ArticleNeurochemical research2025
The Role of Insular Cortex and Prefrontal Cortex in the Pathogenesis of Fibromyalgia: Biochemical and Electrophysiological Rodent Study.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Neuroimaging implicates the medial prefrontal cortex (mPFC) and insula in fibromyalgia (FM), but synaptic and network mechanisms are unclear. To verify mPFC hypersynapticity in a reserpine-induced FM model and test whether anterior insular deep brain stimulation (DBS) restores mPFC oscillations and pain behavior. Thirty-six male Sprague-Dawley rats received reserpine (1 mg·kg⁻¹ i.p., days 1-3) or vehicle. For Objective 1, mPFC tissue was analyzed by ELISA for glutamate, γ-aminobutyric acid (GABA), C-FOS, nerve growth factor (NGF), synaptophysin, and postsynaptic density protein-95 (PSD-95). For Objective 2, rats were assigned to control-sham, control-DBS, FM-sham, or FM-DBS. Monopolar DBS (130 Hz, 60 µs, 100 µA; 15 min·day⁻¹ for 3 days) targeted the anterior insula; local field potentials were recorded from mPFC, and thermal nociception was assessed by tail immersion and hot-plate tests. Reserpine increased glutamate, C-FOS, NGF, synaptophysin, and PSD-95 and reduced GABA (all p < 0.001), confirming hypersynapticity. Insular DBS increased delta-band normalized ratios (NR) in FM and controls (p < 0.0001), normalized FM-associated theta reductions, decreased alpha/beta NR in controls, and suppressed elevated gamma NR in FM (p < 0.0001). DBS increased withdrawal latencies in FM, indicating improved pain thresholds (p < 0.001). Reserpine induces biochemical hypersynapticity in mPFC, and brief anterior insular DBS rebalances mPFC oscillations and alleviates hyperalgesia. Insular DBS may correct cortical network dysfunction in FM.
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