scholarly journals An increase in dendritic plateau potentials is associated with experience-dependent cortical map reorganization

2021 ◽  
Vol 118 (9) ◽  
pp. e2024920118
Author(s):  
Stéphane Pagès ◽  
Nicolas Chenouard ◽  
Ronan Chéreau ◽  
Vladimir Kouskoff ◽  
Frédéric Gambino ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Pyramidal Neurons ◽  
Higher Order ◽  
Cortical Circuits ◽  
Plateau Potentials ◽  
Sensory Map ◽  
Whisker Map ◽  
Cortical Map ◽  
Cortical Representations

The organization of sensory maps in the cerebral cortex depends on experience, which drives homeostatic and long-term synaptic plasticity of cortico-cortical circuits. In the mouse primary somatosensory cortex (S1) afferents from the higher-order, posterior medial thalamic nucleus (POm) gate synaptic plasticity in layer (L) 2/3 pyramidal neurons via disinhibition and the production of dendritic plateau potentials. Here we address whether these thalamocortically mediated responses play a role in whisker map plasticity in S1. We find that trimming all but two whiskers causes a partial fusion of the representations of the two spared whiskers, concomitantly with an increase in the occurrence of POm-driven N-methyl-D-aspartate receptor-dependent plateau potentials. Blocking the plateau potentials restores the archetypical organization of the sensory map. Our results reveal a mechanism for experience-dependent cortical map plasticity in which higher-order thalamocortically mediated plateau potentials facilitate the fusion of normally segregated cortical representations.

scholarly journals An increase in dendritic plateau potentials is associated with experience-dependent cortical map reorganization

2020 ◽  
Author(s):  
Stéphane Pages ◽  
Nicolas Chenouard ◽  
Ronan Chéreau ◽  
Vladimir Kouskoff ◽  
Frédéric Gambino ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Pyramidal Neurons ◽  
Higher Order ◽  
Cortical Circuits ◽  
Plateau Potentials ◽  
Sensory Map ◽  
Whisker Map ◽  
Cortical Map ◽  
Cortical Representations

ABSTRACTThe organization of sensory maps in the cerebral cortex depends on experience, which drives homeostatic and long-term synaptic plasticity of cortico-cortical circuits. In the mouse primary somatosensory cortex (S1) afferents from the higher-order, posterior medial thalamic nucleus (POm) gate synaptic plasticity in layer (L) 2/3 pyramidal neurons via disinhibition and the production of dendritic plateau potentials. Here we address whether these thalamocortically mediated responses play a role in whisker map plasticity in S1. We find that trimming all but two whiskers causes a partial fusion of the representations of the two spared whiskers, concomitantly with an increase in the occurrence of POm-driven, N-methyl-D-aspartate receptor (NMDAR)-dependent plateau potentials. Blocking the plateau potentials restores the archetypical organization of the sensory map. Our results reveal a novel mechanism for experience-dependent cortical map plasticity in which higher-order thalamocortically mediated plateau potentials facilitate the fusion of normally segregated cortical representations.

scholarly journals Synergy between vesicular and non-vesicular gliotransmission regulates synaptic plasticity and working memory

2021 ◽  
Author(s):  
Ulyana Lalo ◽  
Seyed Rasooli-Nejad ◽  
Alexander Bogdanov ◽  
Lorenzo More ◽  
Wuhyun Koh ◽  
...  
Keyword(s):  
Working Memory ◽  
Synaptic Plasticity ◽  
Small Molecule ◽  
Environmental Enrichment ◽  
Pyramidal Neurons ◽  
Active Element ◽  
Spatial Working Memory ◽  
Phasic Response ◽  
Cortical Astrocytes

Astrocytes are an active element of brain signalling, capable of release of small molecule gliotransmitters by vesicular and channel-mediated mechanisms. However, specific physiological roles of astroglial exocytosis of glutamate and D-Serine remain controversial. Our data demonstrate that cortical astrocytes can release glutamate and D-Serine by combination of SNARE-dependent exocytosis and non-vesicular mechanisms dependent on TREK-1 and Best1 channels. Astrocyte-derived glutamate and D-serine elicited complex multicomponent phasic response in neocortical pyramidal neurons, which is mediated by extra-synaptic GluN2B receptors. Impairment of either pathway of gliotransmission (in the TREK1 KO, Best-1 KO or dnSNARE mice) strongly affected the NMDAR-dependent long-term synaptic plasticity in the hippocampus and neocortex. Moreover, impairment of astroglial exocytosis in dnSNARE mice led to the deficit in the spatial working memory which was rescued by environmental enrichment. We conclude that synergism between vesicular and non-vesicular gliotransmission is crucial for astrocyte-neuron communication and astroglia-driven regulation of synaptic plasticity and memory.

