Involvement of spinal glutamate transporter-1 in the development of mechanical allodynia and hyperalgesia associated with type 2 diabetes

Shi, Jing‐Shan; Jiang, Ke; Li, Zhao-duan

doi:10.2147/jpr.s118412

Cited by 9 publications

(12 citation statements)

References 38 publications

(39 reference statements)

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“…Our data agree with previous studies assessing the antinociceptive effect of CFX in models of inflammatory pain, such as carrageenan, acetic acid, and surgical incision (Macaluso et al, 2013;Ochoa-Aguilar et al, 2018;Stepanovic-Petrovic et al, 2014). Moreover, it has been reported that CFX is partially effective in models of neuropathic pain in rodents (Amin et al, 2012;Eljaja et al, 2011;Gunduz et al, 2011;Hajhashemi et al, 2013;Hu et al, 2010;Ochoa-Aguilar et al, 2017;Pottabathini et al, 2016;Ramos et al, 2010;Shi et al, 2016).…”

Section: Discussionsupporting

confidence: 92%

“…However, at these concentrations, formalin resembles neuropathic rather than inflammatory pain (Bráz & Basbaum, 2010; Salinas-Abarca, Avila-Rojas, Barragán-Iglesias, Pineda-Farias, & Granados-Soto, 2017). Notwithstanding, acute pretreatment with CFX induces only a slight (Hu et al, 2010;Ramos et al, 2010;Shi et al, 2016) or null (Amin et al, 2012;Hajhashemi et al, 2013) antiallodynic effect in neuropathic pain model in rodents, although some have reported that 7 days pretreatment of CFX (400 mg/kg) induces a strong anti-hyperalgesic effect (Hajhashemi et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

“…CFX is used against gram-positive and gram-negative bacteria and broadly recommended for nervous central system infections (McLeod, Nahata, & Barson, 1985;Perry & Schentag, 2001). Pioneer studies have shown that this antibiotic induces antinociceptive effects in chronic constriction nerve or streptozotocin injury-induced neuropathic pain (Amin, Hajhashemi, Abnous, & Hosseinzadeh, 2014;Amin, Hajhashemi, Hosseinzadeh, & Abnous, 2012;Gunduz, Oltulu, Buldum, Guven, & Ulugol, 2011;Hajhashemi, Hosseinzadeh, & Amin, 2013;Hu et al, 2010;Pottabathini, Kumar, Bhatnagar, Garg, & Ekavali, 2016;Shi, Jiang, & Li, 2016;Ochoa-Aguilar et al, 2017;Eljaja, Bjerrum, Honoré, & Abrahamsen, 2011). However, this compound has been less studied in inflammatory pain (Ochoa-Aguilar et al, 2018;Stepanovic-Petrovic, Micov, Tomic, Kovacevic, & Boškovic, 2014).…”

Section: Introductionmentioning

confidence: 99%

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Antinociceptive effects of ceftriaxone in formalin‐induced nociception

Baeza‐Flores

Rodríguez‐Palma

Reyes‐Pérez

et al. 2020

Drug Development Research

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Ceftriaxone (CFX) is a β‐lactam antibiotic with analgesic properties. However, its role in the formalin‐induced nociception remains unknown. The purpose of this study was to investigate the antinociceptive effect of CFX in the 1% formalin test in rats. Formalin induced a typical nociceptive response (flinching behavior) of two phases. Local peripheral pretreatment (20 min) with CFX (400–800 μg/paw) slightly attenuated the flinching behavior in phase 2, but not phase 1. Acute intraperitoneal pretreatment (20 min) also reduced phase 2 of the formalin test. In both cases, CFX induced a dose‐dependent antinociception. We also tested the effect of CFX 1 day after its administration and in two schedules of repeated administration. One‐day pretreatment with CFX (50–400 mg/kg, ip) induced a dose‐dependent antinociceptive effect in formalin‐treated rats. Repeated administration (daily during 3 or 7 days) with CFX (50–400 mg/kg, ip) diminished formalin‐induced nociception. Results suggest that local or systemic as well as single or repeated administration of CFX reduces formalin‐induced nociception.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Antinociceptive effects of ceftriaxone in formalin‐induced nociception

Baeza‐Flores

Rodríguez‐Palma

Reyes‐Pérez

et al. 2020

Drug Development Research

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“…Ceftriaxone (CFX), a b-lactam antimicrobial molecule (BLM) [Donnelly et al, 2017] has shown antinociceptive effects after repeated administration in NP models [Hu et al, 2010;Gunduz et al, 2011;Hajhashemi et al, 2013;Shi et al, 2016] and can enhance the analgesic effect of nonsteroidal antiinflammatory drugs (NSAIDs) in inflammatory and visceral models [Stepanovic-Petrovic et al, 2014]. CFX also has neuroprotective [Cui et al, 2014] and antiepileptic properties [Uyanikgil et al, 2016], inhibits drug-seeking reinstatement [Sari et al, 2009], and can release DA from the nucleus accumbens [Althobaiti et al, 2016].…”

