ArticleThe Eurasian journal of medicine2024
The Expression of Neurodegeneration-Related Genes in the Hippocampus of Hypothyroid Rats Following Long-Term Potentiation.
Article in The Eurasian journal of medicine, 2024. 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
backgroundIn our research, we examined how the induction of long-term potentiation (LTP) in the hippocampus of hypothyroid rats afects the mRNA levels of several proteins involved with neurodegeneration, including Gsk3, Cdk5, Akt1, Mapt, P35 (Anxa), Capn1, Bace1, and Psen2.
methodsWistar-albino rats, consisting of 12 males, were used in the research, and they were separated into 2 groups: control (n=6) and hypothyroidism (n=6). To induce hypothyroidism, propylthiouracil was added to drinking water at a dosage of 20 mg/kg/day. The test stimulus intensity was calculated, basal recordings were acquired, and LTP was induced by administering 100 Hz high-frequency stimulation (HFS) for 1 second with a 5-minute delay when the rats were aged 60 days. The population spike (PS) amplitude and excitatory postsynaptic potential (EPSP) slope were measured in the granule cell layer of the dentate gyrus. Using reverse transcription polymerase chain reaction, the mRNA levels of neurodegenerative genes were assessed in induced hippocampal tissues after the LTP protocol. The free T4 levels in plasma were measured using a plate reader with the commercial ELISA kit.
resultsFollowing HFS, LTP was solely induced in the EPSP slope and PS amplitude in the control group. The impaired LTP response of the hypothyroidism group was accompanied by an increase in Akt1-mRNA expression and a decrease in Gsk3ß expression, whereas the value genes' mRNA expression levels did not difer significantly from those of the control group.
conclusionThe hypothyroidism-related LTP impairment could be caused by a reduction in PI3K/AKT signaling. Further investigation of this path is required to elucidate the pathophysiology of impaired synaptic plasticity in hypothyroidism.
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