Transplanted Embryonic Neurons Improve Functional Recovery by Increasing Activity in Injured Cortical Circuits

2020 ◽  
Vol 30 (8) ◽  
pp. 4708-4725
Author(s):  
Evgenia Andreoli ◽  
Volodymyr Petrenko ◽  
Paul Eugène Constanthin ◽  
Alessandro Contestabile ◽  
Riccardo Bocchi ◽  
...  
Keyword(s):  
Functional Recovery ◽  
Pyramidal Neurons ◽  
Functional Integration ◽  
Epileptic Seizures ◽  
Behavioral Tests ◽  
Cortical Circuits ◽  
Functional Deficits ◽  
Promising Strategy ◽  
Neuronal Precursors

Abstract Transplantation of appropriate neuronal precursors after injury is a promising strategy to reconstruct cortical circuits, but the efficiency of these approaches remains limited. Here, we applied targeted apoptosis to selectively ablate layer II/III pyramidal neurons in the rat juvenile cerebral cortex and attempted to replace lost neurons with their appropriate embryonic precursors by transplantation. We demonstrate that grafted precursors do not migrate to replace lost neurons but form vascularized clusters establishing reciprocal synaptic contacts with host networks and show functional integration. These heterotopic neuronal clusters significantly enhance the activity of the host circuits without causing epileptic seizures and attenuate the apoptotic injury-induced functional deficits in electrophysiological and behavioral tests. Chemogenetic activation of grafted neurons further improved functional recovery, and the persistence of the graft was necessary for maintaining restored functions in adult animals. Thus, implanting neuronal precursors capable to form synaptically integrated neuronal clusters combined with activation-based approaches represents a useful strategy for helping long-term functional recovery following brain injury.

Layer-specific serotonergic facilitation of IPSC in layer 2/3 pyramidal neurons of the visual cortex

2012 ◽  
Vol 107 (1) ◽  
pp. 407-416 ◽  
Author(s):  
Hyun-Jong Jang ◽  
Kwang-Hyun Cho ◽  
Sung-Won Park ◽  
Myung-Jun Kim ◽  
Shin Hee Yoon ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Visual Cortex ◽  
Pyramidal Neurons ◽  
Inhibitory Influence ◽  
Inhibitory Transmission ◽  
Layer 2 ◽  
Specific Manner ◽  
Intracellular Ca ◽  
Stimulation Of

Serotonin (5-hydroxytryptamine, 5-HT) inhibits the induction of long-term synaptic plasticity in layer 2/3 of the visual cortex at the end of its critical period in rats. However, the cellular and molecular mechanisms remain unclear. Since inhibitory influence is crucial in the induction of synaptic plasticity, the effect of 5-HT on inhibitory transmission was investigated in layer 2/3 pyramidal neurons of the primary visual cortex. The amplitude of inhibitory postsynaptic current (IPSC), but not excitatory postsynaptic current, evoked by stimulation of the underlying layer 4, was increased by ∼20% with a bath application of 5-HT. The amplitude of miniature IPSC was also increased by the application of 5-HT, while the paired-pulse ratio was not changed. The facilitating effect of 5-HT on IPSC was mediated by the activation of 5-HT2 receptors. An increase in intracellular Ca2+ via release from inositol 1,4,5-trisphosphate (IP3)-sensitive stores, which was confirmed by confocal Ca2+ imaging, and activation of Ca2+/calmodulin-dependent kinase II (CaMKII) were involved in the facilitation of IPSC by 5-HT. However, 5-HT failed to facilitate IPSC evoked by the stimulation of layer 1. These results suggest that activation of 5-HT2 receptors releases intracellular Ca2+ via IP3-sensitive stores, which facilitates GABAAergic transmission via the activation of CaMKII in layer 2/3 pyramidal neurons of the visual cortex in a layer-specific manner. Thus facilitation of inhibitory transmission by 5-HT might be involved in regulating the information flow and the induction of long-term synaptic plasticity, in a pathway-specific manner.

