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Journal of Neuroscience, ISSN 0270-6474, 12/2009, Volume 29, Issue 48, pp. 15245 - 15257
Olfactory bulb (OB) interneurons are continuously renewed throughout an animal's lifespan. Despite extensive investigation of this phenomenon, little is known... 
FOREBRAIN | INHIBITION | MEMORY | DISCRIMINATION | BORN NEURONS | STIMULATED NEUROGENESIS | GAMMA-OSCILLATIONS | GRANULE CELLS | NEUROSCIENCES | NEWBORN NEURONS | BRAIN | Interneurons - physiology | Cytarabine - pharmacology | gamma-Aminobutyric Acid - metabolism | Male | Phosphopyruvate Hydratase - metabolism | Green Fluorescent Proteins - genetics | Nerve Net - drug effects | Nerve Net - physiology | Odorants | Smell - physiology | Time Factors | Exploratory Behavior - drug effects | Olfactory Perception - physiology | Discrimination (Psychology) - drug effects | Lysine - metabolism | Neurogenesis - drug effects | Bromodeoxyuridine - metabolism | Electric Stimulation - methods | Immunosuppressive Agents - pharmacology | Potassium Channel Blockers - pharmacology | Locomotion - drug effects | Olfactory Bulb - cytology | Lysine - analogs & derivatives | Mice, Inbred C57BL | Interneurons - drug effects | Biophysics | Hindlimb Suspension - methods | Association Learning - physiology | Association Learning - drug effects | Evoked Potentials - drug effects | Patch-Clamp Techniques | Ablation Techniques - methods | Animals | Recognition (Psychology) - drug effects | Sensory Thresholds - physiology | Discrimination (Psychology) - physiology | Mice | Locomotion - physiology | Inhibitory Postsynaptic Potentials - drug effects | Sensory Thresholds - drug effects
Journal Article
Psychopharmacology, ISSN 0033-3158, 10/2016, Volume 233, Issue 19-20, pp. 3647 - 3657
The N-methyl-d-aspartate (NMDA) receptor antagonists, including R-ketamine and rapastinel (formerly GLYX-13), show rapid antidepressant effects in animal... 
Antidepressant | R-ketamine | Rapastinel | Brain-derived neurotrophic factor | Synaptogenesis | PATH | FUNCTIONAL PARTIAL AGONIST | BDNF | PSYCHIATRY | D-ASPARTATE ANTAGONIST | NEUROSCIENCES | TRIAL | GLYX-13 | PHARMACOLOGY & PHARMACY | SUSTAINED ANTIDEPRESSANT | RAPID-ONSET | Nucleus Accumbens - metabolism | Disks Large Homolog 4 Protein - metabolism | Disks Large Homolog 4 Protein - drug effects | Male | Hippocampus - drug effects | Brain - metabolism | Brain-Derived Neurotrophic Factor - drug effects | Depression - drug therapy | CA3 Region, Hippocampal - drug effects | Prefrontal Cortex - drug effects | Dentate Gyrus - drug effects | Stress, Psychological - metabolism | CA3 Region, Hippocampal - metabolism | Antidepressive Agents - pharmacology | Brain-Derived Neurotrophic Factor - metabolism | Swimming | Receptor, trkB - drug effects | Receptors, AMPA - metabolism | Disease Models, Animal | Dentate Gyrus - metabolism | Excitatory Amino Acid Antagonists - pharmacology | Hindlimb Suspension | Brain - drug effects | Hippocampus - metabolism | Animals | Prefrontal Cortex - metabolism | Mice | Ketamine - pharmacology | Nucleus Accumbens - drug effects | Oligopeptides - pharmacology | Receptor, trkB - metabolism | Receptors, AMPA - drug effects | Ketamine | Antidepressants | Depression, Mental | Comparative analysis | Drug therapy | Stress (Psychology) | Health aspects | Psychopharmacology | Stress | Original Investigation
Journal Article
The Journal of clinical investigation, ISSN 0021-9738, 01/2005, Volume 115, Issue 1, pp. 118 - 127
Journal Article
Experimental Gerontology, ISSN 0531-5565, 09/2013, Volume 48, Issue 9, pp. 973 - 984
Loss of myonuclei by apoptosis is thought to contribute to sarcopenia. We have previously shown, that the leucine metabolite, β-hydroxy-β-methylbutyrate (HMB)... 
