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12 results on '"Pablo Galeano"'

1. Platelets Bioenergetics Screening Reflects the Impact of Brain Aβ Plaque Accumulation in a Rat Model of Alzheimer

Author

A. Claudio Cuello, Pamela V. Martino Adami, Laura Morelli, Eduardo M. Castaño, Pablo Galeano, Sonia Do Carmo, and Federico A. Prestia

Subjects
Blood Platelets, 0301 basic medicine, medicine.medical_specialty, CIENCIAS MÉDICAS Y DE LA SALUD, Bioenergetics, Plaque, Amyloid, Oxidative phosphorylation, AMYLOID β, Carbohydrate metabolism, Hippocampal formation, medicine.disease_cause, Hippocampus, Biochemistry, Amyloid beta-Protein Precursor, 03 medical and health sciences, Cellular and Molecular Neuroscience, 0302 clinical medicine, Alzheimer Disease, Internal medicine, medicine, Animals, Neurochemistry, Platelet, PLATELET BIOENERGETIC, business.industry, General Medicine, BLOOD-BASED BIOENERGETIC PROFILING, Bioquímica y Biología Molecular, Mitochondria, Rats, 3. Good health, Medicina Básica, 030104 developmental biology, Endocrinology, ALZHEIMER'S DISEASE, BRAIN DYSFUNCTION, Biomarker (medicine), Rats, Transgenic, Energy Metabolism, business, TRANSGENIC RAT, 030217 neurology & neurosurgery, Oxidative stress
Abstract

Alzheimer’s disease (AD) is associated to depressed brain energy supply and impaired cortical and hippocampal synaptic function. It was previously reported in McGill-R-Thy1-APP transgenic (Tg(+/+)) rats that Aβ deposition per se is sufficient to cause abnormalities in glucose metabolism and neuronal connectivity. These data support the utility of this animal model as a platform for the search of novel AD biomarkers based on bioenergetic status. Recently, it has been proposed that energy dysfunction can be dynamically tested in platelets (PLTs) of nonhuman primates. PLTs are good candidates to find peripheral biomarkers for AD because they may reflect in periphery the bioenergetics deficits and the inflammatory and oxidative stress processes taking place in AD brain. In the present study, we carried out a PLTs bioenergetics screening in advanced-age (12–14 months old) control (WT) and Tg(+/+) rats. Results indicated that thrombin-activated PLTs of Tg(+/+) rats showed a significantly lower respiratory rate, as compared to that measured in WT animals, when challenged with the same dose of FCCP (an uncoupler of oxidative phosphorylation). In summary, our results provide original evidence that PLTs bioenergetic profiling may reflect brain bioenergetics dysfunction mediated by Aβ plaque accumulation. Further studies on human PLTs from control and AD patients are required to validate the usefulness of PLTs bioenergetics as a novel blood-based biomarker for AD. Fil: Prestia, Federico A.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Galeano, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Martino Adami, Pamela Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Do Carmo, Sonia. McGill University; Canadá Fil: Castaño, Eduardo Miguel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Cuello, A. Claudio. McGill University; Canadá Fil: Morelli, Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina

Published
2018
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2. Synaptosomal bioenergetic defects are associated with cognitive impairment in a transgenic rat model of early Alzheimer's disease

Author

Pamela V. Martino Adami, Laura Morelli, Sonia Do Carmo, Adriana Cassina, Pablo Galeano, Maria Celeste Leal, Pablo Evelson, Natalia Magnani, Eduardo M. Castaño, Claudio Cuello, and Cecilia Quijano

Subjects
0301 basic medicine, medicine.medical_specialty, CIENCIAS MÉDICAS Y DE LA SALUD, Diet therapy, Amyloid beta, Transgene, Neurociencias, PQQ Cofactor, Mitochondrion, Neuroprotection, 03 medical and health sciences, 0302 clinical medicine, Alzheimer Disease, hippocampal bioenergetics status, Internal medicine, medicine, Animals, Cognitive Dysfunction, Electron Transport Complex I, biology, Neurodegeneration, synaptosomes, Original Articles, early-Alzheimer, medicine.disease, Mitochondria, Rats, Disease Models, Animal, Medicina Básica, 030104 developmental biology, Endocrinology, Neurology, Mitochondrial biogenesis, biology.protein, Neurology (clinical), Rats, Transgenic, Alzheimer's disease, Energy Metabolism, Cardiology and Cardiovascular Medicine, Neuroscience, 030217 neurology & neurosurgery, Diet Therapy, Synaptosomes
Abstract

Synaptic bioenergetic deficiencies may be associated with early Alzheimer's disease (AD). To explore this concept, we assessed pre-synaptic mitochondrial function in hemizygous (+/-)TgMcGill-R-Thy1-APP rats. The low burden of Aβ and the wide array of behavioral and cognitive impairments described in 6-month-old hemizygous TgMcGill-R-Thy1-APP rats (Tg(+/-)) support their use to investigate synaptic bioenergetics deficiencies described in subjects with early Alzheimer's disease (AD). In this report, we show that pre-synaptic mitochondria from Tg(+/-) rats evidence a decreased respiratory control ratio and spare respiratory capacity associated with deficits in complex I enzymatic activity. Cognitive impairments were prevented and bioenergetic deficits partially reversed when Tg(+/-) rats were fed a nutritionally complete diet from weaning to 6-month-old supplemented with pyrroloquinoline quinone, a mitochondrial biogenesis stimulator with antioxidant and neuroprotective effects. These results provide evidence that, as described in AD brain and not proven in Tg mice models with AD-like phenotype, the mitochondrial bioenergetic capacity of synaptosomes is not conserved in the Tg(+/-) rats. This animal model may be suitable for understanding the basic biochemical mechanisms involved in early AD Fil: Martino Adami, Pamela Victoria. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquimicas de Buenos Aires; Argentina Fil: Quijano, Cecilia. Universidad de la Republica; Uruguay Fil: Magnani, Natalia Daniela. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular; Argentina Fil: Galeano, Pablo. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquimicas de Buenos Aires; Argentina Fil: Evelson, Pablo Andres. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular; Argentina Fil: Cassina, Adriana. Universidad de la Republica; Uruguay Fil: Do Carmo, Sonia. Mc Gill University; Canadá Fil: Leal, Maria Celeste. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquimicas de Buenos Aires; Argentina Fil: Castaño, Eduardo Miguel. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquimicas de Buenos Aires; Argentina Fil: Cuello, Claudio. Mc Gill University; Canadá Fil: Morelli, Laura. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquimicas de Buenos Aires; Argentina

