Josep Tomàs

ORCID: 0000-0002-0406-0006
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About
Contact & Profiles
Research Areas
  • Ion channel regulation and function
  • Neuroscience and Neuropharmacology Research
  • Nerve injury and regeneration
  • Neuroscience and Neural Engineering
  • Cellular transport and secretion
  • Neurogenesis and neuroplasticity mechanisms
  • Receptor Mechanisms and Signaling
  • Attention Deficit Hyperactivity Disorder
  • Neurobiology and Insect Physiology Research
  • Adenosine and Purinergic Signaling
  • Amyotrophic Lateral Sclerosis Research
  • Lipid Membrane Structure and Behavior
  • Laser Applications in Dentistry and Medicine
  • Peripheral Neuropathies and Disorders
  • Photoreceptor and optogenetics research
  • Cholinesterase and Neurodegenerative Diseases
  • Muscle Physiology and Disorders
  • Genetic Neurodegenerative Diseases
  • Hereditary Neurological Disorders
  • Plant and Biological Electrophysiology Studies
  • Signaling Pathways in Disease
  • Medical research and treatments
  • Nicotinic Acetylcholine Receptors Study
  • Advanced Neuroimaging Techniques and Applications
  • Functional Brain Connectivity Studies

Universitat Rovira i Virgili
2015-2024

Institut d'Investigació Sanitària Pere Virgili
2024

Zero to Three
2023

Vall d'Hebron Hospital Universitari
2005-2023

Universitat Autònoma de Barcelona
2004

Fundación Ciencias Exactas y Naturales
2003

University of Buenos Aires
2003

Osmania University
1996

Universitat de Barcelona
1976-1992

10.1007/bf01691806 article EN Bulletin of Environmental Contamination and Toxicology 1987-07-01

The neurotrophin Brain-derived neurotrophic factor (BDNF) acts via tropomyosin-related kinase B receptor (TrkB) to regulate synapse maintenance and function in the neuromuscular system. potentiation of ACh release by BDNF requires TrkB phosphorylation Protein Kinase C (PKC) activation. is secreted an activity-dependent manner but it not known if pre- and/or postsynaptic activities enhance expression vivo at junction (NMJ). Here, we investigated whether nerve muscle cell presynaptic...

10.3389/fnmol.2017.00147 article EN cc-by Frontiers in Molecular Neuroscience 2017-05-18

Abstract We studied the presynaptic muscarinic autoreceptor subtypes controlling ACh release and their relationship with voltage‐dependent calcium channels in neuromuscular synapses of Levator auris longus muscle from adult (30–40 days) newborn (3–6 15 days postnatal) rats. Using intracellular recording, we how several antagonists affected evoked endplate potentials. In some experiments previously incubated channel blockers (nitrendipine, ω‐conotoxin‐GVIA ω‐Agatoxin‐IVA) before determining...

10.1046/j.1460-9568.2003.02428.x article EN European Journal of Neuroscience 2003-01-01

Abstract We have used intracellular recording to investigate the existence of a functional link between muscarinic presynaptic acetylcholine (ACh) autoreceptors, serine‐threonine kinases‐mediated transduction pathways and transmitter release in motor nerve terminals adult rats. found following. (1) Transmitter was reduced by M1 receptor (mAChR) blocker pirenzepine enhanced M2 methoctramine. The unselective mAChR atropine increased ACh release, which suggests unmasking another parallel...

10.1111/j.1460-9568.2006.04753.x article EN European Journal of Neuroscience 2006-04-01

The neurotrophin brain-derived neurotrophic factor (BDNF), neurotrophin-4 (NT-4) and the receptors tropomyosin-related kinase B (trkB) p75 NTR are present in nerve terminals on neuromuscular junctions (NMJs) of levator auris longus muscle adult mouse. Exogenously added BDNF or NT-4 increased evoked ACh release after 3 h. This presynaptic effect (the size spontaneous potentials is not affected) specific because it produced by neurotrophin-3 (NT-3) prevented preincubation with trkB-IgG chimera...

10.1523/jneurosci.2676-10.2010 article EN cc-by-nc-sa Journal of Neuroscience 2010-12-08

The development of the nervous system involves an initially exuberant production neurons that make excessive number synaptic contacts. initial overproduction synapses promotes connectivity. Hebbian competition between axons with different activities (the least active are punished) leads to loss roughly half overproduced elements and this refines connectivity increases specificity. neuromuscular junction is innervated by a single axon at end synapse elimination process and, because its...

10.1186/s13041-016-0248-9 article EN cc-by Molecular Brain 2016-06-23

Abstract Vanadium (in the form of NaVO 3 ) was given in drinking water to groups 10 male Sprague‐Dawley rats over a period months at concentrations 0, 5, and 50 ppm. accumulated dose‐dependently kidneys spleen. Appearance, behaviour, food consumption, growth mortality treated all were not affected during 3‐month period. Histopathological investigation showed only mild though dose‐dependent lesions The plasma urea uric acid increased highest exposure groups.

10.1002/jat.2550050616 article EN Journal of Applied Toxicology 1985-12-01

Neurotrophins and their receptors, the trk receptor tyrosine kinases (trks) p75 NTR , are differentially expressed among cell types that make up synapses. It is important to determine precise location of these molecules involved in neurotransmission. Here we use immunostaining Western blotting study localization expression neurotrophin brain‐derived neurotrophic factor (BDNF) neurotrophin‐4 (NT‐4) receptors tropomyosin‐related kinase b (trkB) at adult neuromuscular junction. Our confocal...

