Experts and Doctors on spinal cord in United States


Locale: United States
Topic: spinal cord

Top Publications

  1. Hua F, Ricketts B, Reifsteck A, Ardell J, Williams C. Myocardial ischemia induces the release of substance P from cardiac afferent neurons in rat thoracic spinal cord. Am J Physiol Heart Circ Physiol. 2004;286:H1654-64 pubmed
  2. Madiai F, Goettl V, Hussain S, Clairmont A, Stephens R, Hackshaw K. Anti-fibroblast growth factor-2 antibodies attenuate mechanical allodynia in a rat model of neuropathic pain. J Mol Neurosci. 2005;27:315-24 pubmed
    ..These results suggest that endogenous astroglial FGF-2 contributes to maintaining NP tactile allodynia associated with reactivity of spinal cord astrocytes and that inhibition of spinal FGF-2 ameliorates NP pain signs. ..
  3. Naphade S, Kigerl K, Jakeman L, Kostyk S, Popovich P, Kuret J. Progranulin expression is upregulated after spinal contusion in mice. Acta Neuropathol. 2010;119:123-33 pubmed publisher
    ..These data demonstrate that progranulin is dramatically induced in myeloid cells after experimental spinal cord injury and is positioned appropriately both spatially and temporally to influence recovery after injury. ..
  4. Ziskind Conhaim L, Mentis G, Wiesner E, Titus D. Synaptic integration of rhythmogenic neurons in the locomotor circuitry: the case of Hb9 interneurons. Ann N Y Acad Sci. 2010;1198:72-84 pubmed publisher
    ..Our findings suggest that the rhythmogenic Hb9 INs are integral components of the sensorimotor circuitry that regulate locomotor-like activity in the spinal cord. ..
  5. Medina J, Abrams K, Falcone S, Bhatia R. Spinal imaging findings in spontaneous intracranial hypotension. AJR Am J Roentgenol. 2010;195:459-64 pubmed publisher
    ..Encountering these findings on spinal images may suggest the diagnosis of spontaneous intracranial hypotension and therefore can influence patient treatment. ..
  6. Sohn M, Culver D, Judson M, Scott T, Tavee J, Nozaki K. Spinal cord neurosarcoidosis. Am J Med Sci. 2014;347:195-8 pubmed publisher
    ..Spinal cord neurosarcoidosis (SN) is problematic to diagnose because it mimics other inflammatory neurologic diseases. The authors report the clinical features of 29 SN cases...
  7. Turner S, Hoyt A, Elmallah M, Falk D, Byrne B, Fuller D. Neuropathology in respiratory-related motoneurons in young Pompe (Gaa(-/-)) mice. Respir Physiol Neurobiol. 2016;227:48-55 pubmed publisher
    ..The data support early therapeutic intervention in Pompe disease. ..
  8. Klein R, Smeyne R, Wurst W, Long L, Auerbach B, Joyner A, et al. Targeted disruption of the trkB neurotrophin receptor gene results in nervous system lesions and neonatal death. Cell. 1993;75:113-22 pubmed
    ..These findings illustrate the role of the gp145trkB protein-tyrosine kinase receptor in the ontogeny of the mammalian nervous system. ..
  9. Scarisbrick I, Towner M, Isackson P. Nervous system-specific expression of a novel serine protease: regulation in the adult rat spinal cord by excitotoxic injury. J Neurosci. 1997;17:8156-68 pubmed
    ..Together, these observations indicate that MSP is in a position to play a fundamental role in normal homeostasis and in the response of the spinal cord to injury. ..

More Information

Publications437 found, 100 shown here

  1. Adamus G, Machnicki M, Amundson D, Adlard K, Offner H. Similar pattern of MCP-1 expression in spinal cords and eyes of Lewis rats with experimental autoimmune encephalomyelitis associated anterior uveitis. J Neurosci Res. 1997;50:531-8 pubmed
    ..MCP-1 seems to contribute to the initial recruitment of inflammatory cells into both the tissues of the eye and CNS over the course of disease. ..
  2. Zhou Q, Anderson D. The bHLH transcription factors OLIG2 and OLIG1 couple neuronal and glial subtype specification. Cell. 2002;109:61-73 pubmed
    ..Our results suggest that in the spinal cord, Olig and proneural genes comprise a combinatorial code for the specification of neurons, astrocytes, and oligodendrocytes, the three fundamental cell types of the central nervous system. ..
  3. Becher B, Durell B, Noelle R. Experimental autoimmune encephalitis and inflammation in the absence of interleukin-12. J Clin Invest. 2002;110:493-7 pubmed
    ..These studies show that a molecule other than IL-12 p70, which uses the p40 subunit, fulfills the functions previously attributed to IL-12 with regard to the development and pathogenesis of this autoimmune disease. ..
  4. De Vries G, Rissman E, Simerly R, Yang L, Scordalakes E, Auger C, et al. A model system for study of sex chromosome effects on sexually dimorphic neural and behavioral traits. J Neurosci. 2002;22:9005-14 pubmed
    ..Moreover, two male groups differing only in the form of their Sry gene showed differences in behavior. The results show that sex chromosome genes contribute directly to the development of a sex difference in the brain. ..
  5. Jones T, Ankeny D, Guan Z, McGaughy V, Fisher L, Basso D, et al. Passive or active immunization with myelin basic protein impairs neurological function and exacerbates neuropathology after spinal cord injury in rats. J Neurosci. 2004;24:3752-61 pubmed
    ..These data are consistent with the conventional view of myelin-reactive T-cells as pathological effector cells. ..
  6. Nakatsuka T, Chen M, Takeda D, King C, Ling J, Xing H, et al. Substance P-driven feed-forward inhibitory activity in the mammalian spinal cord. Mol Pain. 2005;1:20 pubmed
    ..Our findings reveal a fundamental role of SP in recruiting inhibitory activity for sensory processing, which may have important therapeutic implications in treating pathological pain conditions using SP receptors as targets. ..
  7. Flint J, Hansen B, Fey M, Schmidig D, King M, Vestergaard Poulsen P, et al. Cellular-level diffusion tensor microscopy and fiber tracking in mammalian nervous tissue with direct histological correlation. Neuroimage. 2010;52:556-61 pubmed publisher
    ..These methods provide a way to directly validate fiber tracking techniques with histology so that contemporary tracking techniques may be compared and refined using the microstructural details of a biological template as a ground truth. ..
  8. Hoelzer B, Knievel S, Michiels W, McGlothlen G, Grigsby E. Meningismus associated with malpositioned intraspinal catheter for drug delivery. Pain Pract. 2011;11:103-6 pubmed publisher
    ..Determining the etiology of a postimplant headache is important particularly when considering the possibility of a life-threatening infection...
  9. Falk D, Mah C, Soustek M, Lee K, Elmallah M, Cloutier D, et al. Intrapleural administration of AAV9 improves neural and cardiorespiratory function in Pompe disease. Mol Ther. 2013;21:1661-7 pubmed publisher
    ..These results further implicate a role for the CNS in Pompe disease pathology and the critical need to target the neurologic aspects in developing therapeutic strategies. ..
  10. Iwasaki K, Taguchi M, Bonkowsky J, Kuwada J. Expression of arginine vasotocin receptors in the developing zebrafish CNS. Gene Expr Patterns. 2013;13:335-42 pubmed publisher
    ..One hypothesis consistent with this anatomy is that AVT signaling mediates or gates sensory input to motor circuits in the hindbrain and spinal cord. ..
  11. Terman G, Eastman C, Chavkin C. Mu opiates inhibit long-term potentiation induction in the spinal cord slice. J Neurophysiol. 2001;85:485-94 pubmed
    ..These studies suggest that mu opioids exert their inhibitory effects presynaptically, likely through the inhibition of glutamate release from primary afferent terminals, and thereby inhibit the induction of LTP in the spinal dorsal horn...
  12. Liu R, Cai J, Hu X, Tan M, Qi Y, German M, et al. Region-specific and stage-dependent regulation of Olig gene expression and oligodendrogenesis by Nkx6.1 homeodomain transcription factor. Development. 2003;130:6221-31 pubmed
    ..In the hindbrain, unlike in the spinal cord, Olig1 and Olig2 can be expressed both inside and outside the Nkx6.1-expressing domains and oligodendrogenesis in this region is not dependent on Nkx6.1 activity. ..
  13. Yezierski R, Yu C, Mantyh P, Vierck C, Lappi D. Spinal neurons involved in the generation of at-level pain following spinal injury in the rat. Neurosci Lett. 2004;361:232-6 pubmed
    ..The results suggest that the substrate for at-level pain following spinal cord injury includes a population of spinal neurons expressing the neurokinin-1 receptor in the superficial laminae of the spinal cord. ..
  14. Rodriguez M, Zoecklein L, Gamez J, Pavelko K, Papke L, Nakane S, et al. STAT4- and STAT6-signaling molecules in a murine model of multiple sclerosis. FASEB J. 2006;20:343-5 pubmed
    ..Thus, virus infection of STAT4-/- mice results in a model that may allow for dissection of the immune events predisposing to late-onset demyelination in MS. ..
  15. Lang S, Eskioglu E, A Mericle R. Intraoperative angiography for neurovascular disease in the prone or three-quarter prone position. Surg Neurol. 2006;65:283-9; discussion 289 pubmed
    ..However, the transradial route has the disadvantage of working from an unfamiliar approach, especially for spinal arteriovenous malformations. ..
  16. Huang D, Shi F, Jung S, Pien G, Wang J, Salazar Mather T, et al. The neuronal chemokine CX3CL1/fractalkine selectively recruits NK cells that modify experimental autoimmune encephalomyelitis within the central nervous system. FASEB J. 2006;20:896-905 pubmed
    ..These results are the first to define a chemokine that governs NK cell migration to the CNS, and the findings suggest novel therapeutic manipulation of CX3CR1+ NK cells. ..
  17. Reynolds J, Liu Q, Brittingham K, Liu Y, Gruenthal M, Gorgun C, et al. Deficiency of fatty acid-binding proteins in mice confers protection from development of experimental autoimmune encephalomyelitis. J Immunol. 2007;179:313-21 pubmed
    ..This study reveals that metabolic-inflammatory pathway cross-regulation by FABPs contributes to adaptive immune responses and subsequent autoimmune inflammation. ..
  18. Souayah N, Sharovetskaya A, Kurnellas M, Myerson M, Deitch J, Elkabes S. Reductions in motor unit number estimates (MUNE) precede motor neuron loss in the plasma membrane calcium ATPase 2 (PMCA2)-heterozygous mice. Exp Neurol. 2008;214:341-346 pubmed publisher
  19. Patel S, Sullivan P, Lyttle T, Rabchevsky A. Acetyl-L-carnitine ameliorates mitochondrial dysfunction following contusion spinal cord injury. J Neurochem. 2010;114:291-301 pubmed publisher
    ..05) spared gray matter. In summary, ALC treatment maintains mitochondrial bioenergetics following contusion SCI and, thus, holds great potential as a neuroprotective therapy for acute SCI. ..
  20. Bevan A, Duque S, Foust K, Morales P, Braun L, Schmelzer L, et al. Systemic gene delivery in large species for targeting spinal cord, brain, and peripheral tissues for pediatric disorders. Mol Ther. 2011;19:1971-80 pubmed publisher
    ..Our findings support the use of AAV9 for gene transfer to the CNS for disorders in pediatric populations. ..
  21. Hoffman M, Nichols N, MacFarlane P, Mitchell G. Phrenic long-term facilitation after acute intermittent hypoxia requires spinal ERK activation but not TrkB synthesis. J Appl Physiol (1985). 2012;113:1184-93 pubmed publisher
    ..Thus, there are clear mechanistic distinctions between AIH-induced pLTF (i.e., BDNF synthesis and MEK/ERK dependent) versus adenosine 2A receptor-induced pMF (i.e., TrkB synthesis and PI3K/Akt dependent). ..
  22. Lavrov I, Gerasimenko Y, Burdick J, Zhong H, Roy R, Edgerton V. Integrating multiple sensory systems to modulate neural networks controlling posture. J Neurophysiol. 2015;114:3306-14 pubmed publisher
  23. Tsuzuki K, Ase A, Séguéla P, Nakatsuka T, Wang C, She J, et al. TNP-ATP-resistant P2X ionic current on the central terminals and somata of rat primary sensory neurons. J Neurophysiol. 2003;89:3235-42 pubmed
    ..These results suggest that TNP-ATP-resistant P2X receptor subtypes are expressed on capsaicin-insensitive A delta-afferent fibers and play a role in modulating sensory transmission to lamina V neurons. ..
