A5058483077- Adenosine and Purinergic Signaling
- Neuroscience and Neuropharmacology Research
- Receptor Mechanisms and Signaling
- Neuroinflammation and Neurodegeneration Mechanisms
- Vagus Nerve Stimulation Research
- Alzheimer's disease research and treatments
- Cannabis and Cannabinoid Research
- Pharmacological Receptor Mechanisms and Effects
- Ion channel regulation and function
- Tryptophan and brain disorders
- Nerve injury and regeneration
- Coffee research and impacts
- Parkinson's Disease Mechanisms and Treatments
- Neurotransmitter Receptor Influence on Behavior
- Nicotinic Acetylcholine Receptors Study
- Biochemical effects in animals
- Neurological Complications and Syndromes
- Sleep and Wakefulness Research
- Neuroscience of respiration and sleep
- Neurological disorders and treatments
- Memory and Neural Mechanisms
- Neuroendocrine regulation and behavior
- Genetics and Neurodevelopmental Disorders
- Bipolar Disorder and Treatment
- Adipose Tissue and Metabolism
University of Coimbra
2016-2025
Instituto Politécnico de Santarém
2025
Centro de Neurociências e Biologia Celular
2011-2024
University of Minho
2024
Centre for Human Drug Research
2022
Leiden University
2022
University of Bonn
2022
Universidade Federal de Santa Catarina
2022
University of Rio Grande and Rio Grande Community College
2022
Universidade Federal do Rio Grande do Sul
2022
The functional role of heteromers G-protein-coupled receptors is a matter debate. In the present study, we demonstrate that heteromerization adenosine A 1 (A Rs) and 2A allows to exert fine-tuning modulation glutamatergic neurotransmission. By means coimmunoprecipitation, bioluminescence time-resolved fluorescence resonance energy transfer techniques, showed existence R–A R in cell surface cotransfected cells. Immunogold detection coimmunoprecipitation experiments indicated are colocalized...
Adenosine is a neuromodulator that operates via the most abundant inhibitory adenosine A1 receptors (A1Rs) and less abundant, but widespread, facilitatory A2ARs. It commonly assumed A1Rs play key role in neuroprotection since they decrease glutamate release hyperpolarize neurons. In fact, A1R activation at onset of neuronal injury attenuates brain damage, whereas its blockade exacerbates damage adult animals. However, there down-regulation central chronic noxious situations. contrast, A2ARs...
Alzheimer's disease (AD) is characterized by memory impairment, neurochemically accumulation of β-amyloid peptide (namely Aβ 1-42 ) and morphologically an initial loss nerve terminals. Caffeine consumption prevents dysfunction in different models, which mimicked antagonists adenosine A 2A receptors (A Rs), are located synapses. Thus, we now tested whether R blockade the early -induced synaptotoxicity what underlying signaling pathways. The intracerebral administration soluble (2 nmol) rats...
Significance Epidemiological studies show that individuals exposed to repeated stress, a major trigger of depression, increase their caffeine intake, which correlates inversely with the incidence depression. However, mechanism underlying this protective effect is unknown. We used an animal model chronic unpredictable stress (CUS) prevents maladaptive changes caused by CUS in manner mimicked selective blockade adenosine A 2A receptors (A R). enhanced R synapses, and elimination neuronal...
Abstract Synaptic plasticity in the autoassociative network of recurrent connections among hippocampal CA3 pyramidal cells is thought to enable storage episodic memory. Impaired memory an early manifestation cognitive deficits Alzheimer’s disease (AD). In APP/PS1 mouse model AD amyloidosis, we show that associative long-term synaptic potentiation (LTP) abolished at stage. This caused by activation upregulated neuronal adenosine A 2A receptors (A R) rather than dysregulation NMDAR signalling...
Brain-derived neurotrophic factor (BDNF) has been shown to control microglial responses in neuropathic pain. Since adenosine A2A receptors (A2ARs) neuroinflammation, as well the production and function of BDNF, we tested see if A2AR controls microglia-dependent secretion BDNF proliferation cells, a crucial event neuroinflammation.Murine N9 cells were challenged with lipopolysaccharide (LPS, 100 ng/mL) absence or presence antagonist, SCH58261 (50 nM), other modulators signaling. The cellular...
Abstract Flickering light stimulation has emerged as a promising non-invasive neuromodulation strategy to alleviate neuropsychiatric disorders. However, the lack of neurochemical underpinning hampered its therapeutic development. Here, we demonstrate that flickering triggered an immediate and sustained increase (up 3 h after flickering) in extracellular adenosine levels primary visual cortex (V1) other brain regions, function frequency intensity, with maximal effects observed at 40 Hz 4000...
Abstract: The release of adenosine and ATP evoked by electrical field stimulation in rat hippocampal slices was investigated with the following two patterns stimulation: (1) a brief, high‐frequency burst (trains stimuli at 100 Hz for 50 ms applied every 2 s 1 min), to mimic long‐term potentiation (LTP) paradigm, (2) more prolonged (3 min) low‐frequency (5 Hz) train stimulation, depression (LTD) paradigm. greater whereas [ 3 H]adenosine slightly stimulation. To investigate source...
Despite the profound effect of cannabinoids on motor function, and their therapeutic potential in Parkinson's Huntington's diseases, cellular subcellular distributions striatal CB 1 receptors are not well defined. Here, we show that primarily located GABAergic (vesicular GABA transporter-positive) glutamatergic [vesicular glutamate transporter-1 (VGLUT-1)- VGLUT-2-positive] nerve terminals present presynaptic active zone, postsynaptic density, as extrasynaptic membrane. Both nonselective...
ATP analogs substituted in the γ-phosphorus (ATPγS, β,γ-imido-ATP, and β,γ-methylene-ATP) were used to probe involvement of P 2 receptors modulation synaptic transmission hippocampus, because their extracellular catabolism was virtually not detected CA1 slices. γ-substituted equipotent inhibit pyramid synapses (IC 50 17–22 μ m ). The inhibitory effect γ-phosphorus-substituted (30 ) modified by receptor antagonist suramin (100 ), inhibited 42–49% ecto-5′-nucleotidase inhibitor α,β-methylene...