10.1111/j.1529-8027.2010.00250.x article EN Journal of the Peripheral Nervous System 2010-03-01

Myofascial pain syndrome is one of the most common forms muscle pain. In this syndrome, originated by so-called trigger points, which consists a set palpable contraction knots in muscle. It has been proposed that high, spontaneous neurotransmission may be involved generation these knots. To confirm hypothesis, we exposed mouse muscles to an anticholinesterasic agent increase neurotransmision synaptic cleft two different conditions, vivo and ex experiments. Using intracellular recordings,...

10.1152/japplphysiol.00248.2018 article EN Journal of Applied Physiology 2018-10-11

Bidirectional communication between presynaptic and postsynaptic components contribute to the homeostasis of synapse. In neuromuscular synapse, arrival nerve impulse at terminal triggers molecular mechanisms associated with ACh release, which can be retrogradely regulated by resulting muscle contraction. This retrograde regulation, however, has been poorly studied. At junction (NMJ), protein kinase A (PKA) enhances neurotransmitter phosphorylation molecules release machinery including...

10.1186/s11658-023-00431-2 article EN cc-by Cellular & Molecular Biology Letters 2023-03-03

Individual skeletal muscle fibers in most new-born rodents are innervated at a single endplate by several motor axons. During the first postnatal weeks, polyneuronal innervation decreases process of synaptic elimination. Previous studies showed that naturally occurring serine-protease thrombin mediates activity-dependent synapse reduction neuromuscular junction (NMJ) vitro and thrombin-receptor activation may modulate nerve terminal consolidation through protein kinase mechanism. To test...

10.1002/1097-4547(20010215)63:4<330::aid-jnr1027>3.0.co;2-w article EN Journal of Neuroscience Research 2001-01-01

Using intracellular recording and immunohistochemistry, we studied the presynaptic muscarinic autoreceptor subtypes controlling ACh release in neuromuscular junctions of newborn (3-6 days postnatal) adult (30-40 days) rat. In Levator auris longus muscles both rats, acetylcholine was modified by M1-receptor selective antagonists pirenzepine (10 microM) MT-7 (100 nM) M2-receptor methoctramine (1 AF-DX 116 microM). The M4-receptor tropicamide MT-3 can also modify neurotransmitter certain...

10.14670/hh-20.733 article EN PubMed 2005-07-01

The distribution of acetylcholine receptors (AChRs) within and around the neuromuscular junction changes dramatically during first postnatal weeks, a period which polyneuronal innervation is eliminated. We reported previously that protein kinase C (PKC) activation accelerates synapse loss. Because close relationship between axonal retraction AChR cluster dispersal, we hypothesize PKC can modulate morphological maturation clusters in postsynaptic membrane neonatal reduction. applied...

10.1002/jnr.10122 article EN Journal of Neuroscience Research 2002-01-29

We use immunohistochemistry to describe the localization of brain-derived neurotrophic factor (BDNF) and its receptors trkB p75(NTR) in neuromuscular synapses postnatal rats (P6-P7) during synapse elimination period. The receptor protein is present nerve terminal, muscle cell glial Schwann whereas BDNF proteins can be detected mainly pre- postsynaptic elements. Exogenously applied (10 nM for 3 hr or 50 1 hr) increases ACh release from singly dually innervated synapses. This effect may...

10.1002/jnr.22320 article EN Journal of Neuroscience Research 2009-12-22

Abstract Immunocytochemistry shows that purinergic receptors (P1Rs) type A1 and A2A (A 1 R A 2 , respectively) are present in the nerve endings at P6 P30 Levator auris longus ( LAL ) mouse neuromuscular junctions NMJ s). As described elsewhere, 25 μ m adenosine reduces (50%) acetylcholine release high Mg 2+ or d ‐tubocurarine paralysed muscle. We hypothesize more preserved neurotransmission machinery conditions (blocking voltage‐dependent sodium channel of muscle cells with μ‐conotoxin GIIIB...

10.1111/ejn.12220 article EN European Journal of Neuroscience 2013-04-22

Adenosine receptors (ARs) are present in the motor terminals at mouse neuromuscular junction. ARs and presynaptic muscarinic acetylcholine (mAChRs) share functional control of We analysed their mutual interaction transmitter release modulation. In electrophysiological experiments with unaltered synaptic transmission (muscles paralysed by blocking voltage-dependent sodium channel muscle cells μ-conotoxin GIIIB), we found that: (i) a collaborative action between different AR subtypes reduced...

10.1111/ejn.12922 article EN European Journal of Neuroscience 2015-04-17

Protein kinase C (PKC) regulates a variety of neural functions, including neurotransmitter release. Although various PKC isoforms can be expressed at the synaptic sites and specific cell distribution may contribute to their functional diversity, little is known about isoform-specific functions PKCs in neuromuscular synapse. The present study designed examine location novel isoform nPKCε junction (NMJ), activity-related expression changes, its regulation by muscle contraction, possible...

10.1186/s13041-015-0098-x article EN cc-by Molecular Brain 2015-02-09
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