Potentiel postsynaptique

Résumé

Un potentiel postsynaptique (PPS), encore appelé potentiel gradué ou potentiel électro-tonique, est le signal unitaire produit en aval d'une synapse. Il s'agit d'un changement transitoire et local de la différence de potentiel électrochimique établie de part et d'autre de la membrane. La plaque motrice est la zone synaptique entre le neurone et la cellule musculaire. Le neurotransmetteur mis en jeu est l'acétylcholine qui va se fixer sur un récepteur et va ainsi entraîner une dépolarisation. Ce potentiel est retrouvé à l’extrémité d'un neurone sensoriel (ex : Corpuscule de Pacini au niveau du derme profond). D'un point de vue informationnel, il y a deux types de PPS : le potentiel postsynaptique excitateur (PPSE) correspond à une dépolarisation de la membrane, ce qui augmente la probabilité que le neurone décharge un potentiel d'action (les ions Na+, présents en grande partie à l'extérieur de l'axone, pénètrent dans le neurone et le chargent positivement augmentant ainsi son potentiel) ; le potentiel postsynaptique inhibiteur (PPSI) correspond à une hyperpolarisation de la membrane qui diminue la probabilité de la décharge. L'ouverture des canaux potassiques permet aux ions K+ de sortir de la cellule, ce qui hyperpolarise celle-ci (perte excessive d'ions K+). Les ions Cl- présents en grande partie à l'extérieur de l'axone peuvent également entrer dans le neurone et le chargent négativement diminuant ainsi son potentiel. D'un point de vue cinétique, on décrit des « PPS lents » et des « PPS rapides ». La génération des PPS rapides est due à l'activation de canaux ioniques via des récepteurs ionotropes, alors que celle des PPS lents est due à l'activation directe de récepteurs métabotropes. La variation du potentiel de membrane va se propager depuis le site d'origine jusqu'aux zones voisines de la membrane plasmique qui sont encore au potentiel de repos. Cette propagation est multidirectionnelle. La circulation est dite « décrémentielle » c'est-à-dire que l'intensité de la dépolarisation diminue puis disparaît avec la distance.

Source officielle

https://fr.wikipedia.org/wiki/Potentiel_postsynaptique

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Animals are capable of evaluating sensory cues for possible threats and adapting their behaviours accordingly. Fear learning is an evolutionarily conserved behaviour crucial for animal survival, during which sensory percepts with a negative reinforcing quality, also called unconditioned stimuli (US), influence the valence of initially neutral sensory cues (conditioned stimulus, CS). The lateral amygdala (LA) is thought to integrate information about sensory cues like tones (the CS), and information about primary reinforcers like painful stimuli (the US). Nevertheless, synaptic afferents to the LA and upstream brain areas remain understudied in fear learning. The posterior insular cortex (pInsCx) has been shown to project to the LA and is known to be a multimodal sensory area which processes auditory, somatosensory-nociceptive, and interoceptive information, making it an interesting brain area with a putative role in fear learning. My PhD thesis therefore aimed to investigate a possible connection from the pInsCx to the LA, and the role of this pathway in the fear learning circuitry. I first used anatomical anterograde and retrograde tracing strategies in the mouse to study the afferents to the LA. Besides previously known inputs, I found that the granular (GI) and the dysgranular (DI) areas of the pInsCx strongly project to the anterior LA. With optogenetically-assisted circuit mapping (OACM), I found a glutamatergic monosynaptic connection from the pInsCx to LA principal neurons that, in agreement with the anatomical findings, was localized more to the anterior LA. In comparison, a well-studied auditory thalamic (MGm/PIN) input was localized more to the posterior LA. Despite this regional input specificity, ~30% LA principal neurons received projections from both areas. Thus, in the first part, using anatomical tracing and OACM, I have unambiguously shown a robust functional excitatory connection from the pInsCx (GI/DI) to the LA.In the second part of my thesis, I aimed to characterize the role of the pInsCx and the pInsCx-LA pathway in fear learning. Using archaerhodopsin-mediated optogenetic inhibition, I found that silencing of footshock-driven activity of pInsCx neurons in-vivo, partially blocks auditory-cued fear memory. These results were also supported by chemogenetic silencing of the pInsCx during the training day, which led to a modest impairment of fear retrieval a day later. Next, to investigate the role of the pInsCx-LA projection more specifically, I used a retrograde expression approach to silence LA-projectors during the footshock, which again, suppressed fear memory one day later. In further ex-vivo experiments, I found that EPSCs at the pInsCx-LA connection exhibited an increased AMPA/NMDA ratio following fear learning, indicating that plasticity occurs at this pathway during fear learning. Finally, miniature microscopic Ca2+ imaging of LA neurons combined with halorhodopsin-mediated axon inhibition, showed that the pInsCx-LA excitatory synapse contributes to transmitting footshock information to a sub-population of LA neurons. This study unravels the relationship between two serial nodes, the pInsCx and the LA, in the fear learning network. Thus, the pInsCx-LA connection is a novel pathway in auditory-cued fear memory that is strengthened with learning and that partly provides aversive information to the amygdala.