scholarly journals Active dendrites, potassium channels and synaptic plasticity

2003 ◽  
Vol 358 (1432) ◽  
pp. 667-674 ◽  
Author(s):  
Daniel Johnston ◽  
Brian R. Christie ◽  
Andreas Frick ◽  
Richard Gray ◽  
Dax A. Hoffman ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Potassium Channels ◽  
Potassium Channel ◽  
Pyramidal Neurons ◽  
Back Propagation ◽  
Dendritic Tree ◽  
Long Term Potentiation ◽  
Synaptic Potentials ◽  
Dendritic Excitability

The dendrites of CA1 pyramidal neurons in the hippocampus express numerous types of voltage-gated ion channel, but the distributions or densities of many of these channels are very non-uniform. Sodium channels in the dendrites are responsible for action potential (AP) propagation from the axon into the dendrites (back-propagation); calcium channels are responsible for local changes in dendritic calcium concentrations following back-propagating APs and synaptic potentials; and potassium channels help regulate overall dendritic excitability. Several lines of evidence are presented here to suggest that back-propagating APs, when coincident with excitatory synaptic input, can lead to the induction of either long-term depression (LTD) or long-term potentiation (LTP). The induction of LTD or LTP is correlated with the magnitude of the rise in intracellular calcium. When brief bursts of synaptic potentials are paired with postsynaptic APs in a theta-burst pairing paradigm, the induction of LTP is dependent on the invasion of the AP into the dendritic tree. The amplitude of the AP in the dendrites is dependent, in part, on the activity of a transient, A-type potassium channel that is expressed at high density in the dendrites and correlates with the induction of the LTP. Furthermore, during the expression phase of the LTP, there are local changes in dendritic excitability that may result from modulation of the functioning of this transient potassium channel. The results support the view that the active properties of dendrites play important roles in synaptic integration and synaptic plasticity of these neurons.

scholarly journals Inhibitory Sharpening of Receptive Fields Contributes to Whisker Map Plasticity in Rat Somatosensory Cortex

2005 ◽  
Vol 94 (6) ◽  
pp. 4387-4400 ◽  
Author(s):  
Elisabeth Foeller ◽  
Tansu Celikel ◽  
Daniel E. Feldman
Keyword(s):  
Receptive Field ◽  
Receptive Fields ◽  
Gaba A ◽  
Layer 4 ◽  
Adolescent Rats ◽  
Rat Somatosensory Cortex ◽  
Sr 95531 ◽  
Sensory Map ◽  
Whisker Map ◽  
Cortical Map

The role of inhibition in sensory cortical map plasticity is not well understood. Here we tested whether inhibition contributes to expression of receptive field plasticity in developing rat somatosensory (S1) cortex. In normal rats, microiontophoresis of gabazine (SR 95531), a competitive γ-aminobutyric acid (GABA)-A receptor antagonist, preferentially disinhibited surround whisker responses relative to principal whisker responses, indicating that GABAA inhibition normally acts to sharpen whisker tuning. Plasticity was induced by transiently depriving adolescent rats of all but one whisker; this causes layer 2/3 (L2/3) receptive fields to shift away from the deprived principal whisker and toward the spared surround whisker. In units with shifted receptive fields, gabazine preferentially disinhibited responses to the deprived principal whisker, unlike in controls, suggesting that GABAA inhibition was acting to preferentially suppress these responses relative to spared whisker responses. This effect was not observed for L2/3 units that did not express receptive field plasticity or in layer 4, where receptive field plasticity did not occur. Thus GABAA inhibition promoted expression of sensory map plasticity by helping to sharpen receptive fields around the spared input.

scholarly journals Disinhibitory circuitry gates associative synaptic plasticity in olfactory cortex

2020 ◽  
Author(s):  
Martha Canto-Bustos ◽  
F. Kathryn Friason ◽  
Constanza Bassi ◽  
Anne-Marie M. Oswald
Keyword(s):  
Synaptic Plasticity ◽  
Pyramidal Neurons ◽  
Piriform Cortex ◽  
Inhibitory Neuron ◽  
Long Term Potentiation ◽  
Inhibitory Interneurons ◽  
Sensory Stimuli ◽  
Term Potentiation ◽  
Cortical Responses

AbstractInhibitory microcircuits play an essential role in regulating cortical responses to sensory stimuli. Interneurons that inhibit dendritic or somatic integration in pyramidal neurons act as gatekeepers for neural activity, synaptic plasticity and the formation of sensory representations. Conversely, interneurons that specifically inhibit other interneurons can open gates through disinhibition. In the rodent piriform cortex, relief of dendritic inhibition permits long-term potentiation (LTP) of the recurrent synapses between pyramidal neurons (PNs) thought to underlie ensemble odor representations. We used an optogenetic approach to identify the inhibitory interneurons and disinhibitory circuits that regulate LTP. We focused on three prominent inhibitory neuron classes-somatostatin (SST), parvalbumin (PV), and vasoactive intestinal polypeptide (VIP) interneurons. We find that VIP interneurons inhibit SST interneurons and promote LTP through subthreshold dendritic disinhibition. Alternatively, suppression of PV-interneuron inhibition promotes LTP but requires suprathreshold spike activity. Thus, we have identified two disinhibitory mechanisms to regulate synaptic plasticity during olfactory processing.

scholarly journals IGF-1 facilitates extinction of conditioned fear

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Laura E Maglio ◽  
José A Noriega-Prieto ◽  
Irene B Maroto ◽  
Jesús Martin-Cortecero ◽  
Antonio Muñoz-Callejas ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Transmission ◽  
Pyramidal Neurons ◽  
Conditioned Fear ◽  
Long Term Potentiation ◽  
Fear Extinction ◽  
Neuronal Firing ◽  
Term Potentiation ◽  
Extinction Memory

Insulin-like growth factor-1 (IGF-1) plays a key role in synaptic plasticity, spatial learning and anxiety-like behavioral processes. While IGF-1 regulates neuronal firing and synaptic transmission in many areas of the central nervous system, its signaling and consequences on excitability, synaptic plasticity, and animal behavior dependent on the prefrontal cortex remain unexplored. Here, we show that IGF-1 induces a long-lasting depression of the medium and slow post-spike afterhyperpolarization (mAHP and sAHP), increasing the excitability of layer 5 pyramidal neurons of the rat infralimbic cortex. Besides, IGF-1 mediates a presynaptic long-term depression of both inhibitory and excitatory synaptic transmission in these neurons. The net effect of this IGF-1 mediated synaptic plasticity is a long-term potentiation of the postsynaptic potentials. Moreover, we demonstrate that IGF-1 favors the fear extinction memory. These results show novel functional consequences of IGF-1 signaling, revealing IGF-1 as a key element in the control of the fear extinction memory.

scholarly journals Higher-order thalamocortical inputs gate synaptic long-term potentiation via disinhibition

2018 ◽  
Author(s):  
Leena E. Williams ◽  
Anthony Holtmaat
Keyword(s):  
Pyramidal Neurons ◽  
Sensory Information ◽  
Long Term Potentiation ◽  
Higher Order ◽  
Synaptic Circuits ◽  
Term Potentiation ◽  
Cortical Pyramidal Neurons ◽  
Whisker Stimulation ◽  
Synaptic Circuitry

SUMMARYSensory experience and perceptual learning changes the receptive field properties of cortical pyramidal neurons, largely mediated by long-term potentiation (LTP) of synapses. The circuit mechanisms underlying cortical LTP remain unclear. In the mouse somatosensory cortex (S1), LTP can be elicited in layer (L) 2/3 pyramidal neurons by rhythmic whisker stimulation. We combined electrophysiology, optogenetics, and chemogenetics in thalamocortical slices to dissect the synaptic circuitry underlying this LTP. We found that projections from higher-order, posteriormedial thalamic complex (POm) to S1 are key to eliciting NMDAR-dependent LTP of intracortical synapses. Paired activation of intracortical and higher-order thalamocortical pathways increased vasoactive intestinal peptide (VIP) interneuron and decreased somatostatin (SST) interneuron activity, which was critical for inducing LTP. Our results reveal a novel circuit motif in which higher-order thalamic feedback gates plasticity of intracortical synapses in S1 via disinhibition. This motif may allow contextual feedback to shape synaptic circuits that process first-order sensory information.

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