التفاصيل البيبلوغرافية
| العنوان: |
P2Y1 receptor inhibition rescues impaired synaptic plasticity and astroglial Ca2+-dependent activity in the epileptic hippocampus |
| المؤلفون: |
Christian Bonansco, Marco Fuenzalida, Felipe Guiffa, Andrés Martorell, Mario Wellmann |
| المصدر: |
Neurobiology of Disease, Vol 146, Iss, Pp 105132-(2020) |
| بيانات النشر: |
Elsevier, 2020. |
| سنة النشر: |
2020 |
| مصطلحات موضوعية: |
0301 basic medicine, Gliotransmission, Gliotransmitter, Hippocampus, Synaptic plasticity, lcsh:RC321-571, 03 medical and health sciences, chemistry.chemical_compound, Epilepsy, 0302 clinical medicine, medicine, Calcium Signaling, Cognitive decline, Neurotransmitter, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, musculoskeletal, neural, and ocular physiology, Long-term potentiation, medicine.disease, 030104 developmental biology, medicine.anatomical_structure, Neurology, chemistry, nervous system, Astrocytes, Neuroglia, Purinergic receptors, Neuroscience, 030217 neurology & neurosurgery |
| الوصف: |
Indexación Scopus Epilepsy is characterized by a progressive predisposition to suffer seizures due to neuronal hyperexcitability, and one of its most common co-morbidities is cognitive decline. In animal models of chronic epilepsy, such as kindling, electrically induced seizures impair long-term potentiation (LTP), deteriorating learning and memory performance. Astrocytes are known to actively modulate synaptic plasticity and neuronal excitability through Ca2+-dependent gliotransmitter release. It is unclear, however, if astroglial Ca2+ signaling could contribute to the development of synaptic plasticity alterations in the epileptic hippocampus. By employing electrophysiological tools and Ca2+ imaging, we found that glutamatergic CA3-CA1 synapses from kindled rats exhibit an impairment in theta burst (TBS) and high frequency stimulation (HFS)-induced LTP, which is accompanied by an increased probability of neurotransmitter release (Pr) and an abnormal pattern of astroglial Ca2+-dependent transients. Both the impairment in LTP and the Pr were reversed by inhibiting purinergic P2Y1 receptors (P2Y1R) with the specific antagonist MRS2179, which also restored the spontaneous and TBS-induced pattern of astroglial Ca2+-dependent signals. Two consecutive, spaced TBS protocols also failed to induce LTP in the kindled group, however, this impairment was reversed and a strong LTP was induced when the second TBS was applied in the presence of MRS2179, suggesting that the mechanisms underlying the alterations in TBS-induced LTP are likely associated with an aberrant modulation of the induction threshold for LTP. Altogether, these results indicate that P2Y1R inhibition rescues both the pattern of astroglial Ca2+-activity and the plastic properties of CA3-CA1 synapses in the epileptic hippocampus, suggesting that astrocytes might take part in the mechanisms that deteriorate synaptic plasticity and thus cause cognitive decline in epileptic patients. © 2020 https://www-sciencedirect-com.recursosbiblioteca.unab.cl/science/article/pii/S0969996120304071?via%3Dihub |
| وصف الملف: |
application/pdf |
| اللغة: |
English |
| تدمد: |
0969-9961 |
| URL الوصول: |
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::84f29e56902796208db74f4cc5279e79
http://www.sciencedirect.com/science/article/pii/S0969996120304071 |
| حقوق: |
OPEN |
| رقم الأكسشن: |
edsair.doi.dedup.....84f29e56902796208db74f4cc5279e79 |
| قاعدة البيانات: |
OpenAIRE |
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