Publication List

@article{Racz2008,
title = {Interferon-gamma is a critical modulator of CB(2) cannabinoid receptor signaling during neuropathic pain.},
author = {Racz, Ildiko and Nadal, Xavier and Alferink, Judith and Baños, Josep E and Rehnelt, Jennifer and Martín, Miquel and Pintado, Belén and Gutierrez-Adan, Alfonso and Sanguino, Elena and Bellora, Nicolas and Manzanares, Jorge and Zimmer, Andreas and Maldonado, Rafael},
url = {http://www.ncbi.nlm.nih.gov/pubmed/19005078},
issn = {1529-2401},
year = {2008},
date = {2008-01-01},
journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
volume = {28},
number = {46},
pages = {12136--45},
abstract = {Nerve injuries often lead to neuropathic pain syndrome. The mechanisms contributing to this syndrome involve local inflammatory responses, activation of glia cells, and changes in the plasticity of neuronal nociceptive pathways. Cannabinoid CB(2) receptors contribute to the local containment of neuropathic pain by modulating glial activation in response to nerve injury. Thus, neuropathic pain spreads in mice lacking CB(2) receptors beyond the site of nerve injury. To further investigate the mechanisms leading to the enhanced manifestation of neuropathic pain, we have established expression profiles of spinal cord tissues from wild-type and CB(2)-deficient mice after nerve injury. An enhanced interferon-gamma (IFN-gamma) response was revealed in the absence of CB(2) signaling. Immunofluorescence stainings demonstrated an IFN-gamma production by astrocytes and neurons ispilateral to the nerve injury in wild-type animals. In contrast, CB(2)-deficient mice showed neuronal and astrocytic IFN-gamma immunoreactivity also in the contralateral region, thus matching the pattern of nociceptive hypersensitivity in these animals. Experiments in BV-2 microglia cells revealed that transcriptional changes induced by IFN-gamma in two key elements for neuropathic pain development, iNOS (inducible nitric oxide synthase) and CCR2, are modulated by CB(2) receptor signaling. The most direct support for a functional involvement of IFN-gamma as a mediator of CB(2) signaling was obtained with a double knock-out mouse strain deficient in CB(2) receptors and IFN-gamma. These animals no longer show the enhanced manifestations of neuropathic pain observed in CB(2) knock-outs. These data clearly demonstrate that the CB(2) receptor-mediated control of neuropathic pain is IFN-gamma dependent.},
keywords = {Animals, Astrocytes, Astrocytes: immunology, Cannabinoid, CB2, CB2: genetics, CB2: immunology, CB2: metabolism, CCR2, CCR2: immunology, CCR2: metabolism, Cells, Cultured, Gene Knockout Techniques, Gene Knockout Techniques: methods, Hyperalgesia, Hyperalgesia: immunology, Hyperalgesia: physiopathology, Interferon-gamma, Interferon-gamma: genetics, Interferon-gamma: immunology, Interferon-gamma: metabolism, Knockout, Male, Mice, Microglia, Microglia: drug effects, Microglia: immunology, Microglia: metabolism, Neuralgia, Neuralgia: genetics, Neuralgia: immunology, Neuralgia: metabolism, Neurons, Neurons: immunology, Nitric Oxide Synthase Type II, Nitric Oxide Synthase Type II: immunology, Nitric Oxide Synthase Type II: metabolism, Peripheral Nerves, Peripheral Nerves: immunology, Peripheral Nerves: injuries, Peripheral Nerves: physiopathology, Peripheral Nervous System Diseases, Peripheral Nervous System Diseases: genetics, Peripheral Nervous System Diseases: immunology, Peripheral Nervous System Diseases: metabolism, Receptor, Receptors, Signal Transduction, Signal Transduction: genetics, Signal Transduction: immunology, Spinal Cord, Spinal Cord: immunology, Spinal Cord: metabolism, Spinal Cord: physiopathology, Up-Regulation, Up-Regulation: immunology}
}

@article{Gibbs2004,
title = {Genome sequence of the Brown Norway rat yields insights into mammalian evolution.},
author = {Gibbs, Richard A and Et al.},
url = {http://www.ncbi.nlm.nih.gov/pubmed/15057822},
issn = {1476-4687},
year = {2004},
date = {2004-01-01},
journal = {Nature},
volume = {428},
number = {6982},
pages = {493--521},
abstract = {The laboratory rat (Rattus norvegicus) is an indispensable tool in experimental medicine and drug development, having made inestimable contributions to human health. We report here the genome sequence of the Brown Norway (BN) rat strain. The sequence represents a high-quality 'draft' covering over 90% of the genome. The BN rat sequence is the third complete mammalian genome to be deciphered, and three-way comparisons with the human and mouse genomes resolve details of mammalian evolution. This first comprehensive analysis includes genes and proteins and their relation to human disease, repeated sequences, comparative genome-wide studies of mammalian orthologous chromosomal regions and rearrangement breakpoints, reconstruction of ancestral karyotypes and the events leading to existing species, rates of variation, and lineage-specific and lineage-independent evolutionary events such as expansion of gene families, orthology relations and protein evolution.},
keywords = {Animals, Base Composition, Centromere, Centromere: genetics, Chromosomes, CpG Islands, CpG Islands: genetics, DNA, DNA Transposable Elements, DNA Transposable Elements: genetics, Evolution, Gene Duplication, Genome, Genomics, Humans, Inbred BN, Inbred BN: genetics, Introns, Introns: genetics, Male, Mammalian, Mammalian: genetics, Mice, Mitochondrial, Mitochondrial: genetics, Models, Molecular, Mutagenesis, Nucleic Acid, Nucleic Acid: genetics, Polymorphism, Rats, Regulatory Sequences, Retroelements, Retroelements: genetics, RNA, RNA Splice Sites, RNA Splice Sites: genetics, Sequence Analysis, Single Nucleotide, Single Nucleotide: genetics, Telomere, Telomere: genetics, Untranslated, Untranslated: genetics}
}