Published
2016
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3. Palmitoylethanolamide prevents neuroinflammation, reduces astrogliosis and preserves recognition and spatial memory following induction of neonatal anoxia-ischemia

Author

Juan Ignacio Romero, Fernando Rodríguez de Fonseca, Emilio Fernández-Espejo, Mariana Inés Holubiec, Eduardo Blanco, Juan Suárez, Manuel Portavella, and Pablo Galeano

Subjects
0301 basic medicine, CIENCIAS MÉDICAS Y DE LA SALUD, Neonatal anoxia, Pharmacology toxicology, Neurociencias, Ischemia, Oleic Acids, Palmitic Acids, Pharmacology, Hippocampus, Neonatal anoxia-ischemia, Rats, Sprague-Dawley, 03 medical and health sciences, Oleoylethanolamide, chemistry.chemical_compound, 0302 clinical medicine, Neuroinflammation, ASTROGLIOSIS, medicine, Animals, PPAR alpha, Palmitoylethanolamide, MEMORY IMPAIRMENT, Spatial Memory, business.industry, Recognition, Psychology, medicine.disease, Lipid Metabolism, Amides, Astrogliosis, Rats, Medicina Básica, Disease Models, Animal, 030104 developmental biology, Glucose, chemistry, Ethanolamines, Hypoxia-Ischemia, Brain, Female, business, 030217 neurology & neurosurgery, Locomotion, Endocannabinoids
Abstract

Rational: Neonatal anoxia-ischemia (AI) particularly affects the central nervous system. Despite the many treatments that have been tested, none of them has proven to be completely successful. Palmitoylethanolamide (PEA) and oleoylethanolamide (OEA) are acylethanolamides that do not bind to CB1 or CB2 receptors and thus they do not present cannabinoid activity. These molecules are agonist compounds of peroxisome proliferator-activator receptor alpha (PPARα), which modulates the expression of different genes that are related to glucose and lipid metabolism, inflammation, differentiation and proliferation. Objective: In the present study, we analyzed the effects that the administration of PEA or OEA, after a neonatal AI event, has over different areas of the hippocampus. Methods: To this end, 7-day-old rats were subjected to AI and then treated with vehicle, OEA (2 or 10 mg/kg) or PEA (2 or 10 mg/kg). At 30 days of age, animals were subjected to behavioral tests followed by immunohistochemical studies. Results: Results showed that neonatal AI was associated with decreased locomotion, as well as recognition and spatial memory impairments. Furthermore, these deficits were accompanied with enhanced neuroinflammation and astrogliosis, as well as a decreased PPARα expression. PEA treatment was able to prevent neuroinflammation, reduce astrogliosis and preserve cognitive functions. Conclusions: These results indicate that the acylethanolamide PEA may play an important role in the mechanisms underlying neonatal AI, and it could be a good candidate for further studies regarding neonatal AI treatments. Fil: Holubiec, Mariana Ines. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina. Hospital Regional Universitario de Málaga; España Fil: Romero, Juan Ignacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina. Hospital Regional Universitario de Málaga; España Fil: Suárez, Juan. Hospital Regional Universitario de Málaga; España Fil: Portavella, Manuel. Universidad de Sevilla; España Fil: Fernández Espejo, Emilio. Universidad de Sevilla; España Fil: Blanco, Eduardo. Universidad de Lleida. Instituto de Recerca Biomédica; España Fil: Galeano, Pablo. Hospital Regional Universitario de Málaga; España. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Rodríguez de Fonseca, Fernando. Hospital Regional Universitario de Málaga; España

Published
2018

4. Acylethanolamides and endocannabinoid signaling system in dorsal striatum of rats exposed to perinatal asphyxia

Author

Tamara Maite Ayelén Logica Tornatore, Juan Ignacio Romero, Eduardo Blanco, Juan Suárez, Fernando Rodríguez de Fonseca, Pablo Galeano, Mariana Inés Holubiec, and Francisco Capani

Subjects
0301 basic medicine, Nape-Pld, Cannabinoid receptor, Striatum, Cb1, Rats, Sprague-Dawley, Oleoylethanolamide, chemistry.chemical_compound, 0302 clinical medicine, Receptor, Cannabinoid, CB1, Receptor, Asphyxia Neonatorum, biology, General Neuroscience, purl.org/becyt/ford/3.1 [https], Endocannabinoid system, Medicina Básica, lipids (amino acids, peptides, and proteins), purl.org/becyt/ford/3 [https], Signal Transduction, Perinatal Asphyxia, medicine.medical_specialty, CIENCIAS MÉDICAS Y DE LA SALUD, Neurociencias, Neuroprotection, Dorsal Striatum, 03 medical and health sciences, Internal medicine, Phospholipase D, medicine, Animals, PPAR alpha, Daglα, Pparα, medicine.disease, Corpus Striatum, Rats, Perinatal asphyxia, Disease Models, Animal, Lipoprotein Lipase, 030104 developmental biology, Endocrinology, Animals, Newborn, nervous system, chemistry, biology.protein, NeuN, Neuroscience, 030217 neurology & neurosurgery, Endocannabinoids
Abstract