Muscle hypertrophy | Sarcopenia | Muscle atrophy | Muscle function | Satellite cells | Nutrition | OXIDATIVE STRESS | REGULATORY FACTORS | BODY-COMPOSITION | OLD RATS | GERIATRICS & GERONTOLOGY | SKELETAL-MUSCLE | YOUNG | HINDLIMB SUSPENSION | RESISTANCE EXERCISE | GASTROCNEMIUS-MUSCLES | GROWTH | TOR Serine-Threonine Kinases - metabolism | Isometric Contraction - drug effects | Rats, Inbred F344 | Body Weight - drug effects | Male | Muscular Disorders, Atrophic - physiopathology | Stem Cells - metabolism | Valerates - pharmacology | Satellite Cells, Skeletal Muscle - pathology | Muscular Disorders, Atrophic - drug therapy | Valerates - therapeutic use | Muscle, Skeletal - drug effects | Muscular Disorders, Atrophic - pathology | Drug Evaluation, Preclinical | Rats | Nuclear Proteins - metabolism | MyoD Protein - metabolism | Hindlimb Suspension | Aging - pathology | Eating - drug effects | Satellite Cells, Skeletal Muscle - drug effects | Organ Size - drug effects | Animals | Aging - physiology | Signal Transduction - drug effects | Cell Differentiation - drug effects | Muscle, Skeletal - physiopathology | Stem Cells - drug effects | Stem Cells - pathology | Signal Transduction - physiology | Cell Proliferation - drug effects | Muscle, Skeletal - pathology | Dietary Supplements | Myogenin - metabolism | Paired Box Transcription Factors - metabolism | Aging - metabolism
Journal Article
Nature Neuroscience, ISSN 1097-6256, 10/2009, Volume 12, Issue 10, pp. 1333 - 1342
After complete spinal cord transections that removed all supraspinal inputs in adult rats, combinations of serotonergic agonists and epidural electrical... 
HINDLIMB-STEPPING ABILITY | RECOVERY | CATS | ADULT RATS | EPIDURAL STIMULATION | CENTRAL PATTERN GENERATOR | INJURY | LOCOMOTION | INTRASPINAL MICROSTIMULATION | CORD STIMULATION | NEUROSCIENCES | Motor Activity - physiology | Neural Pathways - drug effects | Reflex - physiology | Recovery of Function - drug effects | Quipazine - therapeutic use | Motor Activity - drug effects | Neuronal Plasticity - drug effects | Nerve Net - drug effects | Gait - physiology | Nerve Net - physiology | Spinal Cord Injuries - pathology | Hindlimb - physiopathology | Neuronal Plasticity - physiology | Time Factors | Recovery of Function - physiology | Female | Neural Pathways - physiopathology | Spinal Cord Injuries - therapy | Electric Stimulation - methods | Principal Component Analysis | Physical Conditioning, Animal | Disease Models, Animal | Locomotion - drug effects | Oncogene Proteins v-fos - metabolism | Rats | 8-Hydroxy-2-(di-n-propylamino)tetralin - therapeutic use | Biomechanical Phenomena - physiology | Rats, Sprague-Dawley | Serotonin Receptor Agonists - therapeutic use | Gait - drug effects | Animals | Analysis of Variance | Muscle, Skeletal - physiopathology | Brain - pathology | Spinal Cord Injuries - physiopathology | Muscle, Skeletal - pathology | Electromyography - methods | Locomotion - physiology | Physiological aspects | Sensorimotor integration | Neural transmission | Spinal cord | Neural circuitry | Research
Journal Article
Journal Article
Journal Article
Biological Psychiatry, ISSN 0006-3223, 2012, Volume 72, Issue 7, pp. 528 - 536
Background Mood disorders are polygenic disorders in which the alteration of several susceptibility genes results in dysfunctional mood regulation. However,... 
Psychiatry | Antidepressant | CREB | fluoxetine | BDNF | mood disorders | neuroplasticity genes regulation | transcriptional coactivator | major depression | PSYCHIATRY | NEUROTROPHIC FACTOR | ELEMENT-BINDING PROTEIN | ANGER ATTACKS | BIPOLAR DISORDER | ANTIDEPRESSANT DRUGS | CAMP RESPONSE | NEUROSCIENCES | BDNF TRANSCRIPTION | SUICIDE ATTEMPTS | ANIMAL-MODELS | Fear - drug effects | Neuronal Plasticity - drug effects | Male | Receptor, trkB - genetics | Orphan Nuclear Receptors - metabolism | Arabidopsis Proteins - metabolism | Brain - metabolism | Nesting Behavior - drug effects | Sexual Behavior, Animal - physiology | Swimming - psychology | Exploratory Behavior - drug effects | Brain-Derived Neurotrophic Factor - metabolism | Sexual Behavior, Animal - drug effects | Disease Models, Animal | Fluoxetine - pharmacology | Maze Learning - physiology | Food Preferences - drug effects | Antidepressive Agents, Second-Generation - pharmacology | Signal Transduction - genetics | Hindlimb Suspension | Depressive Disorder - metabolism | Maternal Behavior - drug effects | Orphan Nuclear Receptors - genetics | Mice, Knockout | Signal Transduction - drug effects | Brain - pathology | Mice | Biogenic Monoamines - metabolism | Aggression - physiology | Brain-Derived Neurotrophic Factor - genetics | Electroshock - adverse effects | Food Preferences - physiology | Transcription Factors - deficiency | Depressive Disorder - drug therapy | Chromatography, High Pressure Liquid | Antidepressive Agents, Second-Generation - therapeutic use | Exploratory Behavior - physiology | Neuronal Plasticity - genetics | Social Behavior | Fear - psychology | Female | Corticosterone - blood | Fluoxetine - therapeutic use | Depressive Disorder - genetics | Enzyme-Linked Immunosorbent Assay | Gene Expression Regulation - genetics | Mice, Inbred C57BL | Nesting Behavior - physiology | Maternal Behavior - physiology | Maze Learning - drug effects | Intramolecular Transferases - metabolism | Transcription Factors - metabolism | Animals | Aggression - drug effects | Receptor, trkB - metabolism | Neurosciences | Fluoxetine | Analysis | Genes | Depression, Mental | Disease susceptibility | Genetic transcription | Adenylic acid | Protein binding
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 04/2009, Volume 29, Issue 13, pp. 4200 - 4209
Although the tryptophan-degrading enzyme, indoleamine 2,3-dioxygenase (IDO), is a pivotal mediator of inflammation-induced depression, its mechanism of... 
