Erica Hurtado

Universidad Rovira i Virgili

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

María A. Lanuza

Universidad Rovira i Virgili

Josep Tomàs

Universidad Rovira i Virgili

Marta Tomás

Universidad Rovira i Virgili

Neus García

Case Western Reserve University

Víctor Cilleros‐Mañé

Universidad Rovira i Virgili

Laura Nadal

Universidad Rovira i Virgili

Anna Simó

Universidad Rovira i Virgili

Laia Just‐Borràs

Universidad Rovira i Virgili

Manel M. Santafé

Universidad Rovira i Virgili

Teresa Obis

Almirall (Spain)

Cooperative Institutions

Universidad Rovira i Virgili

Institute of Predictive and Personalized Medicine of Cancer

Universitat de Barcelona

Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol

Loma Linda University

Centre National de la Recherche Scientifique

Institut d'Investigació Sanitària Pere Virgili

George Washington University

Children's National

University of Buenos Aires

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Adenosine A2B and A3 receptor location at the mouse neuromuscular junction

Journal of Anatomy (2014)

Neus García Mercedes Priego Erica Hurtado Teresa Obis Manel M. Santafé

Abstract To date, four subtypes of adenosine receptors have been cloned (A 1 R, A 2A R, A 2B R, and A 3 R). In a previous study we used confocal immunocytochemistry to identify A 1 R and A 2A R receptors at mouse neuromuscular junctions ( NMJ s). The data shows that these receptors are localized differently in the three cells (muscle, nerve and glia) that configure the NMJ s. A 1 R localizes in the terminal teloglial S chwann cell and nerve terminal, whereas A 2A R localizes in the postsynaptic muscle and in the axon and nerve terminal. Here, we use W estern blotting to investigate the presence of A 2B R and A 3 R receptors in striated muscle and immunohistochemistry to localize them in the three cells of the adult neuromuscular synapse. The data show that A 2B R and A 3 R receptors are present in the nerve terminal and muscle cells at the NMJ s. Neither A 2B R nor A 3 R receptors are localized in the S chwann cells. Thus, the four subtypes of adenosine receptors are present in the motor endings. The presence of these receptors in the neuromuscular synapse allows the receptors to be involved in the modulation of transmitter release.

10.1111/joa.12188

Cite

Citations (15)

Presynaptic muscarinic acetylcholine autoreceptors (M1, M2 and M4 subtypes), adenosine receptors (A1 and A2A) and tropomyosin-related kinase B receptor (TrkB) modulate the developmental synapse elimination process at the neuromuscular junction

Molecular Brain (2016)

Laura Nadal Neus García Erica Hurtado Anna Simó Marta Tomás

The development of the nervous system involves an initially exuberant production of neurons that make an excessive number of synaptic contacts. The initial overproduction of synapses promotes connectivity. Hebbian competition between axons with different activities (the least active are punished) leads to the loss of roughly half of the overproduced elements and this refines connectivity and increases specificity. The neuromuscular junction is innervated by a single axon at the end of the synapse elimination process and, because of its relative simplicity, has long been used as a model for studying the general principles of synapse development. The involvement of the presynaptic muscarinic ACh autoreceptors may allow for the direct competitive interaction between nerve endings through differential activity-dependent acetylcholine release in the synaptic cleft. Then, the most active ending may directly punish the less active ones. Our previous results indicate the existence in the weakest axons on the polyinnervated neonatal NMJ of an ACh release inhibition mechanism based on mAChR coupled to protein kinase C and voltage-dependent calcium channels. We suggest that this mechanism plays a role in the elimination of redundant neonatal synapses.Here we used confocal microscopy and quantitative morphological analysis to count the number of brightly fluorescent axons per endplate in P7, P9 and P15 transgenic B6.Cg-Tg (Thy1-YFP)16 Jrs/J mice. We investigate the involvement of individual mAChR M1-, M2- and M4-subtypes in the control of axonal elimination after the Levator auris longus muscle had been exposed to agonist and antagonist in vivo. We also analysed the role of adenosine receptor subtypes (A1 and A2A) and the tropomyosin-related kinase B receptor. The data show that postnatal axonal elimination is a regulated multireceptor mechanism that guaranteed the monoinnervation of the neuromuscular synapses.The three receptor sets considered (mAChR, AR and TrkB receptors) intervene in modulating the conditions of the competition between nerve endings, possibly helping to determine the winner or the lossers but, thereafter, the final elimination would occur with some autonomy and independently of postsynaptic maturation.

Adenosine A2A receptor

Curare

10.1186/s13041-016-0248-9

Cite

Citations (40)

BDNF/TrkB signalling, in cooperation with muscarinic signalling, retrogradely regulates PKA pathway to phosphorylate SNAP-25 and Synapsin-1 at the neuromuscular junction

Cell Communication and Signaling (2024)

А. А. Поліщук Víctor Cilleros‐Mañé Marta Balanyà-Segura Laia Just‐Borràs Anton Forniés-Mariné

Protein kinase A (PKA) enhances neurotransmission at the neuromuscular junction (NMJ), which is retrogradely regulated by nerve-induced muscle contraction to promote Acetylcholine (ACh) release through the phosphorylation of molecules involved in synaptic vesicle exocytosis (SNAP-25 and Synapsin-1). However, the molecular mechanism of the retrograde regulation of PKA subunits and its targets by BDNF/TrkB pathway and muscarinic signalling has not been demonstrated until now. At the NMJ, retrograde control is mainly associated with BDNF/TrkB signalling as muscle contraction enhances BDNF levels and controls specific kinases involved in the neurotransmission. Neurotransmission at the NMJ is also highly modulated by muscarinic receptors M

Synapsin

Synapsin I

10.1186/s12964-024-01735-2

Cite

Citations (0)

Running and swimming prevent the deregulation of the BDNF/TrkB neurotrophic signalling at the neuromuscular junction in mice with amyotrophic lateral sclerosis

Cellular and Molecular Life Sciences (2019)

Laia Just‐Borràs Erica Hurtado Víctor Cilleros‐Mañé Olivier Biondi Frédéric Charbonnier

Neuromuscular transmission

10.1007/s00018-019-03337-5

Cite

Citations (35)