Acetylcholine prioritises direct synaptic inputs from entorhinal cortex to CA1 by differential modulation of feedforward inhibitory circuits
Autor: | Jack R. Mellor, Benjamin G. Tehan, Miles Congreve, Alastair J. H. Brown, Pradeep J. Nathan, Matt Udakis, Giles Albert Brown, Jon Palacios-Filardo |
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Přispěvatelé: | Mellor, Jack R [0000-0002-7706-8105], Apollo - University of Cambridge Repository, Mellor, Jack R. [0000-0002-7706-8105] |
Rok vydání: | 2021 |
Předmět: |
Male
Patch-Clamp Techniques hippocampus General Physics and Astronomy Hippocampus CA3 Hippocampal formation Synaptic Transmission CA1 0302 clinical medicine Muscarinic acetylcholine receptor Entorhinal Cortex Feedback Physiological Mice Knockout 0303 health sciences Multidisciplinary 631/378/87 Chemistry 631/378/3920 musculoskeletal neural and ocular physiology Pyramidal Cells 9/74 article Excitatory postsynaptic potential 631/378 Acetylcholine medicine.drug Science Sensory system Biology Cholinergic Agonists Inhibitory postsynaptic potential Neural circuits General Biochemistry Genetics and Molecular Biology 03 medical and health sciences Interneurons medicine Animals Author Correction CA1 Region Hippocampal 631/378/548 030304 developmental biology Receptor Muscarinic M3 entorhinal cortex Excitatory Postsynaptic Potentials General Chemistry Entorhinal cortex Cellular neuroscience acetylcholine Mice Inbred C57BL nervous system Synaptic plasticity Carbachol Neuroscience 030217 neurology & neurosurgery |
Zdroj: | Palacios-Filardo, J, Udakis, M, Mellor, J R & al., E 2021, ' Acetylcholine prioritises direct synaptic inputs from entorhinal cortex to CA1 by differential modulation of feedforward inhibitory circuits ', Nature Communications, vol. 12, no. 1, 5475 . https://doi.org/10.1038/s41467-021-25280-5 Nature Communications Nature Communications, Vol 12, Iss 1, Pp 1-16 (2021) |
Popis: | Funder: Biotechnology and Biological Sciences Research Council Acetylcholine release in the hippocampus plays a central role in the formation of new memory representations. An influential but largely untested theory proposes that memory formation requires acetylcholine to enhance responses in CA1 to new sensory information from entorhinal cortex whilst depressing inputs from previously encoded representations in CA3. Here, we show that excitatory inputs from entorhinal cortex and CA3 are depressed equally by synaptic release of acetylcholine in CA1. However, feedforward inhibition from entorhinal cortex exhibits greater depression than CA3 resulting in a selective enhancement of excitatory-inhibitory balance and CA1 activation by entorhinal inputs. Entorhinal and CA3 pathways engage different feedforward interneuron subpopulations and cholinergic modulation of presynaptic function is mediated differentially by muscarinic M3 and M4 receptors, respectively. Thus, our data support a role and mechanisms for acetylcholine to prioritise novel information inputs to CA1 during memory formation. |
Databáze: | OpenAIRE |
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