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Plasticity of Hippocampal Excitatory-Inhibitory Balance: Missing the Synaptic Control in the Epileptic Brain
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Synaptic plasticity is the capacity generated by experience to modify the neural function and, thereby, adapt our behaviour. Long-term plasticity of glutamatergic and GABAergic transmission occurs in a concerted manner, finely adjusting the excitatory-inhibitory (E/I) balance. Imbalances of E/I function are related to several neurological diseases including epilepsy. Several evidences have demonstrated that astrocytes are able to control the synaptic plasticity, with astrocytes being active partners in synaptic physiology and E/I balance. Here, we revise molecular evidences showing the epileptic stage as an abnormal form of long-term brain plasticity and propose the possible participation of astrocytes to the abnormal increase of glutamatergic and decrease of GABAergic neurotransmission in epileptic networks.
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![Figure 1 Glutamatergic and GABAergic long-term plasticity and tripartite neuronal-astroglial network in normal and epileptic brain. (a) During physiological neuronal activity, coincidence between postsynaptic depolarization and glutamatergic (orange) and GABAergic interneuron (green) simultaneously activated induces increase of synaptic efficacy (i.e., mean amplitude of postsynaptic response) in both glutamatergic [CB1] synapses (LTP) at the same time of a decrease of efficacy of GABAergic transmission (LTD; A). (B) By GABAergic and glutamatergic input integration, the net increase in membrane potential falls below the seizure threshold (ST). (b) During epileptiform neuronal activity, astroglial hyperexcitation through GABAARs, GluRs, and/or eCBsRs activation, which increases the intracellular Ca2+ release of astroglial glutamate, increasing the excitatory neurotransmission while inhibitory transmission remains unchanged (A). (B) In this condition, glutamatergic/GABAergic rate results in an excitatory imbalance, exceeding the seizure threshold.](/paper-figures/f5206e73ffd243729d1c79d5583c2191/plasticity-of-hippocampal-excitatory-inhibitory-balance-missing-the-synaptic-figure-1.jpg)
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“NPTXs could contribute to the long-term E/I imbalance characteristic of epilepsy by altering AMPAR neurotransmission (Bonansco and Fuenzalida 2016; Lopes et al. 2013).”
From Neuronal pentraxins as biomarkers of synaptic activity: from physiological functions to pathological changes in neurodegeneration (2022) · cites this paper as Bonansco and Fuenzalida 2016
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Metadata
- Authors
- Bonansco, C., & Fuenzalida, M.
- Affiliations
- University of Valparaíso (CL)
- Corresponding author
- Bonansco, Christian
- Fuenzalida, Marco
- Venue
- Neural Plasticity
- Publisher
- Wiley
- Published
- 2016
- Volume
- 2016
- Pages
- 1-13
- ISSN
- 1687-5443 (ISSN-L)
- 2090-5904
- PMC
- PMC4783563
- OpenAlex
- W2283621784
- Cited by
- 138
- References
- 168
- Citations by year
- 2026: 10 · 2025: 10 · 2024: 13 · 2023: 23 · 2022: 17 · 2021: 15 · 2020: 20 · 2019: 16 · 2018: 9 · 2017: 4 · 2016: 1
- FWCI
- 1.10
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Neural Plasticity (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Fondo Nacional de Desarrollo Científico y Tecnológico (1130491, 1130614)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Clinical Neurology › Epilepsy research and treatment
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Keywords
- excitation-inhibition balance, synaptic plasticity, epilepsy, astrocytes, long-term plasticity, glutamatergic neurotransmission, GABAergic neurotransmission, epileptic networks, astrocyte-neuron interaction
- MeSH terms
- Animals, Astrocytes, Brain, Epilepsy, gamma-Aminobutyric Acid, Hippocampus, Humans, Synaptic Transmission, Neuronal Plasticity, Synapses, Glutamic Acid
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