Abstract

Depression is commonly observed in patients with chronic pain. Pain can be divided into a sensitive and emotional component processed by different neural circuitries; the emotional component is largely modulated by the structures within the limbic system. The consolidation of pain-related aversive behaviours is attributed to the anterior cingulated cortex, where it has been showed that decreased glial cell density is associated with the development of depressive-like behaviour in stressed animals. Our aim was to investigate the possibility of an association between alterations in cell density in the prefrontal cortex (PFC) and depressive-like behaviour in neuropathic rats. One and two months after inducing spared nerve injury (SNI), neuropathic animals were tested for the presence of depressive-like behaviour (forced-swimming test) and evaluation of locomotor activity (open field test). Stereological analysis of the PFC considered three major areas, the cingulated I (CgI), the pre-limbic (PrL) and the infralimbic (IL) cortices, which were subdivided in three cortical areas, for quantification. The development of depressive-like behaviour was paralleled by a decrease in the number of glial cells in layer II (external granular layer) of the CgI, PrL and IL. Moreover there was a specific decrease in neurone numbers in IL layer II. These data indicate that alterations of glial and neuronal cell content in the PFC contribute to the development of depressive-like behaviour.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.