Ana Paula De Vincenti

University of Buenos Aires

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Gustavo Paratcha

University of Buenos Aires

Fernanda Ledda

Fundación Instituto Leloir

Antonella S. Ríos

Fundación Instituto Leloir

Facundo Ferrero Restelli

University of Buenos Aires

Paula Fontanet

Karolinska Institutet

Mailín Casadei

Consejo Nacional de Investigaciones Científicas y Técnicas

Jorge B. Aquino

Austral University

Tomás L. Falzone

University of Buenos Aires

Antonela Bonafina

University of Buenos Aires

Sonia A. Crichigno

Consejo Nacional de Investigaciones Científicas y Técnicas

Cooperative Institutions

Consejo Nacional de Investigaciones Científicas y Técnicas

University of Buenos Aires

Institute of Astronomy and Space Physics

Karolinska Institutet

National University of Comahue

Fundación Instituto Leloir

Centro Científico Tecnológico - San Juan

Bariloche Atomic Centre

Instituto de Biología Molecular y Celular de Rosario

Austral University

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Social isolation impairs active avoidance performance and decreases neurogenesis in the dorsomedial telencephalon of rainbow trout

Physiology & Behavior (2018)

Maria Soledad Ausas Laura S. Mazzitelli-Fuentes Fernanda R. Román Sonia A. Crichigno Ana Paula De Vincenti

Social Isolation

Social Behavior

10.1016/j.physbeh.2018.10.006

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Citations (18)

New insights into the homeostatic role of Lrig1 in different neurogenic niches: implications for neuronal regeneration

Neural Regeneration Research (2025)

Ana Paula De Vincenti Fernanda Ledda Gustavo Paratcha

Laboratorio de Neurociencia Molecular y Celular, Instituto de Biología Celular y Neurociencias (IBCN)-CONICET-UBA, Facultad de Medicina, Universidad de Buenos Aires (UBA), Buenos Aires, Argentina (De Vincenti AP, Paratcha G) Fundación Instituto Leloir, Instituto de Investigaciones Bioquímicas de Buenos Aires, Buenos Aires, Argentina (Ledda F) *Correspondence to: Gustavo Paratcha, PhD, [email protected]. This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License (http://creativecommons.org/licenses/by-nc-sa/4.0/), which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

Homeostasis

10.4103/nrr.nrr-d-24-01333

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Etv4 regulates nociception by controlling peptidergic sensory neuron development and peripheral tissue innervation

Development (2022)

Antonella S. Ríos Ana Paula De Vincenti Mailín Casadei Jorge B. Aquino Pablo R. Brumovsky

ABSTRACT The perception of noxious environmental stimuli by nociceptive sensory neurons is an essential mechanism for the prevention of tissue damage. Etv4 is a transcriptional factor expressed in most nociceptors in dorsal root ganglia (DRG) during the embryonic development. However, its physiological role remains unclear. Here, we show that Etv4 ablation results in defects in the development of the peripheral peptidergic projections in vivo, and in deficits in axonal elongation and growth cone morphology in cultured sensory neurons in response to NGF. From a mechanistic point of view, our findings reveal that NGF regulates Etv4-dependent gene expression of molecules involved in extracellular matrix (ECM) remodeling. Etv4-null mice were less sensitive to noxious heat stimuli and chemical pain, and this behavioral phenotype correlates with a significant reduction in the expression of the pain-transducing ion channel TRPV1 in mutant mice. Together, our data demonstrate that Etv4 is required for the correct innervation and function of peptidergic sensory neurons, regulating a transcriptional program that involves molecules associated with axonal growth and pain transduction.

