Synaptic and circuit development of the primary sensory cortex

Choi, Se‐Young

doi:10.1038/s12276-018-0029-x

Cited by 12 publications

(15 citation statements)

References 129 publications

(133 reference statements)

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“…All in vitro experiments were performed on fully mature neurons after 21-28 days of cultivation. The evolution of neuronal networks in vitro was characterized by coherent maturation of synaptic connectivity and ECM expression, partially resembling neuronal circuit development in vivo (Choi, 2018). In the course of cultivation, synapse density increased until maturity was reached after 21 days in vitro (DIV) ( Figure S1B, C).…”

Section: Cell Culturesmentioning

confidence: 85%

Extracellular matrix supports excitation-inhibition balance in neuronal networks by stabilizing inhibitory synapses

Dzyubenko

Fleischer

Manrique-Castano

et al. 2020

Preprint

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Maintaining the balance between excitation and inhibition is essential for the appropriate control of neuronal network activity. Sustained excitation-inhibition (E-I) balance relies on the orchestrated adjustment of synaptic strength, neuronal activity and network circuitry. While growing evidence indicates that extracellular matrix (ECM) of the brain is a crucial regulator of neuronal excitability and synaptic plasticity, it remains unclear whether and how ECM contributes to neuronal circuit stability. Here we demonstrate that the integrity of ECM supports the maintenance of E-I balance by retaining inhibitory connectivity. Depletion of ECM in mature neuronal networks preferentially decreases the density of inhibitory synapses and the size of individual inhibitory postsynaptic scaffolds. After ECM depletion, inhibitory synapse strength homeostatically increases via the reduction of presynaptic GABAB receptors. However, the inhibitory connectivity reduces to an extent that inhibitory synapse scaling is no longer efficient in controlling neuronal network state. Our results indicate that the brain ECM preserves the balanced network state by stabilizing inhibitory control.

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Section: Cell Culturesmentioning

confidence: 85%

Extracellular matrix supports excitation-inhibition balance in neuronal networks by stabilizing inhibitory synapses

Dzyubenko

Fleischer

Manrique-Castano

et al. 2020

Preprint

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“…For decades, evidence were collected to demonstrate that neurotrophins operate in a trans-synaptic and bi-directional fashion for regulating synaptic plasticity and strength within active but not resting neuronal networks (Autry and Monteggia, 2012;Bennett and Lagopoulos, 2014;Castren and Antila, 2017;Choi, 2018;Cohen-Cory et al, 2010;Hao et al, 2018;Lessmann, 1998;Lu and Chow, 1999;Park and Poo, 2013;Poo, 2001;Tyler et al, 2002). Two examples: (i) anterograde spread of the trans-synaptic neurotrophin rescued the lack of input activity on post-synaptic cells (Chen et al, 2016;Du et al, 2009), and (ii) retrograde transport of target-derived neurotrophin via signaling endosomes can extend from axon terminals to dendrites where it instructs molecular composition of postsynaptic densities (Sharma et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Neurotrophin and synaptogenesis

Jeanneteau

Arango-Lievano

Chao

2020

Synapse Development and Maturation

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Synaptogenesis is encoded by multiple genes that program the assembly of neural networks in the immature brain during development and later in life, in the experienced brain that must respond to changes of the external world and of proprioception. Processing of neural network activity cannot solely rely on the activity of established synapses as their plasticity can saturate. For this reason, synaptogenesis is reversible. Assembly and disassembly of synapses depend on the exchange of signals between the pre-and post-synaptic terminals. Synaptic trophic factors are paramount for neural network remodeling, homeostasis and survival because they are present in limited supply. Neurotrophins present the necessary attributes to operate as synaptic trophin. It is speculated that many diverse and pleiotropic actions of neurotrophins on the synapse depend on the sources of neurotrophin ligands, its modes of secretion and signaling, all influenced by their locations at the synapse. What information is encoded when synaptic neurotrophin signaling is retrograde or anterograde, paracrine or autocrine? Answers emerged from the characterization of the cells that secrete neurotrophins, the cells that respond to neurotrophins, the various modes of secretion, receptor-signaling pathways, and the temporal constraints imposed by synaptic transmission. Failure to communicate the appropriate synaptic trophic signals impairs neuronal networks maintenance and updated wiring.

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“…They are essential for gain control (Atallah et al, 2012), play a role on feature selectivity (Lee et al, 2012;Duan et al, 2017;Goel et al, 2018), participate in gamma rhythms (Cardin et al, 2009;Sohal et al, 2009). Importantly, in the visual cortex the protracted development of perisomatic inhibition has been implicated in the gating and control of ocular dominance plasticity during the critical period (Huang et al, 1999;Fagiolini et al, 2004; for reviews see Jiang et al, 2005;van Versendaal and Levelt, 2016;Choi, 2018;Hensch and Quinlan, 2018).…”

Section: Introductionmentioning

confidence: 99%

Endocannabinoid Signaling Contributes to Experience-Induced Increase of Synaptic Release Sites From Parvalbumin Interneurons in Mouse Visual Cortex

Huang

Kirkwood

2020

Front. Cell. Neurosci.

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During postnatal development of the visual cortex between eye-opening to puberty, visual experience promotes a gradual increase in the strength of inhibitory synaptic connections from parvalbumin-positive interneurons (PV-INs) onto layer 2/3 pyramidal cells. However, the detailed connectivity properties and molecular mechanisms underlying these developmental changes are not well understood. Using dual-patch clamp in brain slices from G42 mice, we revealed that both connection probability and the number of synaptic release sites contributed to the enhancement of synaptic strength. The increase of release site number was hindered by dark rearing from eye-opening and rescued by 3-days re-exposure to the normal visual environment. The effect of light re-exposure on restoring synaptic release sites in dark reared mice was mimicked by the agonist of cannabinoid-1 (CB1) receptors and blocked by an antagonist of these receptors, suggesting a role for endocannabinoid signaling in lightinduced maturation of inhibitory connectivity from PV-INs to pyramidal cells during postnatal development.

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Synaptic and circuit development of the primary sensory cortex

Cited by 12 publications

References 129 publications

Extracellular matrix supports excitation-inhibition balance in neuronal networks by stabilizing inhibitory synapses

Extracellular matrix supports excitation-inhibition balance in neuronal networks by stabilizing inhibitory synapses

Neurotrophin and synaptogenesis

Endocannabinoid Signaling Contributes to Experience-Induced Increase of Synaptic Release Sites From Parvalbumin Interneurons in Mouse Visual Cortex

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