EPFL2022

Cell-type-specific nicotinic input disinhibits mouse barrel cortex during active sensing

Carl Petersen, Sylvain Crochet, Célia Roxane Gasselin, Benoît Hohl

Fast synaptic transmission relies upon the activation of ionotropic receptors by neurotransmitter release to evoke postsynaptic potentials. Glutamate and GABA play dominant roles in driving highly dynamic activity in synaptically connected neuronal circuits, but ionotropic receptors for other neurotransmitters are also expressed in the neocortex, including nicotinic receptors, which are non-selective cation channels gated by acetylcholine. To study the function of non-glutamatergic excitation in neocortex, we used two-photon microscopy to target whole-cell membrane potential recordings to different types of genetically defined neurons in layer 2/3 of primary somatosensory barrel cortex in awake head-restrained mice combined with pharmacological and optogenetic manipulations. Here, we report a prominent nicotinic input, which selectively depolarizes a subtype of GABAergic neuron expressing vasoactive intestinal peptide leading to disinhibition during active sensorimotor processing. Nicotinic disinhibition of somatosensory cortex during active sensing might contribute importantly to integration of top-down and motor-related signals necessary for tactile perception and learning.

CELL PRESS2021

High potency of the orally-active NMDA-receptor antagonist CGP 40 116 in inhibiting excitatory postsynaptic potentials of rat basolateral amygdala neurones in vitro

Pierre Magistretti, Emilie Pralong

Conventional intracellular recordings were used to monitor postsynaptic potentials of basolateral amygdala neurones (BLA) in brain slices comprising the BLA, the entorhinal cortex (EC) and the hippocampus, in which the EC-BLA connections were preserved. Stimulation of the BLA with a bipolar electrode elicited complex postsynaptic potentials consisting of alpha-amino-3-hydroxy-5-methyl-isoxazoleproprionic acid (AMPA) receptor-mediated fast excitatory postsynaptic potentials (fast EPSPs), gamma-amino-butyric acid [GABA(A)] receptor-mediated fast inhibitory postsynaptic potentials (fast IPSPs) and GABAB receptor-mediated slow IPSPs. Bath application of 10 microM of the AMPA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione and of 10 microM of the GABA(A) receptor antagonist bicuculline methiodide (BMI) revealed a N-methyl-D-aspartate (NMDA) receptor-mediated slow EPSPs, which was occasionally followed by a GABAB receptor-mediated slow IPSPs. Under these conditions, the log concentration-response curve for D-(E)-2-amino-4-methyl-5-phosphono-3-pentanoic acid (CGP 40 116), a newly developed drug with proposed NMDA-receptor antagonist properties, was compared to that obtained with the 'classic' antagonist D(-)-2-amino-5-phosphonopentanoic acid (D-AP5) in inhibiting the NMDA-mediated postsynaptic potentials. CGP 40 116 (IC50: 130 nM) was over 30 times more potent than D-AP5 (IC50: 4100 nM) in reducing NMDA-mediated slow EPSP. In conclusion, the present study indicates that CGP 40 116, a new orally-active NMDA antagonist, shows a very high potency on NMDA receptors in the amygdala and may therefore be a valuable tool for studying the behavioural effect of NMDA-receptor mediated transmission in this structure.

1998

EPFL2022