Publication details

Chemokine CCL2 and its receptor CCR2 in the anterior cingulate cortex after spinal cord contusion

Authors

SVOBODOVÁ Viktorie BRETOVÁ Karolína BAGÓ MAS Anna BOADAS-VAELLO Pere DUBOVÝ Petr

Year of publication 2022
Type Conference abstract
MU Faculty or unit

Faculty of Medicine

Citation
Description The anterior cingulate cortex (ACC) is involved in the regulation of emotional and affective components of neuropathic pain. Activation of the ACC neurons plays a role in pain and fear-related aversive behavior, while inhibition results in analgetic effects. The signal processing in ACC is influenced by pyramidal neurons localized mainly in Layer V and integrating information from different brain areas. Due to the involvement of CCL2/CCR2 in neuronal signal transduction, the study was focused on the distribution of CCL2/CCR2 in the ACC neurons after spinal cord injury (SCI). Female adult CD1 Swiss mice underwent dorsal laminectomy at T8-T9 followed by spinal cord contusion using Weight drop apparatus. Two groups of mice, naive and sham-operated, were used as controls. The operated mice were left to survive for 10 weeks after the operation. Coronal cryostat sections of ACC were cut and immunostained for CCL2/CCR2 detection under the same conditions. The intensities of CCL2/CCR2 immunofluorescence (IF) were measured by image analysis and statistically evaluated. CCL2-IF was found in small and pyramidal neurons of Layer II/III and V, while CCR2-IF was presented only in pyramidal neurons of ACC in all animal groups. CCL2-IF was increased in both small and pyramidal neurons of ACC after SCI compared to naive control. There was no significant difference of CCL2-IF in pyramidal neurons when compared sham with naive controls, but significant increase was detected in small neurons. CCR2-IF was decreased in pyramidal neurons of sham control compared to naive, but with a significant increase after SCI compared to sham controls. These results suggested a role of CCL2/CCR2 in ACC neuronal activation after SCI inducing affective components of neuropathic pain.
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