Literature DB >> 19435601

Spinal glia modulate both adaptive and pathological processes.

Elisabeth G Vichaya1, Kyle M Baumbauer, Luis M Carcoba, James W Grau, Mary W Meagher.   

Abstract

Recent research indicates that glial cells control complex functions within the nervous system. For example, it has been shown that glial cells contribute to the development of pathological pain, the process of long-term potentiation, and the formation of memories. These data suggest that glial cell activation exerts both adaptive and pathological effects within the CNS. To extend this line of work, the present study investigated the role of glia in spinal learning and spinal learning deficits using the spinal instrumental learning paradigm. In this paradigm rats are transected at the second thoracic vertebra (T2) and given shock to one hind limb whenever the limb is extended (controllable shock). Over time these subjects exhibit an increase in flexion duration that reduces net shock exposure. However, when spinalized rats are exposed to uncontrollable shock or inflammatory stimuli prior to testing with controllable shock, they exhibit a learning deficit. To examine the role of glial in this paradigm, spinal glial cells were pharmacologically inhibited through the use of fluorocitrate. Our results indicate that glia are involved in the acquisition, but not maintenance, of spinal learning. Furthermore, the data indicate that glial cells are involved in the development of both shock and inflammation-induced learning deficits. These findings are consistent with prior research indicating that glial cells are involved in both adaptive and pathological processes within the spinal cord.

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Year:  2009        PMID: 19435601      PMCID: PMC2749915          DOI: 10.1016/j.bbi.2009.05.001

Source DB:  PubMed          Journal:  Brain Behav Immun        ISSN: 0889-1591            Impact factor:   7.217


  67 in total

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4.  An in vivo model for studying function of brain tissue temporarily devoid of glial cell metabolism: the use of fluorocitrate.

Authors:  R E Paulsen; A Contestabile; L Villani; F Fonnum
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  18 in total

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2.  Acute spinal cord injury (SCI) transforms how GABA affects nociceptive sensitization.

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4.  Effect of acute intermittent hypoxia on motor function in individuals with chronic spinal cord injury following ibuprofen pretreatment: A pilot study.

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5.  Elevated MMP-9 in the lumbar cord early after thoracic spinal cord injury impedes motor relearning in mice.

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Journal:  Neuroscience       Date:  2011-10-18       Impact factor: 3.590

Review 7.  When Pain Hurts: Nociceptive Stimulation Induces a State of Maladaptive Plasticity and Impairs Recovery after Spinal Cord Injury.

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8.  Evidence That the Central Nervous System Can Induce a Modification at the Neuromuscular Junction That Contributes to the Maintenance of a Behavioral Response.

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9.  Metaplasticity within the spinal cord: Evidence brain-derived neurotrophic factor (BDNF), tumor necrosis factor (TNF), and alterations in GABA function (ionic plasticity) modulate pain and the capacity to learn.

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10.  Ipsilesional Motor Cortex Plasticity Participates in Spontaneous Hindlimb Recovery after Lateral Hemisection of the Thoracic Spinal Cord in the Rat.

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Journal:  J Neurosci       Date:  2018-10-09       Impact factor: 6.167

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