Evaluation of the neonatal streptozotocin model of diabetes in rats: Evidence for a model of neuropathic pain

Barragán-Iglesias, Paulino; Oidor-Chan, Víctor Hugo; Loeza‐Alcocer, Emanuel; Pineda-Farías, Jorge Baruch; Velázquez-Lagunas, Isabel; Salinas-Abarca, Ana Belen; Hong, Enrique; Sánchez-Mendoza, Alicia; Delgado‐Lezama, Rodolfo; Price, Theodore J.; Granados‐Soto, Vinicio

doi:10.1016/j.pharep.2017.09.002

Cited by 30 publications

(16 citation statements)

References 44 publications

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“…Mounting evidence suggests that activation of satellite glial cells indeed participate in neuropathic pain. 39 – 41 Thus, the transient presence of ATF2 in these cells may have a role in neuropathic pain. Our data partially agree with other observations indicating that stimulation of adult DRG neurons by doxorubicin or ultraviolet irradiation ( in vitro ) and axotomy ( in vivo ) induce a rapid (2–24 h) and consistent (3–20 days) down-regulation of ATF2.…”

Section: Discussionmentioning

confidence: 99%

ATF2, but not ATF3, participates in the maintenance of nerve injury-induced tactile allodynia and thermal hyperalgesia

et al. 2018

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Transcription factors are proteins that modulate the transcriptional rate of target genes in the nucleus in response to extracellular or cytoplasmic signals. Activating transcription factors 2 (ATF2) and 3 (ATF3) respond to environmental signals and maintain cellular homeostasis. There is evidence that inflammation and nerve injury modulate ATF2 and ATF3 expression. However, the function of these transcription factors in pain is unknown. The purpose of this study was to investigate the contribution of ATF2 and ATF3 to nerve injury-induced neuropathic pain. L5/6 spinal nerve ligation induced tactile allodynia and thermal hyperalgesia. Moreover, nerve damage enhanced ATF2 and ATF3 protein expression in injured L5/6 dorsal root ganglia and spinal cord but not in uninjured L4 dorsal root ganglia. Nerve damage also enhanced ATF2 immunoreactivity in dorsal root ganglia and spinal cord 7 to 21 days post-injury. Repeated intrathecal post-treatment with a small-interfering RNA targeted against ATF2 (ATF2 siRNA) or anti-ATF2 antibody partially reversed tactile allodynia and thermal hyperalgesia. In contrast, ATF3 siRNA or anti-ATF3 antibody did not modify nociceptive behaviors. ATF2 immunoreactivity was found in dorsal root ganglia and spinal cord co-labeling with NeuN mainly in non-peptidergic (IB4+) but also in peptidergic (CGRP+) neurons. ATF2 was found mainly in small- and medium-sized neurons. These results suggest that ATF2, but not ATF3, is found in strategic sites related to spinal nociceptive processing and participates in the maintenance of neuropathic pain in rats.

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Section: Discussionmentioning

confidence: 99%

ATF2, but not ATF3, participates in the maintenance of nerve injury-induced tactile allodynia and thermal hyperalgesia

et al. 2018

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“…Recently, streptozotocin-induced experimental diabetes has been produced in neonatal rats (nSTZ) and it was demonstrated that in addition to glucose intolerance, the hyperglycemia induced in these animals was much milder than in adults (21). Also, C-fibre nerve conduction velocity in nSTZ animals was reduced in a similar fashion to adults, but it occurred considerably later in neonates following treatment with streptozotocin.…”

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confidence: 99%

“…It is noteworthy that all these characteristics were attended by tactile allodynia to von Frey filament application, substantiating the notion that nSTZ causes nerve injury. The nSTZ diabetic model has been designated as one which mimics type 2 diabetes (22), although more recent authors acknowledged that their findings did not fully support this overall postulation (21). Nevertheless, nSTZ did disclose some of the features of type 2 diabetes and the animals in the nSTZ model were much healthier than those in the type 1 diabetic model (STZ in adult animals).…”

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confidence: 99%

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Neuropathic pain models and outcome measures: a dual translational challenge

Sewell

2018

Ann. Transl. Med

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“…Microglia The role of spinal microglia in neuropathic pain syndromes is complex [137] and, at least for CIPN, is not completely understood. Investigations of the role of microglia in CIPN have presented opposing findings.…”

Section: Immune Cells T-cellsmentioning

confidence: 99%

Chemotherapy-induced peripheral neuropathy: part 1—current state of knowledge and perspectives for pharmacotherapy

Sałat

2020

Pharmacol. Rep

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Background Despite the increasing knowledge of the etiology of neuropathic pain, this type of chronic pain is resistant to available analgesics in approximately 50% of patients and therefore is continuously a subject of considerable interest for physiologists, neurologists, medicinal chemists, pharmacologists and others searching for more effective treatment options for this debilitating condition. Materials and methods The present review article is the first of the two articles focused on chemotherapy-induced peripheral neuropathy (CIPN). Results CIPN is regarded as one of the most common drug-induced neuropathies and is highly pharmacoresistant. The lack of efficacious pharmacological methods for treating CIPN and preventing its development makes CIPN-related neuropathic pain a serious therapeutic gap in current medicine and pharmacotherapy. In this paper, the most recent advances in the field of studies on CIPN caused by platinum compounds (namely oxaliplatin and cisplatin), taxanes, vinca alkaloids and bortezomib are summarized. Conclusions The prevalence of CIPN, potential causes, risk factors, symptoms and molecular mechanisms underlying this pharmacoresistant condition are discussed.

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Evaluation of the neonatal streptozotocin model of diabetes in rats: Evidence for a model of neuropathic pain

Cited by 30 publications

References 44 publications

ATF2, but not ATF3, participates in the maintenance of nerve injury-induced tactile allodynia and thermal hyperalgesia

ATF2, but not ATF3, participates in the maintenance of nerve injury-induced tactile allodynia and thermal hyperalgesia

Neuropathic pain models and outcome measures: a dual translational challenge

Chemotherapy-induced peripheral neuropathy: part 1—current state of knowledge and perspectives for pharmacotherapy

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