Endocannabinoids (eCBs) and acylethanolamides (AEs) have lately received more attention due to their neuroprotective functions in neurological disorders. Here we analyze the alterations induced by perinatal asphyxia (PA) in the main metabolic enzymes and receptors of the eCBs/AEs in the dorsal striatum of rats. To induce PA, we used a model developed by Bjelke et al. (1991). Immunohistochemical techniques were carried out to determine the expression of neuronal and glial markers (NeuN and GFAP), eCBs/AEs synthesis and degradation enzymes (DAGLα, NAPE-PLD and FAAH) and their receptors (CB1 and PPARα). We found a decrease in NAPE-PLD and PPARα expression. Since NAPE-PLD and PPARα take part in the production and reception of biochemical actions of AEs, such as oleoylethanolamide, these results may suggest that PA plays a key role in the regulation of this system. These data agree with previous results obtained in the hippocampus and encourage us to develop further studies using AEs as potential neuroprotective compounds. Fil: Holubiec, Mariana Ines. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Romero, Juan Ignacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Blanco, Eduardo. Universidad de Málaga; España. Universidad de Lleida; España Fil: Logica Tornatore, Tamara Maite Ayelén. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Suarez, Juan. Universidad de Málaga; España Fil: Rodríguez de Fonseca, Fernando. Universidad de Málaga; España Fil: Galeano, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Capani, Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina. Universidad Argentina "John F. Kennedy"; Argentina. Universidad de Chile; Chile

Published
2017

5. Neuronal Damage Induced by Perinatal Asphyxia Is Attenuated by Postinjury Glutaredoxin-2 Administration

Author

Christopher Horst Lillig, Fernando Rodríguez de Fonseca, Mariana Inés Holubiec, Julia Tau, Tamara Maite Ayelén Logica Tornatore, Juan Ignacio Romero, Rodolfo Alberto Kölliker-Frers, Eduardo Blanco, Stéphanie Rivière, Eva-Maria Hanschmann, Pablo Galeano, Francisco Capani, [Ignacio Romero, Juan] UBA CONICET, Fac Med, Inst Invest Cardiol Prof Dr Alberto C Taquini INI, Marcelo T de Alvear 2270,C1122AAJ, Buenos Aires, DF, Argentina, [Ines Holubiec, Mariana] UBA CONICET, Fac Med, Inst Invest Cardiol Prof Dr Alberto C Taquini INI, Marcelo T de Alvear 2270,C1122AAJ, Buenos Aires, DF, Argentina, [Logica Tornatore, Tamara] UBA CONICET, Fac Med, Inst Invest Cardiol Prof Dr Alberto C Taquini INI, Marcelo T de Alvear 2270,C1122AAJ, Buenos Aires, DF, Argentina, [Riviere, Stephanie] UBA CONICET, Fac Med, Inst Invest Cardiol Prof Dr Alberto C Taquini INI, Marcelo T de Alvear 2270,C1122AAJ, Buenos Aires, DF, Argentina, [Alberto Kolliker-Frers, Rodolfo] UBA CONICET, Fac Med, Inst Invest Cardiol Prof Dr Alberto C Taquini INI, Marcelo T de Alvear 2270,C1122AAJ, Buenos Aires, DF, Argentina, [Capani, Francisco] UBA CONICET, Fac Med, Inst Invest Cardiol Prof Dr Alberto C Taquini INI, Marcelo T de Alvear 2270,C1122AAJ, Buenos Aires, DF, Argentina, [Hanschmann, Eva-Maria] Heinrich Heine Univ, Med Fac, Dept Neurol, Dusseldorf, Germany, [Hanschmann, Eva-Maria] Ernst Moritz Arndt Univ Greifswald, Univ Med Greifswald, Inst Med Biochem & Mol Biol, D-17475 Greifswald, Germany, [Lillig, Christopher Horst] Ernst Moritz Arndt Univ Greifswald, Univ Med Greifswald, Inst Med Biochem & Mol Biol, D-17475 Greifswald, Germany, [Tau, Julia] Univ Buenos Aires, Sch Med, Dept Pathol, Lab Ocular Invest, Buenos Aires, DF, Argentina, [Blanco, Eduardo] Univ Lleida, Fac Educ Psicol & Treball Social, Dept Pedag & Psicol, Avda Estudi Gen 4, Lleida 25001, Spain, [Galeano, Pablo] Fdn Inst Leloir, Av Patricias Argentinas 435,C1405BWE, Buenos Aires, DF, Argentina, [Rodriguez de Fonseca, Fernando] Univ Malaga, Hosp Reg Univ Malaga, Inst Invest Biomed Malaga, Unidad Gest Clin Salud Mental, Avda Carlos Haya 82, Malaga 29010, Spain, [Capani, Francisco] Univ Argentina JF Kennedy, Dept Biol, Buenos Aires, DF, Argentina, [Capani, Francisco] Univ Autonoma Chile, Santiago, Chile, Deutsche Forschungsgemeinschaft, Federal Ministry for Science and Education, MINCYT, German Academic Exchange Service DAAD, MINCYT (PROALAR program), National Scientific and Technical Research Council (CONICET, Argentina), Instituto de Salud Carlos III, Ministerio de Economia y Competitividad UE/ERDF, Fundacio 'La Marato de TV3', and University of Buenos Aires

Subjects
Cerebellar granule neurons, 0301 basic medicine, Male, Aging, Mixed disulfide, Redox control, Excitotoxicity, Pharmacology, medicine.disease_cause, Biochemistry, 0302 clinical medicine, Medicine, Neurons, lcsh:Cytology, Glutamate receptor, purl.org/becyt/ford/3.1 [https], General Medicine, Astrogliosis, Medicina Básica, Neurology, Anesthesia, Hypoxia-Ischemia, Brain, purl.org/becyt/ford/3 [https], Thioredoxin, medicine.symptom, Research Article, Perinatal Asphyxia, CIENCIAS MÉDICAS Y DE LA SALUD, Article Subject, Ischemic brain-damage, Neurociencias, Ischemia, Brain damage, Neuroprotection, Neurological reflexes, Neurologia, 03 medical and health sciences, Asphyxia, Cerebral-ischemia, Animals, lcsh:QH573-671, Glutaredoxins, Dopamine-induced apoptosis, Nf-kappa-b, business.industry, Cell Biology, medicine.disease, Perinatal asphyxia, Rats, Treatment, Disease Models, Animal, 030104 developmental biology, Animals, Newborn, Heat-shock-protein, Oxidative stress, Grx2, business, 030217 neurology & neurosurgery
Abstract

