ArticleProceedings of the National Academy of Sciences of the United States of America2014
Postsynaptic activity reverses the sign of the acetylcholine-induced long-term plasticity of GABAA inhibition.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Cholinergic Signaling, Neural Excitability, and Epilepsy.Molecules (Basel, Switzerland) · 2021Review
- The Theta Rhythm of the Hippocampus: From Neuronal and Circuit Mechanisms to Behavior.Frontiers in cellular neuroscience · 2021Article
- Neuromodulation of hippocampal long-term synaptic plasticity.Current opinion in neurobiology · 2019Review
- Molecular, Cellular and Circuit Basis of Cholinergic Modulation of Pain.Neuroscience · 2018Review
- Article
- Bidirectional Hebbian Plasticity Induced by Low-Frequency Stimulation in Basal Dendrites of Rat Barrel Cortex Layer 5 Pyramidal Neurons.Frontiers in cellular neuroscience · 2017Article
- Neuromodulation of the Feedforward Dentate Gyrus-CA3 Microcircuit.Frontiers in synaptic neuroscience · 2016Review
- Muscarinic Long-Term Enhancement of Tonic and Phasic GABAFrontiers in cellular neuroscience · 2016Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acetylcholine (ACh) regulates forms of plasticity that control cognitive functions but the underlying mechanisms remain largely unknown. ACh controls the intrinsic excitability, as well as the synaptic excitation and inhibition of CA1 hippocampal pyramidal cells (PCs), cells known to participate in circuits involved in cognition and spatial navigation. However, how ACh regulates inhibition in function of postsynaptic activity has not been well studied. Here we show that in rat PCs, a brief pulse of ACh or a brief stimulation of cholinergic septal fibers combined with repeated depolarization induces strong long-term enhancement of GABAA inhibition (GABAA-LTP). Indeed, this enhanced inhibition is due to the increased activation of α5βγ2 subunit-containing GABAA receptors by the GABA released. GABAA-LTP requires the activation of M1-muscarinic receptors and an increase in cytosolic Ca(2+). In the absence of PC depolarization ACh triggered a presynaptic depolarization-induced suppression of inhibition (DSI), revealing that postsynaptic activity gates the effects of ACh from presynaptic DSI to postsynaptic LTP. These results provide key insights into mechanisms potentially linked with cognitive functions, spatial navigation, and the homeostatic control of abnormal hyperexcitable states.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.