Section: Introductionmentioning

confidence: 99%

Antiallodynic Activity of Ceftriaxone and Clavulanic Acid in Acute Administration is Associated with Serum TNF‐α Modulation and Activation of Dopaminergic and Opioidergic Systems

Ochoa-Aguilar

Sotomayor-Sobrino

Jaimez

et al. 2017

Drug Development Research

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Preclinical Research The aim of this study was to determine the antiallodynic effect of acute administration of the β-lactam antimicrobials, ceftriaxone (CFX) and clavulanic acid (CLAV), for the control of established pain on a model of neuropathic pain (NP). We also investigated the involvement of dopaminergic and opioidergic pathways as well as alterations in serum concentrations of TNF-α in the antiallodynic actions of these drugs. CFX, CLAV, or gabapentin (GAP), a reference drug, were administered i.p. twelve days after constriction of the sciatic nerve in rats. Mechanic and cold allodynia were evaluated for 3 h and alterations in serum concentration of TNF-α determined. Both CFX and CLAV had antiallodynic effects in response to mechanical and cold stimulation, similar to GAP. The antiallodynic effects of CFX and CLAV were blocked by haloperidol (HAL), a D2 receptor antagonist, and by naloxone (NLX), an opioid receptor antagonist. Additionally, serum TNF-α levels were attenuated following CFX and CLAV administration. These results suggest that acute administration of CFX and CLAV may represent a promising approach for treating the acute allodynia of NP, and that the mechanisms involved in these effects involve activation of dopaminergic and opioidergic pathways as well as modulation of TNF-α production. Drug Dev Res 78 : 105-115, 2017. © 2017 Wiley Periodicals, Inc.

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“…Nerve injury induces changes in the expression of glutamate transporters in the spinal cord and supraspinal brain regions (Gegelashvili & Bjerrum, ; Marcello et al, ; Putatunda, Hala, Chin, & Lepore, ; Sung et al, ; Xin, Weng, & Dougherty, ). Among the five subtypes, GLT1 expression is frequently affected in various animal models of neuropathic pain (Gegelashvili & Bjerrum, ; Marcello et al, ; Putatunda et al, ; Shi, Jiang, & Li, ; Yamamoto et al, ; Yan, Maixner, Li, & Weng, ). Downregulation of GLT1 expression in the spinal dorsal horn is associated with neuropathic pain following chronic constriction of the sciatic nerve and tight ligation of spinal nerves (Gegelashvili & Bjerrum, ; Sung et al, ; Xin et al, ).…”

Section: Introductionmentioning

confidence: 99%

Region‐specific deletions of the glutamate transporter GLT1 differentially affect nerve injury‐induced neuropathic pain in mice

Zhao

Hiraoka

Ogawa

2018

Glia

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Glutamate is a major excitatory neurotransmitter and plays an important role in neuropathic pain, which is frequently caused by nerve damage. According to recent studies, nerve injury induces changes in glutamatergic transmission in the spinal cord and several supraspinal regions, including the periaqueductal gray (PAG). Among glutamate signaling components, accumulating evidence suggests that the glial glutamate transporter GLT1 plays a critical role in neuropathic pain. Indeed, GLT1 expression is reduced in the spinal cord but increased in the PAG after nerve injury, suggesting that the role of GLT1 in neuropathic pain may vary according to the brain region. In this study, we generated PAG-specific and spinal cord-specific GLT1 knockout mice. Nerve injury-induced neuropathic pain was enhanced in spinal cord-specific GLT1 knockout mice but alleviated in PAG-specific GLT1 knockout mice. Thus, nerve injury may enhance glutamatergic neurotransmission from primary sensory neurons to the post-synaptic dorsal horn following downregulation of GLT1 in the spinal cord and result in inadequate descending pain inhibition caused by GLT1 upregulation in the PAG, resulting in neuropathic pain. In addition, ceftriaxone upregulated GLT1 expression in the spinal cord, but not the PAG, of control mice and attenuated tactile hypersensitivity in nerve-injured control mice but not in nerve-injured spinal cord-specific GLT1 knockout mice. Based on these results, the anti-neuropathic pain effect of ceftriaxone is mediated by the upregulation of GLT1 expression in the spinal cord. Thus, selective upregulation of spinal GLT1 and/or downregulation of GLT1 in the PAG represents a potentially novel strategy for the treatment of neuropathic pain.

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Involvement of spinal glutamate transporter-1 in the development of mechanical allodynia and hyperalgesia associated with type 2 diabetes

Cited by 9 publications

References 38 publications

Antinociceptive effects of ceftriaxone in formalin‐induced nociception

Antinociceptive effects of ceftriaxone in formalin‐induced nociception

Antiallodynic Activity of Ceftriaxone and Clavulanic Acid in Acute Administration is Associated with Serum TNF‐α Modulation and Activation of Dopaminergic and Opioidergic Systems

Region‐specific deletions of the glutamate transporter GLT1 differentially affect nerve injury‐induced neuropathic pain in mice

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