QUINOLINIC ACID | TRYPTOPHAN-METABOLISM | IFN-GAMMA | MEDICALLY ILL | IMMUNE ACTIVATION | CENTRAL-NERVOUS-SYSTEM | SICKNESS BEHAVIOR | PROINFLAMMATORY CYTOKINES | TNF-ALPHA | DIFFERENTIAL REGULATION | NEUROSCIENCES | Indoleamine-Pyrrole 2,3,-Dioxygenase - genetics | Indoleamine-Pyrrole 2,3,-Dioxygenase - metabolism | Tumor Necrosis Factor-alpha - metabolism | Immobility Response, Tonic - physiology | Motor Activity - physiology | Chromatography, High Pressure Liquid - methods | Dose-Response Relationship, Immunologic | Mycobacterium bovis - immunology | Depression - pathology | Neuroglia | Brain - enzymology | Motor Activity - drug effects | Male | Interferon-gamma - metabolism | RNA, Messenger - metabolism | Lung - enzymology | Receptors, Tumor Necrosis Factor - therapeutic use | Depression - etiology | Depression - drug therapy | Etanercept | Up-Regulation - physiology | Immobility Response, Tonic - drug effects | Swimming | Animals, Newborn | Cytokines - metabolism | Receptors, Interferon - deficiency | Mice, Inbred C57BL | Cells, Cultured | Depression - microbiology | Immunoglobulin G - therapeutic use | Hindlimb Suspension - methods | Mice, Inbred ICR | Mice, Knockout | Brain - drug effects | Drug Synergism | Up-Regulation - drug effects | Illness Behavior - drug effects | Animals | Anti-Inflammatory Agents, Non-Steroidal - therapeutic use | Interferon-gamma - administration & dosage | Lung - drug effects | Serotonin - metabolism | Tumor Necrosis Factor-alpha - administration & dosage | Mice | Index Medicus
Journal Article
British Journal of Pharmacology, ISSN 0007-1188, 07/2012, Volume 166, Issue 6, pp. 1872 - 1887
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 2/2013, Volume 110, Issue 9, pp. 3573 - 3578
Symptoms of depression can be induced in humans through blockade of acetylcholinesterase (AChE) whereas antidepressant-like effects can be produced in animal... 
Cholinergics | Pain | Genetic variation | Antidepressants | Mice | Anxiety | Cholinergic receptors | Behavioral neuroscience | Hippocampus | Depressive disorders | Affective disorders | Psychosocial stress | SYSTEM | psychosocial stress | ACETYLCHOLINE | MULTIDISCIPLINARY SCIENCES | SCOPOLAMINE | NUCLEUS-ACCUMBENS | ADRENERGIC HYPOTHESIS | affective disorders | ANIMAL-MODEL | MICE | RECEPTORS | ANTIDEPRESSANT-LIKE PROPERTIES | BRAIN | Humans | Male | Anxiety - drug therapy | Hippocampus - drug effects | Cholinergic Antagonists - pharmacology | Gene Knockdown Techniques | Depression - drug therapy | Depression - metabolism | Time Factors | Stress, Psychological - metabolism | Anxiety - complications | Behavior, Animal - drug effects | Depression - complications | Antidepressive Agents - pharmacology | Resilience, Psychological | Fluoxetine - therapeutic use | Anxiety - metabolism | Cholinergic Antagonists - therapeutic use | Fluoxetine - pharmacology | Dependovirus - metabolism | Receptors, Cholinergic - metabolism | Cholinergic Neurons - metabolism | Stress, Psychological - drug therapy | Mice, Inbred C57BL | Anxiety - psychology | Hippocampus - pathology | Physostigmine | Cholinergic Neurons - drug effects | Hindlimb Suspension | Antidepressive Agents - therapeutic use | Hippocampus - metabolism | Phenotype | