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

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

Rok publikování 2022
Druh Konferenční abstrakty
Fakulta / Pracoviště MU

Lékařská fakulta

Citace
Popis 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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