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Τύπος: Άρθρο σε επιστημονικό περιοδικό
Τίτλος: Mice with decreased number of interneurons exhibit aberrant spontaneous and oscillatory activity in the cortex
Συγγραφέας: [EL] Καλεμάκη, Αικατερίνη[EN] Kalemaki, Aikaterinisemantics logo
[EL] Κωνσταντουδάκη, Ξανθίππη[EN] Konstantoudaki, Xanthippisemantics logo
[EN] Tivodar, Simonasemantics logo
[EL] Σιδηροπούλου, Κυριακή[EN] Sidiropoulou, Kyriakisemantics logo
[EL] Καραγωγέως, Δόμνα[EN] Karagogeos, Domnasemantics logo
Ημερομηνία: 31/10/2018
Περίληψη: GABAergic (g-aminobutyric acid) neurons are inhibitory neurons and protect neural tissue from excessive excitation. Cortical GABAergic neurons play a pivotal role for the generation of synchronized cortical network oscillations. Imbalance between excitatory and inhibitory mechanisms underlies many neuropsychiatric disorders and is correlated with abnormalities in oscillatory activity, especially in the gamma frequency range (30– 80 Hz). We investigated the functional changes in cortical network activity in response to developmentally reduced inhibition in the adult mouse barrel cortex (BC). We used a mouse model that displays 50% fewer cortical interneurons due to the loss of Rac1 protein from Nkx2.1/Cre-expressing cells [Rac1 conditional knockout (cKO) mice], to examine how this developmental loss of cortical interneurons may affect basal synaptic transmission, synaptic plasticity, spontaneous activity, and neuronal oscillations in the adult BC. The decrease in the number of interneurons increased basal synaptic transmission, as examined by recording field excitatory postsynaptic potentials (fEPSPs) from layer II networks in the Rac1 cKO mouse cortex, decreased long-term potentiation (LTP) in response to tetanic stimulation but did not alter the pair-pulse ratio (PPR). Furthermore, under spontaneous recording conditions, Rac1 cKO brain slices exhibit enhanced sensitivity and susceptibility to emergent spontaneous activity. We also find that this developmental decrease in the number of cortical interneurons results in local neuronal networks with alterations in neuronal oscillations, exhibiting decreased power in low frequencies (delta, theta, alpha) and gamma frequency range (30–80 Hz) with an extra aberrant peak in high gamma frequency range (80–150 Hz). Therefore, our data show that disruption in GABAergic inhibition alters synaptic properties and plasticity, while it additionally disrupts the cortical neuronal synchronization in the adult BC.
Γλώσσα: Αγγλικά
Σελίδες: 16
DOI: doi: 10.3389/fncir.2018.00096. eCollection 2018.
EISSN: 1662-5110
Θεματική κατηγορία: [EL] Αναπτυξιακή βιολογία[EN] Developmental Biologysemantics logo
[EL] Νευροεπιστήμες[EN] Neurosciencessemantics logo
Λέξεις-κλειδιά: MGE-derived interneuronsRac1synaptic plasticityneuronal oscillationshigh K+ aCSF
Κάτοχος πνευματικών δικαιωμάτων: © 2018 by the author(s)
Όροι και προϋποθέσεις δικαιωμάτων: This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Διατίθεται ανοιχτά στην τοποθεσία: https://pubmed.ncbi.nlm.nih.gov/30429776/
https://www.frontiersin.org/articles/10.3389/fncir.2018.00096/full
Ηλεκτρονική διεύθυνση του τεκμηρίου στον εκδότη: https://www.frontiersin.org/articles/10.3389/fncir.2018.00096/full
Ηλεκτρονική διεύθυνση περιοδικού: https://www.frontiersin.org/journals/neural-circuits
Τίτλος πηγής δημοσίευσης: Frontiers in Neural Circuits
Τόμος: 12
Σελίδες τεκμηρίου (στην πηγή): Article no 96
Σημειώσεις: This study was co-financed through the Operational Program “Education and Lifelong Learning” of the National Strategic Reference Framework – Research Funding Program (EDBM34) by a grant to DK (10040) from the European Union (European Social Fund-ESF) and Greek National Funds
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