The general disruption of redox signaling following an ischemia-reperfusion episode has been proposed as a crucial component in neuronal death and consequently brain damage. Thioredoxin (Trx) family proteins control redox reactions and ensure protein regulation via specific, oxidative posttranslational modifications as part of cellular signaling processes. Trx proteins function in the manifestation, progression, and recovery following hypoxic/ischemic damage. Here, we analyzed the neuroprotective effects of postinjury, exogenous administration of Grx2 and Trx1 in a neonatal hypoxia/ischemia model. P7 Sprague-Dawley rats were subjected to right common carotid ligation or sham surgery, followed by an exposure to nitrogen. 1 h later, animals were injected i.p. with saline solution, 10 mg/kg recombinant Grx2 or Trx1, and euthanized 72 h postinjury. Results showed that Grx2 administration, and to some extent Trx1, attenuated part of the neuronal damage associated with a perinatal hypoxic/ischemic damage, such as glutamate excitotoxicity, axonal integrity, and astrogliosis. Moreover, these treatments also prevented some of the consequences of the induced neural injury, such as the delay of neurobehavioral development. To our knowledge, this is the first study demonstrating neuroprotective effects of recombinant Trx proteins on the outcome of neonatal hypoxia/ischemia, implying clinical potential as neuroprotective agents that might counteract neonatal hypoxia/ischemia injury Fil: Romero, Juan Ignacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Holubiec, Mariana Ines. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Tornatore, Tamara Logica. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Rivière, Stéphanie. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Hanschmann, Eva Maria. Heinrich Heine University; Argentina Fil: Kölliker Frers, Rodolfo Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Tau, Julia. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Patología; Argentina Fil: Blanco, Eduardo. Universidad de Lleida; España Fil: Galeano, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Rodríguez de Fonseca, Fernando. Universidad de Málaga; España Fil: Lillig, Christopher Horst. Heinrich Heine University; Alemania Fil: Capani, Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina. Universidad de Chile; Chile. Universidad Argentina "John F. Kennedy"; Argentina

Published
2017

6. Worsening of memory deficit induced by energy-dense diet in a rat model of early-Alzheimer's disease is associated to neurotoxic Aβ species and independent of neuroinflammation

Author

Goar Gevorkian, Celia Quijano, Laura Morelli, Alejandro Rabossi, A. Claudio Cuello, Sonia Do Carmo, Rafael Radi, ML Wallinger, Natividad Olivar, Pamela V. Martino Adami, Pablo Galeano, Carlos F. Reyes Toso, Daniel P. Cardinali, Luis I. Brusco, Eleonora Samanta Pagano, and Eduardo M. Castaño

Subjects
Male, 0301 basic medicine, Saturated fat, Hippocampal formation, Hippocampus, Amyloid beta-Protein Precursor, Cognition, 0302 clinical medicine, Amyloid precursor protein, Bioenergetic Health Index, ENFERMEDAD DE ALZHEIMER, ENFERMEDADES METABOLICAS, Cognitive decline, Dietary Fat, Adiposity, biology, Microglia, Early Alzheimer, DIETA, Pyrrolidonecarboxylic Acid, Cognitive Decline, Medicina Básica, medicine.anatomical_structure, Biochemistry, MEMORIA, Molecular Medicine, Rats, Transgenic, medicine.medical_specialty, CIENCIAS MÉDICAS Y DE LA SALUD, Neurociencias, App Processing And Pyroglutamate-AΒ, Blood–brain barrier, Neuroprotection, 03 medical and health sciences, Alzheimer Disease, Internal medicine, medicine, Animals, Humans, Molecular Biology, Neuroinflammation, HIPERTENSION, Inflammation, Memory Disorders, ENFERMEDADES NEURODEGENERATIVAS, Rats, Disease Models, Animal, 030104 developmental biology, Endocrinology, Diet, Western, biology.protein, Energy Metabolism, Gene Deletion, 030217 neurology & neurosurgery
Abstract

Fil: Martino Adami, Pamela V. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Martino Adami, Pamela V. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires. Laboratory of Amyloidosis and Neurodegeneration; Argentina Fil: Galeano, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Galeano, Pablo. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires. Laboratory of Amyloidosis and Neurodegeneration; Argentina Fil: Galeano, Pablo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Wallinger, Marina L. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas. Unidad Académica II; Argentina Fil: Quijano, Celia. Universidad de la República. Facultad de Medicina. Department of Biochemistry Center for Free Radical and Biomedical Research; Uruguay Fil: Rabossi, Alejandro. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires. Laboratory of Biochemistry and Molecular Biology of Development; Argentina Fil: Rabossi, Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Pagano, Eleonora Samanta. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas. Unidad Académica II; Argentina Fil: Olivar, Natividad. Universidad de Buenos Aires. Facultad de Medicina. Centro de Neuropsiquiatría y Neurología de la Conducta. Unidad Académica II. Departamento de Ciencias Fisiológicas; Argentina Fil: Reyes Toso, Carlos F. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas. Unidad Académica II; Argentina Fil: Cardinali, Daniel Pedro. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas. Unidad Académica II; Argentina Fil: Brusco, Luis I. Universidad de Buenos Aires. Facultad de Medicina. Centro de Neuropsiquiatría y Neurología de la Conducta. Unidad Académica II. Departamento de Ciencias Fisiológicas; Argentina Fil: Do Carmo, Sonia. McGill University. Department of Pharmacology and Therapeutics; Canadá Fil: Radi, Rafael. Universidad de la República. Facultad de Medicina. Department of Biochemistry Center for Free Radical and Biomedical Research; Uruguay Fil: Gevorkian, Goar. Universidad Nacional Autónoma de México. Instituto de Investigaciones Biomédicas; México Fil: Castaño, Eduardo M. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires. Laboratory of Amyloidosis and Neurodegeneration; Argentina Fil: Castaño, Eduardo M. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Cuello, A. Claudio. McGill University. Department of Pharmacology and Therapeutics; Canadá Fil: Laura Morelli. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires. Laboratory of Amyloidosis and Neurodegeneration; Argentina Fil: Laura Morelli. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Abstract: Diet is a modifiable risk factor for Alzheimer's disease (AD), but the mechanisms linking alterations in peripheral metabolism and cognition remain unclear. Since it is especially difficult to study long-term effects of high-energy diet in individuals at risk for AD, we addressed this question by using the McGill-R-Thy1-APP transgenic rat model (Tg(+/-)) that mimics presymptomatic AD. Wild-type and Tg(+/-) rats were exposed during 6months to a standard diet or a Western diet (WD), high in saturated fat and sugar. Results from peripheral and hippocampal biochemical analysis and in situ respirometry showed that WD induced a metabolic syndrome and decreased presynaptic bioenergetic parameters without alterations in hippocampal insulin signaling or lipid composition. Cognitive tests, ELISA multiplex, Western blot, immunohistochemistry and RT-qPCR indicated that WD worsened cognition in Tg(+/-) rats, increased hippocampal levels of monomeric Aβ isoforms and oligomeric species, promoted deposits of N-Terminal pyroglutamate-Aβ (AβN3(pE)) in CA1 pyramidal neurons and interneurons, decreased transcript levels of genes involved in neuroprotective pathways such as Sirtuin-1 and increased nitrated proteins. Our results support the concept that in the presence of early Aβ pathology, diet-induced metabolic dysfunctions may contribute as a "second hit" to impair cognition. Noteworthy, such effect is not mediated by higher microglia activation or disruption of blood brain barrier. However, it may be attributed to increased amyloidogenic processing of amyloid precursor protein, generation of AβN3(pE) and dysregulation of pathways governed by Sirtuin-1. This evidence reinforces the implementation of prophylactic interventions in individuals at risk for AD.

