Laura Oliveira

ORCID: 0000-0002-8620-077X
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About
Contact & Profiles
Research Areas
  • Ion channel regulation and function
  • Adenosine and Purinergic Signaling
  • Neuroscience and Neuropharmacology Research
  • Receptor Mechanisms and Signaling
  • Neonatal Respiratory Health Research
  • Nicotinic Acetylcholine Receptors Study
  • Healthcare Regulation
  • Myasthenia Gravis and Thymoma
  • Nerve injury and regeneration
  • Nitric Oxide and Endothelin Effects
  • Peripheral Neuropathies and Disorders
  • Neonatal Health and Biochemistry
  • Autoimmune Neurological Disorders and Treatments
  • Vagus Nerve Stimulation Research
  • Muscle and Compartmental Disorders
  • Polyomavirus and related diseases
  • Diabetic Foot Ulcer Assessment and Management
  • Spinal Cord Injury Research
  • Photochromic and Fluorescence Chemistry
  • Pharmacological Receptor Mechanisms and Effects
  • Drilling and Well Engineering
  • Regulation of Appetite and Obesity
  • Healthcare during COVID-19 Pandemic
  • Cardiac electrophysiology and arrhythmias
  • Cooperative Communication and Network Coding

Universidade do Porto
2005-2024

Fundação Faculdade de Medicina
2024

Duke University
2007-2017

Abstract The crosstalk between adenosine and muscarinic autoreceptors regulating evoked [ 3 H]‐acetylcholine ([ H]‐ACh) release was investigated on rat phrenic nerve‐hemidiaphragm preparations. Motor nerve terminals possess facilitatory M 1 inhibitory 2 that can be activated by McN‐A‐343 (1–30 µ m ) oxotremorine (0.3–100 ), respectively. receptor antagonist, dicyclomine (3 n −10 caused a biphasic (inhibitory/facilitatory) effect, indicating ‐facilitation prevails during 5 Hz stimulation...

10.1046/j.1460-9568.2002.02020.x article EN European Journal of Neuroscience 2002-06-01

Nicotinic receptor (nAChR) subtypes involved in pre- and postjunctional actions underlying tetanic fade were studied rat phrenic-nerve hemidiaphragms. We investigated the ability of subtype-specific nAChR antagonists to depress nerve-evoked contractions [(3)H]-acetylcholine ([(3)H]-ACh) release. Muscle tension was transiently increased during brief high frequency trains (50 Hz for 5 sec). The rank potency order reduce peak alpha-bungarotoxin > d-tubocurarine >> mecamylamine hexamethonium....

10.1002/syn.10211 article EN Synapse 2003-04-23

At synapses, ATP is released and metabolised through ecto‐nucleotidases forming adenosine, which modulates neurotransmitter release inhibitory A 1 or facilitatory 2A receptors, according to the amounts of extracellular adenosine. Neuromuscular junctions possess an ecto‐AMP deaminase that can dissociate catabolism from adenosine formation. In this study we have investigated pattern its conversion into probe role in controlling acetylcholine rat phrenic nerve terminals. Nerve‐evoked was 28 ±...

10.1113/jphysiol.2003.040410 article EN The Journal of Physiology 2003-04-08

At the rat motor endplate, pre-synaptic facilitatory adenosine A2A and muscarinic M1 receptors are mutually exclusive. We investigated whether these share a common intracellular signalling pathway. Suppression of McN-A-343-induced facilitation [3H]ACh release was partially recovered when CGS21680C (an agonist) combined with cyclic AMP antagonist Rp-cAMPS. Forskolin, rolipram 8-bromo-cyclic mimicked blockade facilitation. Both Rp-cAMPs nifedipine reduced augmentation by McN-A-343 CGS21680C....

10.1159/000088642 article EN Neurosignals 2005-01-01

In healthy motor endplates, tetanic depression is overcome by tonic adenosine A(2A) -receptor-mediated facilitation of transmitter release. The receptor operates a coordinated shift from fast-desensitizing Ca(v) 2.1 (P/Q) calcium influx to long-lasting Ca(V) 1 (L) channels on nerve terminals. This study aimed at investigating whether receptors-operated Ca(2+) via (L)-type contribute sustain acetylcholine release evoked 50 Hz-bursts in toxin-induced Myasthenia gravis (TIMG) rats. contrast...

