scholarly journals Peer Review #2 of "Astrocyte activation in the anterior cingulate cortex and altered glutamatergic gene expression during paclitaxel-induced neuropathic pain in mice (v0.2)"

2015 ◽  
Author(s):  
M Sangu
Keyword(s):  
Gene Expression ◽  
Neuropathic Pain ◽  
Anterior Cingulate Cortex ◽  
Peer Review ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Astrocyte Activation

scholarly journals Astrocyte activation in the anterior cingulate cortex and altered glutamatergic gene expression during paclitaxel-induced neuropathic pain in mice

PeerJ ◽  
2015 ◽  
Vol 3 ◽  
pp. e1350 ◽  
Author(s):  
Willias Masocha
Keyword(s):  
Gene Expression ◽  
Neuropathic Pain ◽  
Anterior Cingulate Cortex ◽  
Glutamate Receptor ◽  
Pain Perception ◽  
Thermal Hyperalgesia ◽  
Cingulate Cortex ◽  
Glutamate Transporters ◽  
Anterior Cingulate ◽  
Astrocyte Activation

Spinal astrocyte activation contributes to the pathogenesis of paclitaxel-induced neuropathic pain (PINP) in animal models. We examined glial fibrillary acidic protein (GFAP; an astrocyte marker) immunoreactivity and gene expression of GFAP, glutamate transporters and receptor subunits by real time PCR in the anterior cingulate cortex (ACC) at 7 days post first administration of paclitaxel, a time point when mice had developed thermal hyperalgesia. The ACC, an area in the brain involved in pain perception and modulation, was chosen because changes in this area might contribute to the pathophysiology of PINP. GFAP transcripts levels were elevated by more than fivefold and GFAP immunoreactivity increased in the ACC of paclitaxel-treated mice. The 6 glutamate transporters (GLAST, GLT-1 EAAC1, EAAT4, VGLUT-1 and VGLUT-2) quantified were not significantly altered by paclitaxel treatment. Of the 12 ionotropic glutamate receptor subunits transcripts analysed 6 (GLuA1, GLuA3, GLuK2, GLuK3, GLuK5 and GLuN1) were significantly up-regulated, whereas GLuA2, GLuK1, GLuK4, GLuN2A and GLuN2B were not significantly altered and GLuA4 was lowly expressed. Amongst the 8 metabotropic receptor subunits analysed only mGLuR8 was significantly elevated. In conclusion, during PINP there is astrocyte activation, with no change in glutamate transporter expression and differential up-regulation of glutamate receptor subunits in the ACC. Thus, targeting astrocyte activation and the glutamatergic system might be another therapeutic avenue for management of PINP.

scholarly journals Astrocyte activation in the anterior cingulate cortex and altered glutamatergic gene expression during paclitaxel-induced neuropathic pain in mice

2015 ◽  
Author(s):  
Willias Masocha
Keyword(s):  
Gene Expression ◽  
Neuropathic Pain ◽  
Anterior Cingulate Cortex ◽  
Glutamate Receptor ◽  
Pain Perception ◽  
Thermal Hyperalgesia ◽  
Cingulate Cortex ◽  
Glutamate Transporters ◽  
Anterior Cingulate ◽  
Astrocyte Activation

Spinal astrocyte activation contributes to the pathogenesis of paclitaxel-induced neuropathic pain (PINP) in animal models. We examined gene expression of glial fibrillary acidic protein (GFAP; an astrocyte marker), glutamate transporters and receptor subunits in the anterior cingulate cortex (ACC) by real time PCR at 7 days post first administration of paclitaxel, a time point when mice had developed thermal hyperalgesia. Changes in the ACC, an area in the brain involved in pain perception and modulation, might contribute to the pathophysiology of PINP. GFAP transcripts levels were elevated by more than fivefold in the ACC of paclitaxel-treated mice. The 6 glutamate transporters (GLAST, GLT-1 EAAC1, EAAT4, VGLUT-1 and VGLUT-2) quantified were not significantly altered by paclitaxel treatment. Of the 12 ionotropic glutamate receptor subunits transcripts analysed 6 (GLuA1, GLuA3, GLuK2, GLuK3, GLuK5 and GLuN1) were significantly up-regulated, whereas GLuA2, GLuK1, GLuK4, GLuN2A and GLuN2B were not significantly altered and GLuA4 was lowly expressed. Amongst the 8 metabotropic receptor subunits analysed only mGLuR 8 was significantly elevated. In conclusion, during PINP there is astrocyte activation, no change in glutamate transporter expression and differential up-regulation of glutamate receptor subunits in the ACC. Thus, targeting astrocyte activation and the glutamatergic system might be another therapeutic avenue for management of PINP.

scholarly journals Astrocyte activation in the anterior cingulate cortex and altered glutamatergic gene expression during paclitaxel-induced neuropathic pain in mice

2015 ◽  
Author(s):  
Willias Masocha
Keyword(s):  
Gene Expression ◽  
Neuropathic Pain ◽  
Anterior Cingulate Cortex ◽  
Glutamate Receptor ◽  
Pain Perception ◽  
Thermal Hyperalgesia ◽  
Cingulate Cortex ◽  
Glutamate Transporters ◽  
Anterior Cingulate ◽  
Astrocyte Activation

Spinal astrocyte activation contributes to the pathogenesis of paclitaxel-induced neuropathic pain (PINP) in animal models. We examined glial fibrillary acidic protein (GFAP; an astrocyte marker) immunoreactivity and gene expression of GFAP, glutamate transporters and receptor subunits by real time PCR in the anterior cingulate cortex (ACC) at 7 days post first administration of paclitaxel, a time point when mice had developed thermal hyperalgesia. The ACC, an area in the brain involved in pain perception and modulation, was chosen because changes in this area might contribute to the pathophysiology of PINP. GFAP transcripts levels were elevated by more than fivefold and GFAP immunoreactivity increased in the ACC of paclitaxel-treated mice. The 6 glutamate transporters (GLAST, GLT-1 EAAC1, EAAT4, VGLUT-1 and VGLUT-2) quantified were not significantly altered by paclitaxel treatment. Of the 12 ionotropic glutamate receptor subunits transcripts analysed 6 (GLuA1, GLuA3, GLuK2, GLuK3, GLuK5 and GLuN1) were significantly up-regulated, whereas GLuA2, GLuK1, GLuK4, GLuN2A and GLuN2B were not significantly altered and GLuA4 was lowly expressed. Amongst the 8 metabotropic receptor subunits analysed only mGLuR8 was significantly elevated. In conclusion, during PINP there is astrocyte activation, no change in glutamate transporter expression and differential up-regulation of glutamate receptor subunits in the ACC. Thus, targeting astrocyte activation and the glutamatergic system might be another therapeutic avenue for management of PINP.

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