scholarly journals Author Correction: Acetylcholine prioritises direct synaptic inputs from entorhinal cortex to CA1 by differential modulation of feedforward inhibitory circuits

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jon Palacios-Filardo ◽  
Matt Udakis ◽  
Giles A. Brown ◽  
Benjamin G. Tehan ◽  
Miles S. Congreve ◽  
...  
2020 ◽  
Author(s):  
Jon Palacios-Filardo ◽  
Matt Udakis ◽  
Giles A. Brown ◽  
Benjamin G. Tehan ◽  
Miles S. Congreve ◽  
...  

AbstractAcetylcholine release in the hippocampus plays a central role in the formation of new memory representations by facilitating synaptic plasticity. It is also proposed 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, but this influential theory has not been directly tested. Here, we show that excitatory inputs from entorhinal cortex and CA3 are depressed equally by synaptic release of acetylcholine in CA1. However, greater depression of feedforward inhibition from entorhinal cortex results in an overall enhancement of excitatory-inhibitory balance and CA1 activation. Underpinning the prioritisation of entorhinal inputs, entorhinal and CA3 pathways engage distinct feedforward interneuron subpopulations and depression is mediated differentially by presynaptic muscarinic M3 and M4 receptors respectively. These mechanisms enable acetylcholine to prioritise novel information inputs to CA1 during memory formation and suggest selective muscarinic targets for therapeutic intervention.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jon Palacios-Filardo ◽  
Matt Udakis ◽  
Giles A. Brown ◽  
Benjamin G. Tehan ◽  
Miles S. Congreve ◽  
...  

AbstractAcetylcholine 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.


2014 ◽  
Vol 369 (1635) ◽  
pp. 20120520 ◽  
Author(s):  
Christoph Schmidt-Hieber ◽  
Michael Häusser

Neurons in the medial entorhinal cortex fire action potentials at regular spatial intervals, creating a striking grid-like pattern of spike rates spanning the whole environment of a navigating animal. This remarkable spatial code may represent a neural map for path integration. Recent advances using patch-clamp recordings from entorhinal cortex neurons in vitro and in vivo have revealed how the microcircuitry in the medial entorhinal cortex may contribute to grid cell firing patterns, and how grid cells may transform synaptic inputs into spike output during firing field crossings. These new findings provide key insights into the ingredients necessary to build a grid cell.


2008 ◽  
Vol 64 (6) ◽  
pp. 674-686 ◽  
Author(s):  
Vadym Gnatkovsky ◽  
Laura Librizzi ◽  
Federica Trombin ◽  
Marco de Curtis

2001 ◽  
Vol 112 (10) ◽  
pp. 1822-1827 ◽  
Author(s):  
Carlo Trompetto ◽  
Alessandro Buccolieri ◽  
Lucio Marinelli ◽  
Giovanni Abbruzzese

2021 ◽  
Author(s):  
Sebastian H. Bitzenhofer ◽  
Elena A. Westeinde ◽  
Han-Xiong Bear Zhang ◽  
Jeffry S. Isaacson

SummaryOlfactory information is encoded in lateral entorhinal cortex (LEC) by two classes of layer 2 (L2) principal neurons: fan and pyramidal cells. However, the functional properties of L2 neurons are unclear. Here, we show in awake mice that L2 cells respond rapidly to odors during single sniffs and that LEC is essential for discrimination of odor identity and intensity. Population analyses of L2 ensembles reveals that while rate coding distinguishes odor identity, firing rates are weakly concentration-dependent and changes in spike timing represent odor intensity. L2 principal cells differ in afferent olfactory input and connectivity with local inhibitory circuits and the relative timing of pyramidal and fan cell spikes underlies odor intensity coding. Downstream, intensity is encoded purely by spike timing in hippocampal CA1. Together, these results reveal the unique processing of odor information by parallel LEC subcircuits and highlight the importance of temporal coding in higher olfactory areas.


2019 ◽  
Vol 121 (1) ◽  
pp. 238-254 ◽  
Author(s):  
Stephen Beesley ◽  
Thomas Sullenberger ◽  
Jyotsna Pilli ◽  
Saad Abbasi ◽  
Akash Gunjan ◽  
...  

The subunit composition of N-methyl-d-aspartate receptors (NMDARs) at synaptic inputs onto a neuron can either vary or be uniform depending on the type of neuron and/or brain region. Excitatory pyramidal neurons in the frontal and somatosensory cortices (L5), for example, show pathway-specific differences in NMDAR subunit composition in contrast with the entorhinal cortex (L3), where we now show colocalization of NMDARs with distinct subunit compositions at individual synaptic inputs onto these neurons. Subunit composition was deduced electrophysiologically based on alterations of current-voltage relationship ( I–V) profiles, amplitudes, and decay kinetics of minimally evoked, pharmacologically isolated, NMDAR-mediated excitatory postsynaptic currents by known subunit-preferring antagonists. The I–Vs were outwardly rectifying in a majority of neurons assayed (~80%), indicating expression of GluN1/GluN2/GluN3-containing triheteromeric NMDARs ( t-NMDARs) and of the conventional type, reversing close to 0 mV with prominent regions of negative slope, in the rest of the neurons sampled (~20%), indicating expression of GluN1/GluN2-containing diheteromeric NMDARs ( d-NMDARs). Blocking t-NMDARs in neurons with outwardly rectifying I–Vs pharmacologically unmasked d-NMDARs, with all responses antagonized using D-AP5. Coimmunoprecipitation assays of membrane-bound protein complexes isolated from the medial entorhinal area using subunit-selective antibodies corroborated stoichiometry and together suggested the coexpression of t- and d-NMDARs at these synapses. Colocalization of functionally distinct NMDAR subtypes at individual synaptic inputs likely enhances the repertoire of pyramidal neurons for information processing and plasticity within the entorhinal cortex. NEW & NOTEWORTHY The subunit composition of a N-methyl-d-aspartate (NMDA) receptor, which dictates most aspects of its function, can vary between neurons in different brain regions and/or between synaptic inputs onto single neurons. Here we demonstrate colocalization of tri- and diheteromeric-NMDA receptors at the same/single synaptic input onto excitatory neurons in the entorhinal cortex. Synaptic colocalization of distinct NMDAR subtypes might endow entorhinal cortical neurons with the ability to encode distinct patterns of neuronal activity through single synapses.


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