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<p>Traumatic brain injury (TBI) induces secondary injury cascades characterized by glutamate-mediated excitotoxicity, oxidative stress, and impaired neurotrophic signaling, particularly within the hippocampus, leading to cognitive dysfunction. transcranial Direct Current Stimulation (tDCS) has emerged as a non-invasive neuromodulatory approach with potential neuroprotective effects; however, its mechanistic impact on glutamatergic pathways, redox balance, and BDNF signaling in TBI remains incompletely understood. This study investigated the therapeutic and prophylactic effects of anodal tDCS on hippocampal neurodegeneration, glutamate receptor expression, oxidative stress parameters, BDNF levels, and cognitive performance in a rat model of diffuse traumatic brain injury. Adult male Wistar rats were assigned to four groups: control, TBI, TBI + tDCS, and tDCS + TBI + tDCS (prophylactic). Diffuse TBI was induced using the Marmarou weight-drop model. Anodal tDCS (1&#xa0;mA, 30&#xa0;min) was applied for three consecutive sessions post-injury, with additional preconditioning in the prophylactic group. Motor function was assessed using the Open Field Test, while cognitive function was assessed using the New Object Recognition Test. Hippocampal histopathology was evaluated by H&amp;E staining. NMDAR1, NMDAR2A, and AMPAR1 expression were analyzed immunohistochemically. MDA, SOD, and BDNF levels were measured by ELISA. TBI significantly impaired recognition memory, increased hippocampal neurodegeneration, elevated NMDAR1/NMDAR2A/AMPAR1 immunoreactivity, increased MDA levels, decreased SOD activity, and reduced BDNF levels compared to controls (<i>p</i> &lt; 0.05). Anodal tDCS significantly improved cognitive performance, reduced excitotoxic receptor expression, attenuated lipid peroxidation, restored antioxidant activity, and increased BDNF levels (<i>p</i> &lt; 0.05 vs. TBI). The prophylactic stimulation paradigm demonstrated protective effects relative to post-traumatic stimulation alone. Anodal tDCS mitigates hippocampal neurodegeneration and cognitive dysfunction following TBI through multi-level modulation of excitotoxic, oxidative, and neurotrophic pathways. These findings support the translational potential of tDCS as a non-invasive therapeutic strategy targeting secondary injury mechanisms in traumatic brain injury.</p>

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Anodal tDCS attenuates hippocampal neurodegeneration and cognitive deficits after traumatic brain injury via glutamatergic and redox modulation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月9日

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  • Guven Akcay,
  • Esra Balcioglu,
  • Recep Baydemir,
  • Betul Yalcın,
  • Cagla Celik

摘要

Traumatic brain injury (TBI) induces secondary injury cascades characterized by glutamate-mediated excitotoxicity, oxidative stress, and impaired neurotrophic signaling, particularly within the hippocampus, leading to cognitive dysfunction. transcranial Direct Current Stimulation (tDCS) has emerged as a non-invasive neuromodulatory approach with potential neuroprotective effects; however, its mechanistic impact on glutamatergic pathways, redox balance, and BDNF signaling in TBI remains incompletely understood. This study investigated the therapeutic and prophylactic effects of anodal tDCS on hippocampal neurodegeneration, glutamate receptor expression, oxidative stress parameters, BDNF levels, and cognitive performance in a rat model of diffuse traumatic brain injury. Adult male Wistar rats were assigned to four groups: control, TBI, TBI + tDCS, and tDCS + TBI + tDCS (prophylactic). Diffuse TBI was induced using the Marmarou weight-drop model. Anodal tDCS (1 mA, 30 min) was applied for three consecutive sessions post-injury, with additional preconditioning in the prophylactic group. Motor function was assessed using the Open Field Test, while cognitive function was assessed using the New Object Recognition Test. Hippocampal histopathology was evaluated by H&E staining. NMDAR1, NMDAR2A, and AMPAR1 expression were analyzed immunohistochemically. MDA, SOD, and BDNF levels were measured by ELISA. TBI significantly impaired recognition memory, increased hippocampal neurodegeneration, elevated NMDAR1/NMDAR2A/AMPAR1 immunoreactivity, increased MDA levels, decreased SOD activity, and reduced BDNF levels compared to controls (p < 0.05). Anodal tDCS significantly improved cognitive performance, reduced excitotoxic receptor expression, attenuated lipid peroxidation, restored antioxidant activity, and increased BDNF levels (p < 0.05 vs. TBI). The prophylactic stimulation paradigm demonstrated protective effects relative to post-traumatic stimulation alone. Anodal tDCS mitigates hippocampal neurodegeneration and cognitive dysfunction following TBI through multi-level modulation of excitotoxic, oxidative, and neurotrophic pathways. These findings support the translational potential of tDCS as a non-invasive therapeutic strategy targeting secondary injury mechanisms in traumatic brain injury.