  24. Lewis K, Bates J, Eisen J. Regulation of iro3 expression in the zebrafish spinal cord. Dev Dyn. 2005;232:140-8 pubmed
    ..We discuss our findings in the context of previous studies, suggesting that iro3 represses formation of motoneurons and promotes formation of interneurons. ..
  25. Li X, Gutierrez D, Hanson M, Han J, Mark M, Chiel H, et al. Fast noninvasive activation and inhibition of neural and network activity by vertebrate rhodopsin and green algae channelrhodopsin. Proc Natl Acad Sci U S A. 2005;102:17816-21 pubmed
    ..Thus light-activated vertebrate RO4 and green algae ChR2 allow the antagonistic control of neuronal function within ms to s in a precise, reversible, and noninvasive manner in cultured neurons and intact vertebrate spinal cords. ..
  26. Jacques Fricke B, Seow Y, Gottlieb P, Sachs F, Gomez T. Ca2+ influx through mechanosensitive channels inhibits neurite outgrowth in opposition to other influx pathways and release from intracellular stores. J Neurosci. 2006;26:5656-64 pubmed
  27. Ye J, Zhang J, Xiao C, Kong J. Patch-clamp studies in the CNS illustrate a simple new method for obtaining viable neurons in rat brain slices: glycerol replacement of NaCl protects CNS neurons. J Neurosci Methods. 2006;158:251-9 pubmed
    ..Due to the increase in the number of viable neurons, the new ACSF increases the productivity of experiments. Based on our data, we propose that this glycerol-based solution may protect CNS neurons. ..
  28. Benyamin R, Kramer J, Vallejo R. A case of spinal cord stimulation in Raynaud's Phenomenon: can subthreshold sensory stimulation have an effect?. Pain Physician. 2007;10:473-8 pubmed
    ..The possible role of the sympathetic nervous system in this relationship is also discussed. ..
  29. Zhang G, Mohammad H, Peper B, Raja S, Wilson S, Sweitzer S. Enhanced peripheral analgesia using virally mediated gene transfer of the mu-opioid receptor in mice. Anesthesiology. 2008;108:305-13 pubmed publisher
    ..This gene therapy approach may provide an innovative strategy to enhance peripheral opioid analgesia for the treatment of pain in humans, thereby minimizing centrally mediated opioid side effects such as sedation and addiction. ..
  30. Guerrero A, Quang P, Dekker N, Jordan R, Schmidt B. Peripheral cannabinoids attenuate carcinoma-induced nociception in mice. Neurosci Lett. 2008;433:77-81 pubmed publisher
    ..These findings support the suggestion that cannabinoids are capable of producing antinociception in carcinoma-induced pain. ..
  31. DiMarco A, Kowalski K. High-frequency spinal cord stimulation of inspiratory muscles in dogs: a new method of inspiratory muscle pacing. J Appl Physiol (1985). 2009;107:662-9 pubmed publisher
    ..HF-SCS has the potential to provide an effective method of inspiratory muscle pacing. ..
  32. Perkins E, Warren S, May P. The mesencephalic reticular formation as a conduit for primate collicular gaze control: tectal inputs to neurons targeting the spinal cord and medulla. Anat Rec (Hoboken). 2009;292:1162-81 pubmed publisher
    ..The medial location of these reticulospinal and reticuloreticular neurons suggests this MRF region may be specialized for head movement control. ..
  33. Zivadinov R, Poloni G, Marr K, Schirda C, Magnano C, Carl E, et al. Decreased brain venous vasculature visibility on susceptibility-weighted imaging venography in patients with multiple sclerosis is related to chronic cerebrospinal venous insufficiency. BMC Neurol. 2011;11:128 pubmed publisher
    ..The pathogenesis of these findings has to be further investigated, but they suggest that reduced metabolism and morphological changes of venous vasculature may be taking place in patients with MS. ..
