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  1. Fulltext Effect of radio-frequency electromagnetic radiations (RF-EMR) on passive avoidance behaviour and hippocampal morphology in Wistar rats
    Narayanan SN, Kumar RS, Potu BK, Nayak S, Bhat PG, Mailankot M
    Ups. J. Med. Sci., 2010 May;115(2):91-6.
    PMID: 20095879 DOI: 10.3109/03009730903552661
    The interaction of mobile phone radio-frequency electromagnetic radiation (RF-EMR) with the brain is a serious concern of our society.
    Matched MeSH terms: Avoidance Learning/radiation effects*
  2. Fulltext Possible effects of radiofrequency electromagnetic radiation on contextual fear conditioning, hippocampal perivascular space, apoptosis and adrenal gland microarchitecture in rats
    Narayanan SN, Kumar RS, Kumar N, Prabhakar P, Nayak SB, Bhat PG
    Behav Brain Res, 2025 Mar 12;481:115424.
    PMID: 39788457 DOI: 10.1016/j.bbr.2025.115424
    Whilst the world sees the tremendous growth of mobile phone technology, radiofrequency electromagnetic radiation (RF-EMR) induced possible health effects have emerged as a topic of recent day debate. The current study is designed to test the hypothesis that chronic 900 MHz radiation exposure would potentially dysregulate the stress response system (HPA axis) in vivo, via, its non-thermal mechanisms, leading to alterations in the microarchitecture of the adrenal gland, vulnerable brain regions such as the hippocampus which may results in altered behaviours in rats. Male albino Wistar rats aged four weeks, weighing 50-60 g were subjected to 900 MHz radiation from a mobile phone for four weeks at a rate of one hour per day. On the 29th day, animals from the control, sham exposed and RF-EMR exposed groups were tested for contextual fear conditioning. They were later euthanized to study hippocampal and adrenal gland cytoarchitecture. Bright and dark compartment transitions in the avoidance box were considerably elevated in the RF-EMR exposed group and they exhibited a significant decrease in the latency to enter the dark compartment during the contextual fear conditioning test. Apoptosis was apparent in the CA3 region and perivascular space was significantly increased in the hippocampus of the radiation-exposed group. In addition to lymphocytic infiltrates, congested sinusoids, apoptotic-like changes were evident in the zona fasciculata of the adrenal gland. However, the cytoarchitecture of the adrenal medulla was comparable in all three groups. Chronic RF-EMR exposure caused changes in contextual fear conditioning, enlargement of hippocampal perivascular space, apparent CA3 apoptosis, and apoptotic-like changes in the zona fasciculata of the adrenal gland in rats.
    Matched MeSH terms: Avoidance Learning/radiation effects
  3. Light-Emitting Diode (LED) Therapy Attenuates Neurotoxicity of Methanol-Induced Memory Impairment and Apoptosis in The Hippocampus
    Ghanbari A, Zibara K, Salari S, Ghareghani M, Rad P, Mohamed W, et al.
    CNS Neurol Disord Drug Targets, 2018;17(7):528-538.
    PMID: 29968547 DOI: 10.2174/1871527317666180703111643
    BACKGROUND & OBJECTIVE: The adolescent brain has a higher vulnerability to alcoholinduced neurotoxicity, compared to adult's brain. Most studies have investigated the effect of ethanol consumption on the body, however, methanol consumption, which peaked in the last years, is still poorly explored.

    METHOD: In this study, we investigated the effects of methanol neurotoxicity on memory function and pathological outcomes in the hippocampus of adolescent rats and examined the efficacy of Light- Emitting Diode (LED) therapy. Methanol induced neurotoxic rats showed a significant decrease in the latency period, in comparison to controls, which was significantly improved in LED treated rats at 7, 14 and 28 days, indicating recovery of memory function. In addition, methanol neurotoxicity in hippocampus caused a significant increase in cell death (caspase3+ cells) and cell edema at 7 and 28 days, which were significantly decreased by LED therapy. Furthermore, the number of glial fibrillary acid protein astrocytes was significantly lower in methanol rats, compared to controls, whereas LED treatment caused their significant increase. Finally, methanol neurotoxicity caused a significant decrease in the number of brain-derived neurotrophic factor (BDNF+) cells, but also circulating serum BDNF, at 7 and 28 days, compared to controls, which were significantly increased by LED therapy. Importantly, LED significantly increased the number of Ki-67+ cells and BDNF levels in the serum and hypothalamus in control-LED rats, compared to controls without LED therapy.

    CONCLUSION: In conclusion, chronic methanol administration caused severe memory impairments and several pathological outcomes in the hippocampus of adolescent rats which were improved by LED therapy.

    Matched MeSH terms: Avoidance Learning/radiation effects
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