Chronic neuropathic pain (NP) is a highly prevalent and debilitating neurological condition. On the cellular level, the elevated pain sensitivity is induced by aberrant neuronal plasticity at all stages of the nociceptive pathway. Whereas a lot is known about the mechanisms mediating NP in the peripheral nervous system and in the spinal cord, less is known about these processes in brain areas where pain is eventually perceived.
The Anterior Cingulate Cortex (ACC) is a key area of the nociceptive system, is essential for encoding pain affect and is hyperactive in patients suffering from chronic pain. Also, synaptic and cellular modifications in ACC neurons are necessary for the expression of nociceptive sensitization in animal models of NP.
Recent data suggest that abnormal recruitment of basal ganglia (BG) structures may facilitate the persistence of pain. In this context, we speculate that abnormal nociceptive processing during NP could spread to the BG through aberrant neuronal plasticity in cortico-striatal (CO-ST) neurons of the ACC. However, little is known on how NP affects these neurons.
To gain insight on this, we evaluated the synaptic and cellular modification in CO-ST ACC neurons associated with NP. To do this we combined neuronal identification with fluorescent retrograde tracers and ex-vivo electrophysiological recording (brain slices) in a rodent model of NP. Our preliminary data shows that NP impairs the integration of synaptic inputs into CO-ST ACC neurons.