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Remodelling of supraspinal neuroglial network in neuropathic pain is featured by a reactive gliosis of the nociceptive amygdala
Author(s) -
Marcello L.,
Cavaliere C.,
Colangelo A.M.,
Bianco M.R.,
Cirillo G.,
Alberghina L.,
Papa M.
Publication year - 2013
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1002/j.1532-2149.2012.00255.x
Subject(s) - sni , neuropathic pain , neuroscience , periaqueductal gray , glial fibrillary acidic protein , glutamatergic , gliosis , glutamate receptor , amygdala , medicine , biology , pathology , central nervous system , immunohistochemistry , midbrain , biochemistry , receptor , hydrolysis , acid hydrolysis
Background Many brain areas participate to supraspinal control of nociception. In these regions, few studies have investigated the role of glial cells in supraspinal plasticity and the effect of 7‐day intrathecal nerve growth factor‐like ( BB14 ®, Blueprint Biotech, Milano, Italy) treatment. Methods In male S prague‐ D awley rats, we evaluated by immunohistochemistry the morphological and molecular rearrangement of neuroglial network occurring in several supraspinal brain regions involved in pain processing following spared nerve injury ( SNI ) of the sciatic nerve. In particular, the medial prefrontal cortex, the amygdala ( A my), the nucleus accumbens ( A cb), the thalamus and the periaqueductal gray were analysed. Results Despite the modifications occurring in the dorsal horn of spinal cord following SNI , no significant changes in the I ba1 and glial fibrillary acidic protein ( GFAP ) expression were detected in all the analysed supraspinal regions, except for the A my, showing a remarkable GFAP increase. Interestingly, neuropathic rats also displayed a significant increase of glial transporters ( GTs ) in all the supraspinal regions. Finally, the analysis of vesicular glutamate transporter 1 ( vGLUT1 ) and vesicular gamma‐aminobutyric acid (GABA) transporter (vGAT) expression revealed a significant enhancement of glutamatergic/ GABA ergic ratio in all selected brain regions of SNI animals, except for A cb. Both glial activation in the A my and alteration of GTs and vGLUT/vGAT levels observed in neuropathic animals were largely reversed by BB14 ® treatment. Conclusions All together, these data strengthen the role of supraspinal neuroglial network plasticity in the establishment of neuropathic pain syndrome. The hallmark is represented by the divergence between glial reaction confined to A my and the widespread changes in the GT distribution and glutamate/ GABA ratio detected in the other supraspinal region.