  34. Ziskind Conhaim L. Neuronal correlates of the dominant role of GABAergic transmission in the developing mouse locomotor circuitry. Ann N Y Acad Sci. 2013;1279:43-53 pubmed publisher
  35. Zwischenberger B, Beasley M, Davenport D, Xenos E. Meta-analysis of the correlation between chronic cerebrospinal venous insufficiency and multiple sclerosis. Vasc Endovascular Surg. 2013;47:620-4 pubmed publisher
    ..885, P < .0001) with no significant heterogeneity of the studies (I (2) = 18, P = .279). The meta-analysis demonstrated a correlation between CCSVI and MS. However, there was no evidence that CCSVI has a causative role in MS. ..
  36. Williams J, Trias E, Beilby P, Lopez N, Labut E, Bradford C, et al. Copper delivery to the CNS by CuATSM effectively treats motor neuron disease in SOD(G93A) mice co-expressing the Copper-Chaperone-for-SOD. Neurobiol Dis. 2016;89:1-9 pubmed publisher
    ..All ALS patients also express human CCS, raising the hope that familial SOD ALS patients could respond to CuATSM treatment similarly to the CCSxSOD mice. ..
  37. Clark W, Madden K, Rothlein R, Zivin J. Reduction of central nervous system ischemic injury in rabbits using leukocyte adhesion antibody treatment. Stroke. 1991;22:877-83 pubmed
    ..This protective effect supports the active role of leukocytes in central nervous system reperfusion ischemic injury and offers potential for future therapy. ..
  38. Rodriguez M, Roos R. Pathogenesis of early and late disease in mice infected with Theiler's virus, using intratypic recombinant GDVII/DA viruses. J Virol. 1992;66:217-25 pubmed
    ..However, quantitative analysis of demyelination produced by recombinant GDVII/DA viruses suggest that multiple gene segments influence the number and extent of demyelinating lesions. ..
  39. Nance P. Alpha adrenergic and serotonergic agents in the treatment of spastic hypertonia. Phys Med Rehabil Clin N Am. 2001;12:889-905 pubmed
    ..6. Initiate therapy with a low dosage, and titrate judiciously. 7. Stop the titration when functional goal is achieved. 8. If goal is not achieved or if side effects are intolerable, consider a second medication. ..
  40. Loy D, Magnuson D, Zhang Y, Onifer S, Mills M, Cao Q, et al. Functional redundancy of ventral spinal locomotor pathways. J Neurosci. 2002;22:315-23 pubmed
    ..7 and 6.5, respectively. Our data support a diffuse arrangement of axons within the ventral white matter that may comprise a system of multiple descending pathways subserving spontaneous over-ground locomotion in the intact animal. ..
  41. Dun S, Brailoiu G, Parsons A, Yang J, Zeng Q, Chen X, et al. Metastin-like immunoreactivity in the rat medulla oblongata and spinal cord. Neurosci Lett. 2003;335:197-201 pubmed
    ..The pattern of distribution of MTS-LI in the medulla and spinal cord suggests that this novel peptide may participate in autonomic and sensory neural signaling. ..
  42. Fuller D, Johnson S, Olson E, Mitchell G. Synaptic pathways to phrenic motoneurons are enhanced by chronic intermittent hypoxia after cervical spinal cord injury. J Neurosci. 2003;23:2993-3000 pubmed
    ..05). We conclude that CIH induced spinal cord plasticity-enhanced phrenic motor output. This plasticity required preconditions established by chronic spinal injury. ..
  43. Tsai H, Macklin W, Miller R. Netrin-1 is required for the normal development of spinal cord oligodendrocytes. J Neurosci. 2006;26:1913-22 pubmed
    ..These data indicate that netrin-1 is crucial for both the initial dispersal of spinal cord oligodendrocyte precursors and their subsequent development in the presumptive white matter. ..
  44. Southerland E, Milhorn D, Foreman R, Linderoth B, DeJongste M, Armour J, et al. Preemptive, but not reactive, spinal cord stimulation mitigates transient ischemia-induced myocardial infarction via cardiac adrenergic neurons. Am J Physiol Heart Circ Physiol. 2007;292:H311-7 pubmed
    ..SCS did not alter blood pressure or heart rate. We conclude that preemptive SCS reduces the size of infarcts induced by transient CAO; such cardioprotection involves cardiac adrenergic neurons. ..
