrawal thresholds (MWTs) and thermal withdrawal latencies (TWLs) were measured, and the rats were sacrificed at different time points post-operation. The L4-L6 sections of the spinal cord were removed. Apoptotic changes were evaluated using the TUNEL method. Immunohistochemistry assessed Bcl-2 and caspase-3 expression. TMP treatment increased MWT and TWL values and Bcl-2 expression, but it reduced neuronal apoptosis and caspase-3 expression in laminae I–II of the spinal dorsal horn. These results suggested that the inhibition of neuronal apoptosis via the modulation of Bcl-2 and caspase-3 proteins in the rat spinal dorsal horn contributed to TMP-induced analgesia.
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Shinoda, Masamichi, Satoshi Fujita, Shiori Sugawara, Sayaka Asano, Ryo Koyama, Shintaro Fujiwara, Kumi Soma, et al. "Suppression of Superficial Microglial Activation by Spinal Cord Stimulation Attenuates Neuropathic Pain Following Sciatic Nerve Injury in Rats." International Journal of Molecular Sciences 21, no. 7 (March 30, 2020): 2390. http://dx.doi.org/10.3390/ijms21072390.
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We evaluated the mechanisms underlying the spinal cord stimulation (SCS)-induced analgesic effect on neuropathic pain following spared nerve injury (SNI). On day 3 after SNI, SCS was performed for 6 h by using electrodes paraspinally placed on the L4-S1 spinal cord. The effects of SCS and intraperitoneal minocycline administration on plantar mechanical sensitivity, microglial activation, and neuronal excitability in the L4 dorsal horn were assessed on day 3 after SNI. The somatosensory cortical responses to electrical stimulation of the hind paw on day 3 following SNI were examined by using in vivo optical imaging with a voltage-sensitive dye. On day 3 after SNI, plantar mechanical hypersensitivity and enhanced microglial activation were suppressed by minocycline or SCS, and L4 dorsal horn nociceptive neuronal hyperexcitability was suppressed by SCS. In vivo optical imaging also revealed that electrical stimulation of the hind paw-activated areas in the somatosensory cortex was decreased by SCS. The present findings suggest that SCS could suppress plantar SNI-induced neuropathic pain via inhibition of microglial activation in the L4 dorsal horn, which is involved in spinal neuronal hyperexcitability. SCS is likely to be a potential alternative and complementary medicine therapy to alleviate neuropathic pain following nerve injury.
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Akiyama, T., M. Nagamine, A. Davoodi, M. Iodi Carstens, F. Cevikbas, M. Steinhoff, and E. Carstens. "Intradermal endothelin-1 excites bombesin-responsive superficial dorsal horn neurons in the mouse." Journal of Neurophysiology 114, no. 4 (October 2015): 2528–34. http://dx.doi.org/10.1152/jn.00723.2015.
Full textAbstract:
Endothelin-1 (ET-1) has been implicated in nonhistaminergic itch. Here we used electrophysiological methods to investigate whether mouse superficial dorsal horn neurons respond to intradermal (id) injection of ET-1 and whether ET-1-sensitive neurons additionally respond to other pruritic and algesic stimuli or spinal superfusion of bombesin, a homolog of gastrin-releasing peptide (GRP) that excites spinal itch-signaling neurons. Single-unit recordings were made from lumbar dorsal horn neurons in pentobarbital-anesthetized C57BL/6 mice. We searched for units that exhibited elevated firing after id injection of ET-1 (1 μg/μl). Responsive units were further tested with mechanical stimuli, bombesin (spinal superfusion, 200 μg·ml−1·min−1), heating, cooling, and additional chemicals [histamine, chloroquine, allyl isothiocyanate (AITC), capsaicin]. Of 40 ET-1-responsive units, 48% responded to brush and pinch [wide dynamic range (WDR)] and 52% to pinch only [high threshold (HT)]. Ninety-three percent responded to noxious heat, 50% to cooling, and >70% to histamine, chloroquine, AITC, and capsaicin. Fifty-seven percent responded to bombesin, suggesting that they participate in spinal itch transmission. That most ET-1-sensitive spinal neurons also responded to pruritic and algesic stimuli is consistent with previous studies of pruritogen-responsive dorsal horn neurons. We previously hypothesized that pruritogen-sensitive neurons signal itch. The observation that ET-1 activates nociceptive neurons suggests that both itch and pain signals may be generated by ET-1 to result in simultaneous sensations of itch and pain, consistent with observations that ET-1 elicits both itch- and pain-related behaviors in animals and burning itch sensations in humans.