Published
2017

7. Neuroplasticity and Healthy Lifestyle: How Can We Understand This Relationship?

Author

Pablo Galeano, Azucena Begega, P. Sampedro-Piquero, Luis J. Santín, and Debora Cutuli

Subjects
CIENCIAS MÉDICAS Y DE LA SALUD, Psychotherapist, Neuronal Plasticity, Article Subject, Inmunología, MEDLINE, brain, humans, neuronal plasticity, healthy lifestyle, Brain, Cognition, purl.org/becyt/ford/3.1 [https], lcsh:RC321-571, AGING, Medicina Básica, Editorial, Neurology, Neuroplasticity, COGNITION, Humans, purl.org/becyt/ford/3 [https], Neurology (clinical), Healthy Lifestyle, Psychology, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, NEUROPLASTICITY, Introductory Journal Article
Abstract

Our brain has this extraordinary ability to experience functional and structural changes before environmental stimuli, cognitive demand, or our experience itself. Exercise, diet, an appropriate sleep pattern, and reading habits are among those activities proposed to induce effects on cerebral architecture—an active lifestyle seems to induce changes in the brain function that favour welfare and better quality of life. This special issue is intended to extend the knowledge about the relationship between neuroplasticity and a healthy lifestyle Fil: Begega, Azucena. Universidad de Oviedo; España Fil: Santín, Luis J.. Universidad de Málaga; España Fil: Galeano, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Cutuli, Debora. Universita Di Roma; Italia Fil: Sampedro Piquero, Patricia. Universidad Autonoma de Madrid. Facultad de Psicología. Departamento de Psicología Biológica y de la Salud; España

Published
2017

8. Effects of perinatal asphyxia on rat striatal cytoskeleton

Author

Lisandro Diego Giraldez-Alvarez, M.V. Ayala, Mariana Inés Holubiec, Pablo Galeano, Francisco Capani, R. Kölliker-fres, Maria Sol Badorrey, George E. Barreto, Héctor Coirini, Juan Ignacio Romero, and Gustavo Ezequiel Saraceno

Subjects
medicine.medical_specialty, Pathology, CIENCIAS MÉDICAS Y DE LA SALUD, Dendritic spine, Dendritic Spines, Blotting, Western, Neurociencias, macromolecular substances, Striatum, Biology, Calbindin, Rats, Sprague-Dawley, Synapse, Asphyxia, Cellular and Molecular Neuroscience, Microscopy, Electron, Transmission, Internal medicine, Neuronal Cytoskeleton, medicine, Animals, Cytoskeleton, Map-2, Microscopy, Confocal, Neurodegeneration, Actin cytoskeleton, medicine.disease, Immunohistochemistry, Corpus Striatum, Rats, Disease Models, Animal, Medicina Básica, Endocrinology, Animals, Newborn, nervous system, Female, Immunostaining, Perinatal Asphyxia
Abstract

Perinatal asphyxia (PA) is a medical condition associated with a high short-term morbimortality and different long-term neurological diseases. In previous works, we have shown that neuronal and synaptic changes in rat striatum lead to ubi-protein accumulation in post-synaptic density (PSD) after six months of sub-severe PA. However, very little is known about the synaptic and related structural modifications induced by PA in young rats. In the present work, we studied neuronal cytoskeleton modifications in striatum induced by subsevere PA in 30-day-old rats. We observed a significant decrease in the number of neurons, in particular calbindin immunoreactive neurons after PA. In addition, it was also observed that actin cytoskeleton was highly modified in the PSD as well as an increment of F-actin staining by Phalloidin-alexa 488 in the striatum of PA rats. Using correlative fluorescence-electron microscopy photooxidation, we confirmed and extended confocal observations. F-actin staining augmentation was mostly related with an increment in the number of mushroom-shaped spines. Consistent with microscopic data, Western blot analysis revealed a β-actin increment in PSD in PA rats. On the other hand, MAP-2 immunostaining was decreased after PA, being NF-200 expression unmodified. Although neuronal death was observed, signs of generalized neurodegeneration were absent. Taken together these results showed early post-synaptic F-actin cytoskeleton changes induced by PA with slightly modifications in the other components of the neuronal cytoskeleton, suggesting that F-actin accumulation in the dendritic spines could be involved in the neuronal loss induced by PA. © 2011 Wiley Periodicals, Inc. Fil: Saraceno, Gustavo Ezequiel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Ayala, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Badorrey, Maria Sol. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Holubiec, Mariana Ines. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Romero, Juan Ignacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Galeano, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Barreto, G.. Pontificia Universidad Javeriana; Colombia Fil: Giraldez Alvárez, L. D.. Universidade Federal da Bahia; Brasil Fil: Kolliker Frers, Rodolfo Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Coirini, Hector. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina Fil: Capani, Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina

Published
2011
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9. Cocaine-induced behavioral sensitization decreases the expression of endocannabinoid signaling-related proteins in the mouse hippocampus

Author

Francisco Alén, Juan Suárez, Pablo Galeano, Eduardo Blanco, Patricia Rivera, Fernando Rodríguez de Fonseca, Estela Castilla-Ortega, Juan Decara, Antonio Vargas, Antonia Serrano, Leticia Rubio, Ainhoa Bilbao, Ana Palomino, and Francisco Javier Pavón

Subjects
0301 basic medicine, Male, CIENCIAS MÉDICAS Y DE LA SALUD, Cannabinoid receptor, Time Factors, Neurociencias, Glutamic Acid, Biology, Pharmacology, Depolarization-induced suppression of inhibition, Hippocampus, Amidohydrolases, GLUTAMATE, 03 medical and health sciences, Mice, 0302 clinical medicine, Cocaine, Dopamine Uptake Inhibitors, Fatty acid amide hydrolase, Conditioned locomotion, Animals, Pharmacology (medical), RNA, Messenger, Cannabinoid, Biological Psychiatry, Analysis of Variance, musculoskeletal, neural, and ocular physiology, Endocannabinoid system, Cocaine sensitization, Cocaïna, Monoacylglycerol lipase, Mice, Inbred C57BL, Medicina Básica, Psychiatry and Mental health, 030104 developmental biology, Metabotropic receptor, nervous system, Neurology, Gene Expression Regulation, Receptors, Glutamate, Metabotropic glutamate receptor, lipids (amino acids, peptides, and proteins), Neurology (clinical), 030217 neurology & neurosurgery, Locomotion, Ionotropic effect, Endocannabinoids, Signal Transduction
Abstract

In the reward mesocorticolimbic circuits, the glutamatergic and endocannabinoid systems are implicated in neurobiological mechanisms underlying cocaine addiction. However, the involvement of both systems in the hippocampus, a critical region to process relational information relevant for encoding drug-associated memories, in cocaine-related behaviors remains unknown. In the present work, we studied whether the hippocampal gene/protein expression of relevant glutamate signaling components, including glutamate-synthesizing enzymes and metabotropic and ionotropic receptors, and the hippocampal gene/protein expression of cannabinoid type 1 (CB1) receptor and endocannabinoid metabolic enzymes were altered following acute and/or repeated cocaine administration resulting in conditioned locomotion and locomotor sensitization. Results showed that acute cocaine administration induced an overall down-regulation of glutamate-related gene expression and, specifically, a low phosphorylation level of GluA1. In contrast, locomotor sensitization to cocaine produced an up-regulation of several glutamate receptor-related genes and, specifically, an increased protein expression of the GluN1 receptor subunit. Regarding the endocannabinoid system, acute and repeated cocaine administration were associated with an increased gene/protein expression of CB1 receptors and a decreased gene/protein expression of the endocannabinoid-synthesis enzymes N-acyl phosphatidylethanolamine D (NAPE-PLD) and diacylglycerol lipase alpha (DAGLα). These changes resulted in an overall decrease in endocannabinoid synthesis/degradation ratios, especially NAPE-PLD/fatty acid amide hydrolase and DAGLα/monoacylglycerol lipase, suggesting a reduced endocannabinoid production associated with a compensatory up-regulation of CB1 receptor. Overall, these findings suggest that repeated cocaine administration resulting in locomotor sensitization induces a down-regulation of the endocannabinoid signaling that could contribute to the specifically increased GluN1 expression observed in the hippocampus of cocaine-sensitized mice. Fil: Blanco, Eduardo. Universidad de Málaga; España. Universidad de Lleida; España Fil: Galeano, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Palomino, Ana. Universidad de Málaga; España Fil: Pavon, Francisco J.. Universidad de Málaga; España Fil: Rivera, Patricia. Universidad de Málaga; España Fil: Serrano, Antonia. Universidad de Málaga; España Fil: Alen, Francisco. Universidad de Málaga; España Fil: Rubio, Leticia. Universidad de Málaga; España Fil: Vargas, Antonio. Universidad de Málaga; España Fil: Castilla-Ortega, Estela. Universidad de Málaga; España Fil: Decara, Juan. Universidad de Málaga; España Fil: Bilbao, Ainhoa. Universidad de Málaga; España Fil: Rodríguez de Fonseca, Fernando. Universidad de Málaga; España Fil: Suaréz, Juan. Universidad de Málaga; España

Published
2015

10. Pharmacological blockade of either cannabinoid CB1 or CB2 receptors prevents both cocaine-induced conditioned locomotion and cocaine-induced reduction of cell proliferation in the hippocampus of adult male rat

