Mercury causes disturbances in neurological functions at both the molecular and cellular levels, impacting various regions of the central nervous system and leading to neural dysfunction, which is evident through behavioral changes. This research aimed to assess the neurotoxic effects of mercury (Hg) exposure on wild rodents (Peromyscus spp.) inhabiting areas involved in artisanal mercury mining within the Sierra Gorda Biosphere Reserve in Queretaro, Mexico. Mercury levels were quantified in environmental samples (soil) and the brain tissue of the sampled rodents using atomic absorption spectrophotometry via the cold vapor method. Histopathological assessments of the rodent brains were conducted, focusing on cell enumeration within the dentate gyrus of the hippocampus. We analyzed the expression patterns of four genes linked to three distinct neurotransmitter receptors in the rodent brain tissue using RT-qPCR: the Drd1 gene of the dopaminergic pathway, NR1 and NR2A subunits associated with the NMDA-type ionotropic glutamate receptor, and the γ-3 subunit pertinent to the GABAA receptor. Our findings reveal a significant difference in cerebral mercury concentrations between control and reference groups compared to the rodent cohort near the mining area (p < 0.001). Histological assessments indicated a reduced cellular count within the hippocampal region in rodents with elevated mercury levels (p < 0.001). Furthermore, an inverse correlation was observed between hippocampal cell count and total mercury concentration in the neural tissue, with r = −0.72 (p < 0.05). Notably, gene expression related to the examined receptors remained statistically consistent across all rodent groups. This study highlights the neurotoxic potential of inorganic mercury (Hg2+); wild organisms exposed to this compound exhibit cellular abnormalities within vital central nervous system areas, notably the hippocampus.
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