Neuropathic pain (NP) arises from nerve damage or compression and often extends to the contralateral side of the body (mirror-image pain, MP) and adjacent non-injured areas (extraterritorial pain). This study investigates whether altered sensitivity in these contralateral and peripheral regions is mediated by glial cells, using the chronic constriction injury (CCI) model of NP. Thirty-two male Wistar rats were randomly assigned into four groups (8/group): sham, CCI + vehicle, CCI + minocycline (MIN;10 mg/kg), and CCI + pentoxifylline (PTX;8 mg/kg). The CCI model was employed for NP induction. MIN and PTX were administered intraperitoneally from postoperative days (POD)4 to POD14, once daily. Pain responses were assessed on POD0, 2, 6, 10, and14 using Hargreaves, von Frey, and Tail-flick tests. Western blot analysis was performed on POD14 to measure Iba1 and GFAP protein expression in the spinal cord hemispheres. Results revealed that post-injury treatment with MIN and PTX significantly reduced contralateral thermal hyperalgesia, mechanical allodynia, and tail-flick responses. Correspondingly, the contralateral spinal cord exhibited significantly decreased GFAP and Iba1 protein expression compared to the CCI + vehicle treated group. These findings suggest that post-injury glial cell inhibition effectively mitigates neuropathic pain and prevents the development of MP and extraterritorial pain. This highlights the potential for clinical applications targeting glial cells to manage NP even after nerve injury.