  45. Cramer S, Baggott C, Cain J, Tilghman J, Allcock B, Miranpuri G, et al. The role of cation-dependent chloride transporters in neuropathic pain following spinal cord injury. Mol Pain. 2008;4:36 pubmed publisher
    ..The anti-hyperalgesic effect of NKCC1 inhibition suggests that normal or elevated NKCC1 function and loss of KCC2 function play a role in the development and maintenance of SCI-induced neuropathic pain. ..
  46. Tsai H, Macklin W, Miller R. Distinct modes of migration position oligodendrocyte precursors for localized cell division in the developing spinal cord. J Neurosci Res. 2009;87:3320-30 pubmed publisher
    ..These studies suggest that positional cues are critical for regulating OPC behavior during spinal cord development. ..
  47. Myers S, DeVries W, Andres K, Gruenthal M, Benton R, Hoying J, et al. CD47 knockout mice exhibit improved recovery from spinal cord injury. Neurobiol Dis. 2011;42:21-34 pubmed publisher
  48. Campbell A, Zagon I, McLaughlin P. Opioid growth factor arrests the progression of clinical disease and spinal cord pathology in established experimental autoimmune encephalomyelitis. Brain Res. 2012;1472:138-48 pubmed publisher
    ..Our data substantiate the role of the OGF-OGFr axis in EAE and support the use of OGF as a biotherapy for MS. ..
  49. Jiang Y, Salafranca M, Adhikari S, Xia Y, Feng L, Sonntag M, et al. Chemokine receptor expression in cultured glia and rat experimental allergic encephalomyelitis. J Neuroimmunol. 1998;86:1-12 pubmed
    ..These data identify the rat orthologs of chemokine receptors and demonstrate that brain, spinal cord, and cultured glial cells express chemokine receptors that can be regulated both in vitro and in vivo. ..
  50. Ippolito D, Xu M, Bruchas M, Wickman K, Chavkin C. Tyrosine phosphorylation of K(ir)3.1 in spinal cord is induced by acute inflammation, chronic neuropathic pain, and behavioral stress. J Biol Chem. 2005;280:41683-93 pubmed
    ..The reduction in K(ir)3 channel activity is predicted to enhance neuronal excitability under physiologically relevant conditions and may mediate a component of the adaptive physiological response. ..
  51. Olsen M, Campbell S, Sontheimer H. Differential distribution of Kir4.1 in spinal cord astrocytes suggests regional differences in K+ homeostasis. J Neurophysiol. 2007;98:786-93 pubmed
    ..Taken together, these data support the conclusion that regional differences in astrocytic expression of Kir4.1 channels result in marked changes in potassium clearance rates in these two regions of the spinal cord. ..
  52. Duric V, McCarson K. Neurokinin-1 (NK-1) receptor and brain-derived neurotrophic factor (BDNF) gene expression is differentially modulated in the rat spinal dorsal horn and hippocampus during inflammatory pain. Mol Pain. 2007;3:32 pubmed
    ..modulation of the higher brain structures such as the hippocampus. ..
  53. Mitchell G, Turner D, Henderson D, Foley K. Spinal serotonin receptor activation modulates the exercise ventilatory response with increased dead space in goats. Respir Physiol Neurobiol. 2008;161:230-8 pubmed publisher
    ..We conclude that spinal 5-HT2 receptors modulate the exercise ventilatory response with increased VD in goats. ..
  54. Jha A, Lammertse D, Coll J, Charlifue S, Coughlin C, Whiteneck G, et al. Apolipoprotein E epsilon4 allele and outcomes of traumatic spinal cord injury. J Spinal Cord Med. 2008;31:171-6 pubmed
    ..APOE epsilon4 allele was associated with differences in neurological recovery and longer rehabilitation LOS. Genetic factors may be among the determinants of outcome after SCI and warrant further study. ..
  55. Wilkerson J, Mitchell G. Daily intermittent hypoxia augments spinal BDNF levels, ERK phosphorylation and respiratory long-term facilitation. Exp Neurol. 2009;217:116-23 pubmed publisher
    ..Increased BDNF synthesis may no longer be necessary for phrenic LTF following dAIH preconditioning since BDNF concentration is already elevated. ..
