دورية أكاديمية
أعرض في EDS

Investigating Contributions of Canonical Transient Receptor Potential Channel 3 to Hippocampal Hyperexcitability and Seizure-Induced Neuronal Cell Death.

التفاصيل البيبلوغرافية
العنوان: Investigating Contributions of Canonical Transient Receptor Potential Channel 3 to Hippocampal Hyperexcitability and Seizure-Induced Neuronal Cell Death.
المؤلفون: Phelan KD; Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA., Shwe UT; Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA., Wu H; Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA., Zheng F; Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.; Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
المصدر: International journal of molecular sciences [Int J Mol Sci] 2024 Jun 06; Vol. 25 (11). Date of Electronic Publication: 2024 Jun 06.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI, [2000-
مواضيع طبية MeSH: TRPC Cation Channels*/metabolism , TRPC Cation Channels*/genetics , Cell Death* , Pyramidal Cells*/metabolism , Pyramidal Cells*/pathology , Hippocampus*/metabolism , Hippocampus*/pathology , Seizures*/metabolism , Seizures*/pathology, Animals ; Mice ; Status Epilepticus/metabolism ; Status Epilepticus/pathology ; Status Epilepticus/chemically induced ; Male ; Neurons/metabolism ; Pilocarpine ; Long-Term Potentiation ; Mice, Knockout ; Mice, Inbred C57BL ; Neuronal Plasticity
مستخلص: Canonical transient receptor potential channel 3 (TRPC3) is the most abundant TRPC channel in the brain and is highly expressed in all subfields of the hippocampus. Previous studies have suggested that TRPC3 channels may be involved in the hyperexcitability of hippocampal pyramidal neurons and seizures. Genetic ablation of TRPC3 channel expression reduced the intensity of pilocarpine-induced status epilepticus (SE). However, the underlying cellular mechanisms remain unexplored and the contribution of TRPC3 channels to SE-induced neurodegeneration is not determined. In this study, we investigated the contribution of TRPC3 channels to the electrophysiological properties of hippocampal pyramidal neurons and hippocampal synaptic plasticity, and the contribution of TRPC3 channels to seizure-induced neuronal cell death. We found that genetic ablation of TRPC3 expression did not alter basic electrophysiological properties of hippocampal pyramidal neurons and had a complex impact on epileptiform bursting in CA3. However, TRPC3 channels contribute significantly to long-term potentiation in CA1 and SE-induced neurodegeneration. Our results provided further support for therapeutic potential of TRPC3 inhibitors and raised new questions that need to be answered by future studies.
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معلومات مُعتمدة: R01 NS058503 United States NS NINDS NIH HHS; R01 NS126473 United States NS NINDS NIH HHS; NS050381 and NS126473 United States NS NINDS NIH HHS
فهرسة مساهمة: Keywords: FluoroJade staining; TRPC3 global knockout; cell resistance; excitability; paired-pulse facilitation; resting membrane potential; stereology
المشرفين على المادة: 0 (TRPC3 cation channel)
0 (TRPC Cation Channels)
01MI4Q9DI3 (Pilocarpine)
تواريخ الأحداث: Date Created: 20240619 Date Completed: 20240619 Latest Revision: 20240718
رمز التحديث: 20240718
مُعرف محوري في PubMed: PMC11172528
DOI: 10.3390/ijms25116260
PMID: 38892448
قاعدة البيانات: MEDLINE
الوصف
تدمد:1422-0067
DOI:10.3390/ijms25116260