Introduction
Neuropathic pain is often chronic and hard to treat: its prevalence is 7 to 8% in the general population and higher in patients with chronic post-surgical pain (CPSP). There’s a growing interest toward glial cells, which may also contribute to chronic pain. Understanding their role and physiology could lead to new drugs development and better outcome for the patients.
Microglia is the central nervous system (CNS) macrophage: it modulates the neural environment and is involved in neuro-inflammation. In case of peripheral neural lesion, microglial cells at the corresponding spinal cord levels are activated. This phenomenon is related to membrane current changes, potassium currents among others. Thus, we chose to study the microglial potassium channels in order to better understand this process. We focused on Kv1.3, Kv1.5 and KIR2.1.
Material and method
We worked with spared nerve injury (SNI) model in CX3CR1 – Green fluorescent protein (GFP) mutated mice. The animals were sacrificed at different timings after surgery. We used spinal cord complete tissues from L3-L4-L5 levels and studied them with 2 different technics. First we used immunofluorescence to locate the channels at the microglial membrane. Secondly, we used Western-Blot to quantify the potassium channel expression prior to and after microglial activation.
Results
SNI induces a strong microglial proliferation in the spinal cord. The immunofluorescence shows that Kv1.3 is localized on microglial cells. The same occurs for KIR2.1 in a lesser way, but not for Kv1.5. A strong unspecific background signal prevented us from quantifying the channel expression. The Western Blot couldn’t be interpreted due to unspecific signal. Further experiments need to be done to find the right conditions to analyze the channels expression in a quantitative way.