  56. Barlow S. Central pattern generation involved in oral and respiratory control for feeding in the term infant. Curr Opin Otolaryngol Head Neck Surg. 2009;17:187-93 pubmed publisher
    ..Cross-system interactions among these CPGs represent targets of opportunity for new interventions, which optimize experience-dependent mechanisms to promote safe swallows among newborn and pediatric patients. ..
  57. Boudrias M, McPherson R, Frost S, Cheney P. Output properties and organization of the forelimb representation of motor areas on the lateral aspect of the hemisphere in rhesus macaques. Cereb Cortex. 2010;20:169-86 pubmed publisher
  58. Ramesh G, Borda J, Gill A, Ribka E, Morici L, Mottram P, et al. Possible role of glial cells in the onset and progression of Lyme neuroborreliosis. J Neuroinflammation. 2009;6:23 pubmed publisher
    ..This inflammatory context could potentiate glial and neuronal apoptosis...
  59. Jeffry J, Yu S, Sikand P, Parihar A, Evans M, Premkumar L. Selective targeting of TRPV1 expressing sensory nerve terminals in the spinal cord for long lasting analgesia. PLoS ONE. 2009;4:e7021 pubmed publisher
    ..Preventing nociceptive transmission at the level of the spinal cord can be a useful strategy to treat chronic, debilitating and intractable pain. ..
  60. Riley J, Federici T, Park J, Suzuki M, Franz C, Tork C, et al. Cervical spinal cord therapeutics delivery: preclinical safety validation of a stabilized microinjection platform. Neurosurgery. 2009;65:754-61; discussion 761-2 pubmed publisher
    ..Finally, demonstration of long-term graft viability in future preclinical toxicity studies may require tailored immunosuppressive therapies, an allograft construct, or tailored choice of host species. ..
  61. Sribnick E, Samantaray S, Das A, Smith J, Matzelle D, Ray S, et al. Postinjury estrogen treatment of chronic spinal cord injury improves locomotor function in rats. J Neurosci Res. 2010;88:1738-50 pubmed publisher
    ..These findings suggest that estrogen may be useful as a promising therapeutic agent for prevention of damage and improvement of locomotor function in chronic SCI. (c) 2010 Wiley-Liss, Inc. ..
  62. Horvath R, Landry R, Romero Sandoval E, DeLeo J. Morphine tolerance attenuates the resolution of postoperative pain and enhances spinal microglial p38 and extracellular receptor kinase phosphorylation. Neuroscience. 2010;169:843-54 pubmed publisher
  63. Prudencio M, Durazo A, Whitelegge J, Borchelt D. An examination of wild-type SOD1 in modulating the toxicity and aggregation of ALS-associated mutant SOD1. Hum Mol Genet. 2010;19:4774-89 pubmed publisher
  64. Sharma H, Alilain W, Sadhu A, Silver J. Treatments to restore respiratory function after spinal cord injury and their implications for regeneration, plasticity and adaptation. Exp Neurol. 2012;235:18-25 pubmed publisher
    ..Additionally, it will discuss findings about motor and CNS respiratory plasticity and adaptation with potential clinical and translational implications. ..
  65. Iwasa M, Kawabe K, Sapru H. Activation of melanocortin receptors in the intermediolateral cell column of the upper thoracic cord elicits tachycardia in the rat. Am J Physiol Heart Circ Physiol. 2013;305:H885-93 pubmed publisher
    ..Our results allude to the possibility that cardiac effects of stress may be mediated via melanocortin containing ARCN neurons that project to the IML. ..
  66. Hutchins E, Szaro B. c-Jun N-terminal kinase phosphorylation of heterogeneous nuclear ribonucleoprotein K regulates vertebrate axon outgrowth via a posttranscriptional mechanism. J Neurosci. 2013;33:14666-80 pubmed publisher
    ..Thus, in addition to its known roles in transcription and cytoskeletal organization, JNK acts posttranscriptionally through hnRNP K to regulate translation of proteins crucial for axonogenesis. ..
  67. Moore S, Oglesbee M. Spinal Cord Ependymal Responses to Naturally Occurring Traumatic Spinal Cord Injury in Dogs. Vet Pathol. 2015;52:1108-17 pubmed publisher
    ..Enhanced GFAP expression and changes in E-cadherin expression patterns support additional studies to evaluate the canine SEL as a source of endogenous neural precursors that may be modulated for future clinical interventions after SCI. ..