Author

Estela Castilla-Ortega, Eduardo Blanco-Calvo, Antonio Vargas, Juan Suárez, Sergio Arrabal, Patricia Rivera, Fernando Rodríguez de Fonseca, Pablo Galeano, Leticia Rubio, Francisco Javier Pavón, Antonia Serrano, [Blanco-Calvo,E] Departament de Pedagogia i Psicologia, Facultat de Ciències de l’Educació, Universitat de Lleida, Lleida, Spain. [Blanco-Calvo,E, Rivera,P, Arrabal,S, Vargas,A, Pavón,FJ, Serrano,A, Castilla-Ortega,E, Rodríguez de Fonseca,F] Laboratorio de Investigación-UGC de Salud Mental, Instituto de Investigación Biomédica de Málaga, Universidad de Málaga, Hospital Regional Universitario de Málaga, Málaga, Spain. [Galeano,P] Instituto de Investigaciones Cardiológicas Prof. Dr. Alberto C. Taquini, Universidad de Buenos Aires-CONICET, Ciudad de Buenos Aires, Argentina. [Rubio,L] Departamento de Anatomía y Medicina Legal y Forense, Facultad de Medicina, Universidad de Málaga, Málaga, Spain., and The 7th Framework Program of the European Union [grant number HEALTH-F2-2008-223713, REPROBESITY], the Ministerio de Ciencia e Innovación [grant numbers SAF2010-19087, SAF 2010-20521], the Instituto de Salud Carlos III, the Ministerio de Economía y Competitividad, UE-ERDF [grant number CP12/03109], the Red de Trastornos Adictivos [grant numbers RD12/0028/0001, RD12/0028/0009], the CIBERobn, the Plan Nacional Sobre Drogas, Ministerio de Sanidad y Consumo [grant number PNSD 2010/143], the Consejería de Economía, Innovación y Ciencia, Junta de Andalucía, the UE/ERDF [grant number CTS-433, P-11-CVI-07637], the Consejería de Salud, Junta de Andalucía [grant numbers PI0232/2008, PI0029/2008, SAS111224], and the Fundació La Marató de TV3 [grant number 386/C/2011]. JS is a recipient of a 'Miguel Servet' research contract from the National System of Health (Instituto de Salud Carlos III, grant number CP12/03109). ECO is a recipient of a 'Sara Borrell' research contract from the National System of Health (Instituto de Salud Carlos III, grant number CD12/00455).

Subjects
Cannabinoid receptor, medicine.medical_treatment, striatum, Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Differentiation::Neurogenesis [Medical Subject Headings], Hippocampus, Pharmacology, lcsh:RC346-429, Subgranular zone, Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Proteins::Membrane Proteins::Receptors, Cell Surface::Receptors, G-Protein-Coupled::Receptors, Cannabinoid::Receptor, Cannabinoid, CB1 [Medical Subject Headings], Rimonabant, conditioning, Cocaine, Receptor cannabinoide CB2, Receptor cannabinoide CB1, Cannabinoid receptor type 2, Cocaina, Original Research Article, AM630, Anatomy::Nervous System::Central Nervous System::Brain::Prosencephalon::Telencephalon::Cerebrum::Basal Ganglia::Corpus Striatum::Neostriatum [Medical Subject Headings], Chemistry, Neurogenesis, purl.org/becyt/ford/3.1 [https], Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Proteins::Membrane Proteins::Receptors, Cell Surface::Receptors, G-Protein-Coupled::Receptors, Cannabinoid::Receptor, Cannabinoid, CB2 [Medical Subject Headings], Sensory Systems, 3. Good health, Medicina Básica, medicine.anatomical_structure, purl.org/becyt/ford/3 [https], lipids (amino acids, peptides, and proteins), medicine.drug, CIENCIAS MÉDICAS Y DE LA SALUD, Cognitive Neuroscience, Hipocamp (Cervell), Neurociencias, Subventricular zone, Check Tags::Male [Medical Subject Headings], lcsh:RC321-571, Striatum, Cellular and Molecular Neuroscience, Ratas, cannabinoid receptors, medicine, Hipocampo, Anatomy::Nervous System::Central Nervous System::Brain::Limbic System::Hippocampus [Medical Subject Headings], Cannabinoid receptors, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, lcsh:Neurology. Diseases of the nervous system, Inflammation, Chemicals and Drugs::Heterocyclic Compounds::Alkaloids::Tropanes::Cocaine [Medical Subject Headings], Cocaïna, Rats, Neostriado, Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Rats [Medical Subject Headings], nervous system, inflammation, Receptors cel·lulars, Cannabinoid, Neuroscience
Abstract

Addiction to major drugs of abuse, such as cocaine, has recently been linked to alterations in adult neurogenesis in the hippocampus. The endogenous cannabinoid system modulates this proliferative response as demonstrated by the finding that pharmacological activation/blockade of cannabinoid CB1 and CB2 receptors not only modulates neurogenesis but also modulates cell death in the brain. In the present study, we evaluated whether the endogenous cannabinoid system affects cocaine-induced alterations in cell proliferation. To this end, we examined whether pharmacological blockade of either CB1 (Rimonabant, 3 mg/kg) or CB2 receptors (AM630, 3 mg/kg) would affect cell proliferation (the cells were labeled with BrdU) in the subventricular zone (SVZ) of the lateral ventricle and the dentate subgranular zone (SGZ). Additionally, we measured cell apoptosis (as monitored by the expression of cleaved caspase-3) and glial activation (by analyzing the expression of GFAP and Iba-1) in the striatum and hippocampus during acute and repeated (4 days) cocaine administration (20 mg/kg). The results showed that acute cocaine exposure decreased the number of BrdU-immunoreactive (ir) cells in the SVZ and SGZ. In contrast, repeated cocaine exposure reduced the number of BrdU-ir cells only in the SVZ. Both acute and repeated cocaine exposure increased the number of cleaved caspase-3-, GFAP- and Iba1-ir cells in the hippocampus, and this effect was counteracted by AM630 or rimonabant, which increased the number of BrdU-, GFAP- and Iba1-ir cells in the hippocampus. These results indicate that the changes in neurogenic, apoptotic and gliotic processes that were produced by repeated cocaine administration were normalized by pharmacological blockade of CB1 and CB2. The restorative effects of cannabinoid receptor blockade on hippocampal cell proliferation were associated with the prevention of the induction of conditioned locomotion but not with the prevention of cocaine-induced sensitization. Fil: Blanco Calvo, Eduardo. Universitat de Lleida; España Fil: Rivera, Patricia. Universidad de Malaga; España Fil: Arrabal, Sergio. Universidad de Malaga; España Fil: Vargas, Antonio. Universidad de Malaga; España Fil: Pavon, Francisco Javier. Universidad de Malaga; España Fil: Serrano, Antonia. Universidad de Malaga; España Fil: Castilla Ortega, Estela. Universidad de Malaga; España Fil: Galeano, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina Fil: Rubio, Leticia. Universidad de Malaga; España Fil: Suaréz, Juan. Universidad de Malaga; España Fil: Rodríguez de Fonseca, Fernando. Universidad de Malaga; España