10.1111/j.1471-4159.2011.07216.x article EN Journal of Neurochemistry 2011-02-16

AMP dephosphorylation via ecto-5'-nucleotidase/CD73 is the rate limiting step to generate extracellular adenosine (ADO) from released adenine nucleotides. ADO, A2A receptors (A2ARs), a potent modulator of neuromuscular and immunological responses. The pivotal role ecto-5'-nucleotidase/CD73, in controlling ADO formation, prompted us investigate its rat model experimental autoimmune myasthenia gravis (EAMG). Results show that CD4(+)CD25(+)FoxP3(+) regulatory T cells express lower amounts as...

10.1155/2015/460610 article EN cc-by Mediators of Inflammation 2015-01-01

Motor nerve terminals possess multiple voltage-sensitive calcium channels operating acetylcholine (ACh) release. In this study, we investigated whether facilitation of neuromuscular transmission by adenosine generated during neuronal firing was operated Ca(2+) influx via 'prevalent' P-type or the recruitment 'silent' L-type channels. The release [(3)H]ACh from rat phrenic endings decreased upon increasing stimulation frequency trains (750 pulses) 5 Hz (83 +/- 4 x 10(3) disintegrations per...

10.1113/jphysiol.2004.067595 article EN The Journal of Physiology 2004-08-06

Nitric oxide (NO) production and depression of neuromuscular transmission are closely related, but little is known about the role L-citrulline, a co-product NO biosynthesis, on neurotransmitter release.Muscle tension recordings outflow experiments were performed rat phrenic nerve-hemidiaphragm preparations stimulated electrically.L-citrulline concentration-dependently inhibited evoked [(3)H]ACh release from motor nerve terminals depressed nerve-evoked muscle contractions. The synthase (NOS)...

10.1038/sj.bjp.0707242 article EN British Journal of Pharmacology 2007-04-02

Acetylcholine (ACh) spillover from motor endplates occurs after neuronal firing bursts being potentiated by cholinesterase inhibitors (e.g., neostigmine). Nicotinic α7 receptors (α7nAChR) on perisynaptic Schwann cells (PSCs) can control ACh unknown mechanisms. We hypothesized that adenosine might be the gliotransmitter underlying PSCs-nerve terminal communication. Rat isolated hemidiaphragm preparations were used to measure (1) outflow of [3 H]ACh, (2) real-time transmitter exocytosis...

10.1111/jnc.14975 article EN Journal of Neurochemistry 2020-02-03

Lower limb paralysis from spinal cord injury (SCI) or neurological disease carries a poor prognosis for recovery and remains large societal burden. Neurophysiological neuroprosthetic research have the potential to improve quality of life these patients; however, lack an ethical sustainable nonhuman primate model paraplegia hinders their advancement. Therefore, our multidisciplinary team developed way induce temporary in awake behaving macaques by creating fully implantable lumbar epidural...

10.1152/jn.00327.2017 article EN cc-by-nd Journal of Neurophysiology 2017-07-13

Abstract Acetylcholine (ACh) facilitates its own release acting at muscarinic M 1 receptors on rat motoneurons. While the positive feedback mechanism is operative there a concomitant suppression of ability 2 ‐inhibitory and adenosine A 2A ‐facilitatory to control [ 3 H]ACh release. We aimed investigating whether ‐occlusion function could result from interplay second messengers level. Drugs blocking IP pathway, like LiCl 2‐aminoethoxydiphenylborane (2‐APB), but not selective PKC inhibitor,...

10.1002/sita.200500057 article EN Signal Transduction 2006-02-01

A cirurgia metabólica tem emergido como uma abordagem eficaz no tratamento do diabetes mellitus tipo 2 (DM2), particularmente em pacientes com obesidade. Este estudo apresenta revisão integrativa o objetivo de avaliar impacto dessa intervenção controle DM2, analisando os mecanismos metabólicos subjacentes, a eficácia na remissão da doença e benefícios longo prazo. Foram selecionados estudos publicados entre 2010 2023, utilizando bases dados PubMed, Scopus LILACS. Os resultados demonstraram...

10.51891/rease.v10i10.16223 article PT cc-by Revista Ibero-Americana de Humanidades, Ciências e Educação 2024-10-14

Introdução: A Esteatohepatite Não Alcoólica (NASH) é uma condição progressiva do fígado associada à obesidade e resistência insulina, que pode evoluir para cirrose carcinoma hepatocelular. As intervenções nutricionais têm sido estudadas como abordagem não invasiva retardar a progressão da doença, mas as evidências sobre sua eficácia ainda são dispersas. Objetivo: Esta revisão crítica visa analisar o impacto das na NASH, com ênfase nas mudanças dietéticas suas implicações no controle...

10.51891/rease.v1i01.16224 article PT cc-by Revista Ibero-Americana de Humanidades, Ciências e Educação 2024-10-14
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