<p>Maternal nutrition influences offspring brain development, and omega-3 fatty acids have been linked to neuroprotection. However, their effects on acute responses to traumatic brain injury (TBI) in adult offspring have not been examined. Wistar rat dams (<i>n</i> = 21) received fish oil (0.5&#xa0;g/kg/day), flaxseed oil (0.5&#xa0;g/kg/day), or water by gavage during lactation (postnatal days (PND): 1–21). Adult male offspring (<i>n</i> = 32; 8 per group) underwent diffuse TBI using the modified Marmarou weight-drop model. Electrocorticography (ECoG) was recorded at baseline, 24&#xa0;h, and 72&#xa0;h post-injury. Somatosensory evoked potentials (SSEPs) were measured on day 3, and thalamic tissue was analyzed by immunohistochemistry for NeuN, S100, and GFAP. TBI induced significant prolongation of N2 (<i>p</i> &lt; 0.05) and P3 (<i>p</i> &lt; 0.01) SSEP latencies versus controls, along with significantly reduced thalamic NeuN expression (<i>p</i> &lt; 0.001) and increased S100 (<i>p</i> &lt; 0.01) and GFAP (<i>p</i> &lt; 0.01) immunoreactivity. In the fish oil group, P3 latency was significantly shorter than in TBI (<i>p</i> &lt; 0.05), and NeuN expression was significantly higher (<i>p</i> &lt; 0.05), indicating preserved neuronal integrity. In the flaxseed oil group, GFAP immunoreactivity was significantly lower than in TBI (<i>p</i> &lt; 0.01); however, NeuN did not differ from TBI and was significantly lower than Control (<i>p</i> &lt; 0.05), and S100 was significantly higher than Control (<i>p</i> &lt; 0.05), indicating incomplete normalization. N2 latency did not differ significantly between supplementation groups and TBI. ECoG spectral power analysis revealed no significant intergroup differences across any frequency band (all <i>p</i> &gt; 0.05). These exploratory findings suggest that the two omega-3 sources exerted marker-specific differential effects rather than uniform neuroprotection: maternal fish oil supplementation was associated with preserved thalamic neuronal integrity and shorter late-latency cortical processing time, whereas flaxseed oil was associated with reduced astrocytic GFAP activation. Given the modest sample, and the acute 72-hour observation window, all findings should be regarded as preliminary and hypothesis-generating. Larger, adequately powered, sex-stratified studies with biochemical validation and longer follow-up are needed to confirm these results.</p>

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Maternal Omega-3 Supplementation During Lactation and Acute Electrophysiologic and Thalamic Astroglial Outcomes After Adult Traumatic Brain Injury in Rats

  • H. Fehmi Ozel,
  • Suheda Alpay,
  • Hasan Kazdagli,
  • Hayrunnisa Yesil Sarsmaz,
  • Seren Gülşen Gürgen

摘要

Maternal nutrition influences offspring brain development, and omega-3 fatty acids have been linked to neuroprotection. However, their effects on acute responses to traumatic brain injury (TBI) in adult offspring have not been examined. Wistar rat dams (n = 21) received fish oil (0.5 g/kg/day), flaxseed oil (0.5 g/kg/day), or water by gavage during lactation (postnatal days (PND): 1–21). Adult male offspring (n = 32; 8 per group) underwent diffuse TBI using the modified Marmarou weight-drop model. Electrocorticography (ECoG) was recorded at baseline, 24 h, and 72 h post-injury. Somatosensory evoked potentials (SSEPs) were measured on day 3, and thalamic tissue was analyzed by immunohistochemistry for NeuN, S100, and GFAP. TBI induced significant prolongation of N2 (p < 0.05) and P3 (p < 0.01) SSEP latencies versus controls, along with significantly reduced thalamic NeuN expression (p < 0.001) and increased S100 (p < 0.01) and GFAP (p < 0.01) immunoreactivity. In the fish oil group, P3 latency was significantly shorter than in TBI (p < 0.05), and NeuN expression was significantly higher (p < 0.05), indicating preserved neuronal integrity. In the flaxseed oil group, GFAP immunoreactivity was significantly lower than in TBI (p < 0.01); however, NeuN did not differ from TBI and was significantly lower than Control (p < 0.05), and S100 was significantly higher than Control (p < 0.05), indicating incomplete normalization. N2 latency did not differ significantly between supplementation groups and TBI. ECoG spectral power analysis revealed no significant intergroup differences across any frequency band (all p > 0.05). These exploratory findings suggest that the two omega-3 sources exerted marker-specific differential effects rather than uniform neuroprotection: maternal fish oil supplementation was associated with preserved thalamic neuronal integrity and shorter late-latency cortical processing time, whereas flaxseed oil was associated with reduced astrocytic GFAP activation. Given the modest sample, and the acute 72-hour observation window, all findings should be regarded as preliminary and hypothesis-generating. Larger, adequately powered, sex-stratified studies with biochemical validation and longer follow-up are needed to confirm these results.