Published
2014

11. Hyperactivity induced by the dopamine D-2/D-3 receptor agonist quinpirole is attenuated by inhibitors of endocannabinoid degradation in mice

Author

María Jesús Luque-Rojas, Pablo Galeano, Juan Suárez, Fernando Rodríguez de Fonseca, Eduardo Blanco Calvo, Luis J. Santín, and Pedro Araos

Subjects
Male, CIENCIAS MÉDICAS Y DE LA SALUD, Quinpirole, Endocannabinoid system, Dopamine, Neurociencias, Dopamina, Pharmacology, URB602, chemistry.chemical_compound, Mice, Cocaine, Fatty acid amide hydrolase, Dopamine receptor D2, medicine, Animals, Pharmacology (medical), Psychomotor Agitation, Receptors, Dopamine D2, Receptors, Dopamine D3, purl.org/becyt/ford/3.1 [https], URB597, Monoacylglycerol lipase, Mice, Inbred C57BL, Psychiatry and Mental health, Medicina Básica, chemistry, Benzamides, Dopamine Agonists, purl.org/becyt/ford/3 [https], Carbamates, Stereotyped Behavior, Psychomotor disorder, Stereotyped behaviour, medicine.drug, Endocannabinoids
Abstract

The present study was designed to investigate the effect of pharmacological inhibition of endocannabinoid degradation on behavioural actions of the dopamine D2/D3 receptor agonist quinpirole in male C57Bl/6J mice. In addition, we studied the effects of endocannabinoid degradation inhibition on both cocaine-induced psychomotor activation and behavioural sensitization. We analysed the effects of inhibition of the two main endocannabinoid degradation enzymes: fatty acid amide hydrolase (FAAH), using inhibitor URB597 (1 mg/kg); monoacylglycerol lipase (MAGL), using inhibitor URB602 (10 mg/kg). Administration of quinpirole (1 mg/kg) caused a temporal biphasic response characterized by a first phase of immobility (0–50 min), followed by enhanced locomotion (next 70 min) that was associated with the introduction of stereotyped behaviours (stereotyped jumping and rearing). Pretreatment with both endocannabinoid degradation inhibitors did not affect the hypoactivity actions of quinpirole. However, this pretreatment resulted in a marked decrease in quinpirole-induced locomotion and stereotyped behaviours. Administration of FAAH or MAGL inhibitors did not attenuate the acute effects of cocaine. Furthermore, these inhibitors did not impair the acquisition of cocaine-induced behavioural sensitization or the expression of cocaine-induced conditioned locomotion. Only MAGL inhibition attenuated the expression of an already acquired cocaine-induced behavioural sensitization. These results suggest that pharmacological inhibition of endocannabinoid degradation might exert a negative feedback on D2/D3 receptor-mediated hyperactivity. This finding might be relevant for therapeutic approaches for either psychomotor disorders (dyskinesia, corea) or disorganized behaviours associated with dopamine-mediated hyperactivity. Fil: Luque Rojas, María Jesús. Fundación IMABIS; España Fil: Galeano, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina Fil: Suarez, Juan . Fundación IMABIS; España Fil: Araos, Pedro. Fundación IMABIS; España Fil: Santín Nuñez, Luis Javier. Universidad de Malaga; España Fil: Rodríguez de Fonseca, Fernando. Fundación IMABIS; España Fil: Blanco Calvo, Eduardo. Fundación IMABIS; España. Universidad de Malaga; España

Published
2013

12. Experimental Neurology

Author

George E. Barreto, Pablo Galeano, Laura Aon-Bertolino, Francisco Capani, Valeria Botti, Lisandro Diego Giraldez-Alvarez, Diêgo Madureira de Oliveira, Gustavo Ezequiel Saraceno, and Héctor Coirini

Subjects
Male, SYNAPSE, Calbindins, Electron Microscope Tomography, Time Factors, HYPOXIA, Hypothermia, Synapse, Rats, Sprague-Dawley, Postsynaptic potential, Hypothermia, Induced, Pregnancy, Hypoxia, Brain, Microscopy, Immunoelectron, gamma-Aminobutyric Acid, Neurons, Neuroprotection, Cell biology, Perinatal asphyxia, Medicina Básica, Neurology, Female, medicine.symptom, Subcellular Fractions, CIENCIAS MÉDICAS Y DE LA SALUD, Neurociencias, Biology, S100 Calcium Binding Protein G, Developmental Neuroscience, medicine, Animals, Ubiquitins, NEOSTRIATUM, Analysis of Variance, Ubiquitin, Postsynaptic density, Hypoxia (medical), medicine.disease, Protein ubiquitination, Rats, Neostriatum, Disease Models, Animal, Animals, Newborn, Synapses, Neuroscience, AP
Abstract

Synaptic dysfunction has been associated with neuronal cell death following hypoxia. The lack of knowledge on the mechanisms underlying this dysfunction prompted us to investigate the morphological changes in the postsynaptic densities (PSDs) induced by hypoxia. The results presented here demonstrate that PSDs of the rat neostriatum are highly modified and ubiquitinated 6 months after induction of hypoxia in a model of perinatal asphyxia. Using both two dimensional (2D) and three dimensional (3D) electron microscopic analyses of synapses stained with ethanolic phosphotungstic acid (E-PTA), we observed an increment of PSD thickness dependent on the duration and severity of the hypoxic insult. The PSDs showed clear signs of damage and intense staining for ubiquitin. These morphological and molecular changes were effectively blocked by hypothermia treatment, one of the most effective strategies for hypoxia-induced brain injury available today. Our data suggest that synaptic dysfunction following hypoxia may be caused by long-term misfolding and aggregation of proteins in the PSD. Fil: Capani, Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Saraceno, Gustavo Ezequiel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Botti, Valeria. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina Fil: Aon Bertolino, Maria Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Madureira de Oliveira, Diego. Universidade Federal da Bahia; Brasil Fil: Barreto, George. Consejo Superior de Investigaciones Científicas. Instituto Cajal; España Fil: Galeano, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Giraldez Alvarez, Lisandro Diego. Universidade Federal da Bahia; Brasil Fil: Coirini, Hector. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina

Published
2009
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