Glial Modulation of Pain: A Step Beyond: Figure 1.

Cunha, Thiago M.; Dias, Quintino Moura

doi:10.1523/jneurosci.5938-08.2009

Cited by 6 publications

(6 citation statements)

References 11 publications

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“…The peripheral nerve injury leads to abnormal neuronal inputs from site of injury to CNS and it strongly activates central glial cells (i.e., microglia, astrocytes and oligodendrocytes) as well as peripheral glial cells (i.e., Schwann and satellite cells) (Zhuo et al, 2011). These cells are responsible to release many substances either directly or indirectly acting on neurons of the nociceptive system and subsequently amplifying pain signal in the site of injury to brain and vise-verse (Cunha and Dias, 2009). The contribution of neuron-glia interactions have played major role in the genesis of neuropathic pain and this event produces severe and long-lasting pain-related behaviors via changing the exaggerated release of excitatory neurotransmitters leads to ectopic discharge, long-term potentiation and neuronal plasticity (Cunha and Dias, 2009;Wei et al, 2008;Zhuo et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

“…These cells are responsible to release many substances either directly or indirectly acting on neurons of the nociceptive system and subsequently amplifying pain signal in the site of injury to brain and vise-verse (Cunha and Dias, 2009). The contribution of neuron-glia interactions have played major role in the genesis of neuropathic pain and this event produces severe and long-lasting pain-related behaviors via changing the exaggerated release of excitatory neurotransmitters leads to ectopic discharge, long-term potentiation and neuronal plasticity (Cunha and Dias, 2009;Wei et al, 2008;Zhuo et al, 2011). In addition, the interactions between glial and immune cells are also contributed to induce the chronic neuropathic pain (Benarroch, 2010;Watkins and Maier, 2002).…”

Section: Discussionmentioning

confidence: 99%

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Ameliorative potential of montelukast on ischemia–reperfusion injury induced vasculitic neuropathic pain in rat

2012

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Ameliorative potential of montelukast on ischemia–reperfusion injury induced vasculitic neuropathic pain in rat

2012

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“…Weak points: (1) this is a single case study; (2) the link between the neurotoxin and the direct effect on the primary trigeminal neurons is not missing but is weakly supported by very few references; (3) as the findings are a proof of serendipity, other sensory ganglia were not evaluated.…”

Section: Swo(t) Analysis Of the Case Reportedmentioning

confidence: 95%

“…P eripheral neuropathies can result from any type of neural damage, including that triggered by physical trauma, infection, inflammation, metabolic abnormalities, vascular abnormalities, neurotoxins, chemotherapeutic agents, radiation or autoimmune disease [1].…”

mentioning

confidence: 99%

Trigeminal ganglionic neuronal death in a case positive for the botulinum neurotoxin B

Jianu¹,

Pop²,

Hostiuc³

et al. 2012

RJLM

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Botulinum neurotoxin B (BoNT-B) is a well known lethal agent in humans. In the last years botulinum neurotoxins have been used as therapeutic agents in pain management; their intimate effects on the peripheral nervous ganglia were however not thoroughly described. We present here a rare case of a BoNT-B serologically positive human adult in which trigeminal ganglia were found immunopositive for caspases 3 and 9. Thus the intrinsic apoptotic pathway was proposed as the cell death mechanism involving primary trigeminal neurons. Scavengers such as macrophages and resident satellite glial cells, with a CD68 immunopositivity were also identified, presumably being in the process of eliminating apoptotic remnants. Taking into account that the downregulation of metalloproteinases leads to inactivation of neuronal caspase 3, exogenous metalloproteinases, such as BoNT, may lead to apoptosis. If this causal relation, neurotoxin-to-apoptosis is valid, similar apoptotic processes can be presumed to occur in various ganglia, sensory and autonomic, involved in vital functions of the body. In conclusion, further morphological and experimental studies are needed to extensively evaluate the apoptotic effect of BoNT within the peripheral nervous ganglia in botulinum infections and BoNT treatments.

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“…And it is approved by the FDA for the treatment of multiple myeloma and leprosy as well. Although NP is also associated with an immunological disorder in the CNS,12 whether Tha could alleviate NP remains unclear. Tha can significantly inhibit activation of both astrocytes and microglia in a mouse model of Alzheimer’s disease13 and suppress the production of tumor necrosis factor alpha (TNF-α) 14.…”

Section: Introductionmentioning

confidence: 99%

<p>Systemic Injection of Thalidomide Prevent and Attenuate Neuropathic Pain and Alleviate Neuroinflammatory Response in the Spinal Dorsal Horn</p>

Xu¹,

Dang²,

Cui³

et al. 2019

JPR

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Background and objectiveThalidomide (Tha) has been shown to exert immunomodulatory and anti-inflammatory properties. Whether Tha can alleviate spinal nerve ligation (SNL)-induced neuropathic pain (NP) is still unclear. This study aimed to investigate the therapeutic effect of Tha on the SNL-induced NP and further explore the potential analgesic mechanisms of Tha.MethodsThe effects of Tha on SNL-induced mechanical allodynia were assessed by pain behavioral testing. The expressions of the astrocyte marker glial fibrillary acidic protein (GFAP) and the microglia marker Iba1 in the spinal dorsal horn were evaluated by immunofluorescence histochemistry. Protein expressions of the tumor necrosis factor alpha (TNF-α) in the spinal dorsal horn were tested by Western blot assay. Data were analyzed using one-way ANOVA or two-way ANOVA.ResultsBy the pretreatment with a single intraperitoneal injection, the PWMT in SNL+Tha group was significantly increased from day 1 to day 2 after SNL (P < 0.05 compared with SNL+Veh group). By the posttreatment with a single intraperitoneal injection, the PWMT in SNL+Tha group was also significantly increased from day 3 to day 4 after SNL (P < 0.05 compared with SNL+Veh group). By the posttreatment with multiple intraperitoneal injection, both the PWMT and the PWTL in SNL+Tha group were similarly significantly increased from day 3 to day 14 after SNL (P < 0.05 compared with SNL+Veh group). Furthermore, the GFAP and Iba1 expressions and TNF-α levels of the ipsilateral spinal dorsal horn in SNL+Tha group were significantly weaker from day 3 to day 14 after SNL than those in SNL+Veh group (P < 0.05).ConclusionTha can significantly alleviate NP induced by SNL. The analgesic mechanism may be related to inhibition of astrocyte and microglia activation as well as down-regulation of TNF-α levels in the spinal dorsal horn.

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Glial Modulation of Pain: A Step Beyond: Figure 1.

Cited by 6 publications

References 11 publications

Ameliorative potential of montelukast on ischemia–reperfusion injury induced vasculitic neuropathic pain in rat

Ameliorative potential of montelukast on ischemia–reperfusion injury induced vasculitic neuropathic pain in rat

Trigeminal ganglionic neuronal death in a case positive for the botulinum neurotoxin B

<p>Systemic Injection of Thalidomide Prevent and Attenuate Neuropathic Pain and Alleviate Neuroinflammatory Response in the Spinal Dorsal Horn</p>

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