Nociceptor

Dorsal root ganglion

Sensory neuron

10.1242/dev.200583

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Tetraspanin1 promotes NGF signaling by controlling TrkA receptor proteostasis

Cellular and Molecular Life Sciences (2019)

Facundo Ferrero Restelli Paula Fontanet Ana Paula De Vincenti Tomás L. Falzone Fernanda Ledda

Proteostasis

10.1007/s00018-019-03282-3

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Lrig1 regulates cell fate specification of glutamatergic neurons via FGF-driven Jak2/Stat3 signaling in cortical progenitors

Development (2024)

Ana Paula De Vincenti Antonela Bonafina Fernanda Ledda Gustavo Paratcha

The cell-intrinsic mechanisms underlying the decision of a stem/progenitor cell to either proliferate or differentiate remain incompletely understood. Here, we identify the transmembrane protein Lrig1 as a physiological homeostatic regulator of FGF2-driven proliferation and self-renewal of neural progenitors at early-to-mid embryonic stages of cortical development. We show that Lrig1 is expressed in cortical progenitors (CPs), and its ablation caused expansion and increased proliferation of radial/apical progenitors and of neurogenic transit-amplifying Tbr2+ intermediate progenitors. Notably, our findings identify a previously unreported EGF-independent mechanism through which Lrig1 negatively regulates neural progenitor proliferation by modulating the FGF2-induced IL6/Jak2/Stat3 pathway, a molecular cascade that plays a pivotal role in the generation and maintenance of CPs. Consistently, Lrig1 knockout mice showed a significant increase in the density of pyramidal glutamatergic neurons placed in superficial layers 2 and 3 of the postnatal neocortex. Together, these results support a model in which Lrig1 regulates cortical neurogenesis by influencing the cycling activity of a set of progenitors that are temporally specified to produce upper layer glutamatergic neurons.

Cell fate determination

Progenitor

10.1242/dev.202879

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Mechanisms That Modulate and Diversify BDNF Functions: Implications for Hippocampal Synaptic Plasticity

Frontiers in Cellular Neuroscience (2019)

Ana Paula De Vincenti Antonella S. Ríos Gustavo Paratcha Fernanda Ledda

Brain-Derived Neurotrophic Factor (BDNF) is a neurotrophin that has pleiotropic effects on neuronal morphology and synaptic plasticity that underlie hippocampal circuit development and cognition. Recent advances established that BDNF function is controlled and diversified by molecular and cellular mechanisms including trafficking and subcellular compartmentalization of different Bdnf mRNA species, pre- vs. postsynaptic release of BDNF, control of BDNF signaling by TrkB receptor interactors and conversion of pro-BDNF to mature BDNF and BDNF-propeptide. Defects in these regulatory mechanisms affect dendritic spine formation and morphology of pyramidal neurons as well as synaptic integration of newborn granule cells (GCs) into preexisting circuits of mature hippocampus, compromising the cognitive function. Here, we review recent findings describing novel dynamic mechanisms that diversify and locally control the function of BDNF in hippocampal neurons.

10.3389/fncel.2019.00135

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Citations (124)

Lrig1 and Lrig3 cooperate to control Ret receptor signaling, sensory axonal growth and epidermal innervation

Development (2021)

Ana Paula De Vincenti Fernando C. Alsina Facundo Ferrero Restelli Håkan Hedman Fernanda Ledda

ABSTRACT Negative feedback loops represent a regulatory mechanism that guarantees that signaling thresholds are compatible with a physiological response. Previously, we established that Lrig1 acts through this mechanism to inhibit Ret activity. However, it is unclear whether other Lrig family members play similar roles. Here, we show that Lrig1 and Lrig3 are co-expressed in Ret-positive mouse dorsal root ganglion (DRG) neurons. Lrig3, like Lrig1, interacts with Ret and inhibits GDNF/Ret signaling. Treatment of DRG neurons with GDNF ligands induces a significant increase in the expression of Lrig1 and Lrig3. Our findings show that, whereas a single deletion of either Lrig1 or Lrig3 fails to promote Ret-mediated axonal growth, haploinsufficiency of Lrig1 in Lrig3 mutants significantly potentiates Ret signaling and axonal growth of DRG neurons in response to GDNF ligands. We observe that Lrig1 and Lrig3 act redundantly to ensure proper cutaneous innervation of nonpeptidergic axons and behavioral sensitivity to cold, which correlates with a significant increase in the expression of the cold-responsive channel TrpA1. Together, our findings provide insights into the in vivo functions through which Lrig genes control morphology, connectivity and function in sensory neurons.

Haploinsufficiency

Proto-Oncogene Proteins c-ret

Dorsal root ganglion

10.1242/dev.197020

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Citations (3)