  68. Coovert D, Le T, McAndrew P, Strasswimmer J, Crawford T, Mendell J, et al. The survival motor neuron protein in spinal muscular atrophy. Hum Mol Genet. 1997;6:1205-14 pubmed
    ..We suggest that disruption of SMN(T) in type I patients results in loss of SMN from motor neurons, resulting in the degeneration of these neurons. ..
  69. Gallagher M, Burgess L, Brunden K. Characterization of multiple forms of the human glycine transporter type-2. Brain Res Mol Brain Res. 1999;70:101-15 pubmed
    ..Like rat GlyT2, the high-affinity uptake mediated by hGlyT2 was found to be insensitive to the GlyT1 inhibitor sarcosine. ..
  70. Ness T, Gebhart G. Inflammation enhances reflex and spinal neuron responses to noxious visceral stimulation in rats. Am J Physiol Gastrointest Liver Physiol. 2001;280:G649-57 pubmed
    ..This suggests that the neurophysiological basis for inflammation-induced increases in reflex responses to CRD is increased activity of this neuronal subgroup...
  71. Sribnick E, Wingrave J, Matzelle D, Wilford G, Ray S, Banik N. Estrogen attenuated markers of inflammation and decreased lesion volume in acute spinal cord injury in rats. J Neurosci Res. 2005;82:283-93 pubmed
    ..Further work needs to be done, however, to elucidate the neuroprotective mechanism of estrogen. ..
  72. Ni X, Sullivan G, Martin Caraballo M. Developmental characteristics of AMPA receptors in chick lumbar motoneurons. Dev Neurobiol. 2007;67:1419-32 pubmed
    ..These findings raise the possibility that Ca2+ influx through Ca(2+)-permeable AMPA receptors plays an important role during early embryonic development in chick spinal motoneurons...
  73. Kondo Y, Duncan I. Selective reduction in microglia density and function in the white matter of colony-stimulating factor-1-deficient mice. J Neurosci Res. 2009;87:2686-95 pubmed publisher
    ..These findings demonstrate that this mutant is a valuable model in which to study roles of microglia/macrophages in the pathophysiology of myelin disorders. ..
  74. Dolic K, Weinstock Guttman B, Marr K, Valnarov V, Carl E, Hagemeier J, et al. Risk factors for chronic cerebrospinal venous insufficiency (CCSVI) in a large cohort of volunteers. PLoS ONE. 2011;6:e28062 pubmed publisher
    ..Risk factors for CCSVI differ from established risk factors for peripheral venous diseases. Vascular, infectious and inflammatory factors were associated with higher CCSVI frequency. ..
  75. Hammer L, Zagon I, McLaughlin P. Treatment of a relapse-remitting model of multiple sclerosis with opioid growth factor. Brain Res Bull. 2013;98:122-31 pubmed publisher
    ..These data are the first to demonstrate that OGF prevented relapses in RR-EAE and diminished underlying neuropathology, corroborating the potential of the OGF-OGF receptor pathway for treatment of MS. ..
  76. Morgan D, Davis B, Kearn C, Marcus D, Cook A, Wager Miller J, et al. Mutation of putative GRK phosphorylation sites in the cannabinoid receptor 1 (CB1R) confers resistance to cannabinoid tolerance and hypersensitivity to cannabinoids in mice. J Neurosci. 2014;34:5152-63 pubmed publisher
    ..These mice also validate the approach of mutating GRK phosphorylation sites involved in desensitization as a general means to confer exaggerated signaling to GPCRs in vivo. ..
  77. Chen X, Wang Y, Chen Y, Chen L, Wolpaw J. Ablation of the inferior olive prevents H-reflex down-conditioning in rats. J Neurophysiol. 2016;115:1630-6 pubmed publisher
    ..They help to further define H-reflex conditioning as a model for understanding motor learning and as a new approach to enhancing functional recovery after trauma or disease. ..
  78. Gao B, Stricker C, Ziskind Conhaim L. Transition from GABAergic to glycinergic synaptic transmission in newly formed spinal networks. J Neurophysiol. 2001;86:492-502 pubmed
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