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Schneider, S. P., and E. R. Perl. "Synaptic mediation from cutaneous mechanical nociceptors." Journal of Neurophysiology 72, no. 2 (August 1, 1994): 612–21. http://dx.doi.org/10.1152/jn.1994.72.2.612.
Full textAbstract:
1. Responses of dorsal horn neurons to cutaneous mechanical stimulation were studied in an in vitro preparation of hamster spinal cord with partially intact innervation from an isolated patch of hairy skin. Stable extracellular and intracellular recordings were obtained from cells with different mechanoreceptive properties similar to those reported for other species in vivo. Analyses were made of the intracellular responses of 25 dorsal horn neurons activated selectively by mechanical stimulation to the skin patch. 2. Bath application of the broad spectrum, excitatory amino acid (EAA) receptor antagonist, kynurenic acid (1 mM) blocked excitation of 7 of 8 high-threshold mechanoreceptive units by either cutaneous nerve volleys or mechanical stimulation of the skin. This concentration of kynurenic acid suppressed peripherally evoked responses in 8 of 14 neurons responsive to innocuous mechanical stimuli. 3. High-threshold mechanoreceptive neurons of the superficial dorsal horn exhibited one of three distinctive patterns of postsynaptic potentials in response to electrical stimulation of cutaneous afferent fibers: 1) a simple fast excitatory postsynaptic potential (EPSP), 2) a fast EPSP with a prolonged decay phase lasting between 100 and 1,000 ms, and 3) a multiphasic response dissociable on the basis of stimulus strength consisting of a fast EPSP followed by a hyperpolarizing inhibitory postsynaptic potential (IPSP) (duration 80–100 ms). Gentle mechanical stimuli initiated inhibition from areas adjacent to the high-threshold mechanically excitatory field; this suggests that membrane hyperpolarization in these neurons was evoked by input from low-threshold mechanoreceptors. 4. Bath application of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM), a competitive EAA antagonist selective for non-N-methyl-D-aspartate (non-NMDA) receptor subtypes, substantially or completely (56–100%) suppressed EPSPs evoked from cutaneous afferent fibers in high-threshold mechanoreceptive neurons. CNQX also decreased the membrane depolarization, the frequency of EPSPs, and the frequency of action potentials evoked by mechanical stimulation of the receptive field. 5. CNQX (10 microM) or kynurenic acid (1 mM) had considerably weaker effects on IPSPs than on EPSPs evoked from the periphery in superficial dorsal horn neurons. IPSP amplitudes were unchanged by these agents in some neurons and decreased by only 20–25% in others. 6. We conclude that L-glutamate acting on non-NMDA receptors mediates fast synaptic excitation of superficial dorsal horn neurons from peripheral mechanical nociceptors with myelinated fibers. Furthermore, the observations imply either an agent other than L-glutamate or one acting at different membrane receptors is a synaptic mediator for other peripheral afferent units including some activated by innocuous mechanical stimuli.
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Ingram, Rachel A., Maria Fitzgerald, and Mark L. Baccei. "Developmental Changes in the Fidelity and Short-Term Plasticity of GABAergic Synapses in the Neonatal Rat Dorsal Horn." Journal of Neurophysiology 99, no. 6 (June 2008): 3144–50. http://dx.doi.org/10.1152/jn.01342.2007.
Full textAbstract:
The lower thresholds and increased excitability of dorsal horn neurons in the neonatal rat suggest that inhibitory processing is less efficient in the immature spinal cord. This is unlikely to be explained by an absence of functional GABAergic inhibition because antagonism of γ-aminobutyric acid (GABA) type A receptors augments neuronal firing in vivo from the first days of life. However, it is possible that more subtle deficits in GABAergic signaling exist in the neonate, such as decreased reliability of transmission or greater depression during repetitive stimulation, both of which could influence the relative excitability of the immature spinal cord. To address this issue we examined monosynaptic GABAergic inputs onto superficial dorsal horn neurons using whole cell patch-clamp recordings made in spinal cord slices at a range of postnatal ages (P3, P10, and P21). The amplitudes of evoked inhibitory postsynaptic currents (IPSCs) were significantly lower and showed greater variability in younger animals, suggesting a lower fidelity of GABAergic signaling at early postnatal ages. Paired-pulse ratios were similar throughout the postnatal period, whereas trains of stimuli (1, 5, 10, and 20 Hz) revealed frequency-dependent short-term depression (STD) of IPSCs at all ages. Although the magnitude of STD did not differ between ages, the recovery from depression was significantly slower at immature GABAergic synapses. These properties may affect the integration of synaptic inputs within developing superficial dorsal horn neurons and thus contribute to their larger receptive fields and enhanced afterdischarge.