Transkraniyal doğru akım stimülasyonu deneysel Parkinson hastalığı modelinde nöronal eksitotoksisiteyi düzenleyerek motor ve bilişsel işlevleri iyileştirir

Amaç: Bu çalışmada, 6-hidroksidopamin (6-OHDA) Parkinson hastalığı (PH) sıçanlarında erken ve uzun süreli transkraniyal doğru akım stimülasyonunun (tDAS= terapötik etkileri araştırılmıştır. Gereç ve Yöntem: PH hayvanlarında erken ve uzun süreli tDAS uygulamasından sonra (PH lezyonundan 24 saat sonra başlayarak, 1000 mA anodal tDCS, 30 dakika/gün, 13 gün), tDAS'nin motor ve bilişsel fonksiyon davranışları ve glutamaterjik nöron eksitotoksisitesi üzerindeki etkileri Ca2+, glutamat ve NMDAR1 seviyeleri ile belirlendi. Bulgular: 13 günlük tDAS tedavisi lokomotor aktivite, öğrenme ve hafıza benzeri davranışlarda 6-OHDA kaynaklı motor bozuklukları önemli ölçüde azalttığı görüldü. Biyokimyasal olarak, hipokampal nöronal hasara neden olan Ca2+, glutamat ve NMDAR1 seviyelerini de azalttığı gözlendi. Sonuç: Bu sonuçlar, erken ve uzun süreli tDAS'nin nöroprotektif etkiler gösterebileceğini ve 6-OHDA ile indüklenen PH sıçan modelinde motor ve bilişsel bozuklukların artmasını azaltabileceğini göstermektedir. Bununla birlikte, tDAS'ın PH'de glutamaterjik yolak üzerinde etkisi olduğunu ve nöronal eksitotoksisiteyi önlediğini de göstermektedir. Ayrıca, bu preklinik model terapötik tDAS'nin potansiyel kullanımını arttırabilir ve PH veya diğer bozukluklar için tDAS'nin terapötik mekanizmasını daha fazla açıklamak için bir tedavi yöntemi olabilir.

Anahtar Kelimeler:

Öğrenme, lokomotor aktivite, nöroprotektif tedavi, Parkinson hastalığı, transkraniyal doğru akım stimülasyonu

Transcranial direct current stimulation ameliorates motor and cognitive functions by regulating neuronal excitotoxicity in experimental Parkinson’s disease model

Purpose: In the study, the therapeutic effects of early and long-term transcranial direct current stimulation (tDCS) in Parkinson's disease (PD) rats with 6-hydroxydopamine (6-OHDA) lesions of tDCS were investigated. Materials and Methods: After early and prolonged tDCS administration in PD animals (starting 24 hours after PD lesion, 1000 mA anodal tDCS, 30 min/day, 13 days), the effects of tDCS on motor and cognitive function behaviors and glutamatergic neuron excitotoxicity were determined by Ca2+, glutamate, and NMDAR1 levels. Results: We found that the 13-day tDCS intervention significantly reduced 6-OHDA-induced motor deficits in locomotor activity, learning, and memory-like behavior. Biochemically, we showed that it also reduces Ca2+, glutamate, and NMDAR1 levels, which cause hippocampal neuronal damage. Conclusion: These results suggest that early and long-term tDCS may exert neuroprotective effects and reduce the exacerbation of motor and cognitive impairments in a rat model of 6-OHDA-induced PD. However, it also shows that tDCS has an effect on the glutamatergic pathway in PD and prevents neuronal excitotoxicity. Furthermore, this preclinical model may increase the potential use of therapeutic tDCS and serve as a translation platform to further define the therapeutic mechanism of tDCS for PD or other disorders.

Keywords:

Learning, Locomotor Activity, Neuroprotective Treatment, Parkinson, Transcranial Direct Current Stimulation,

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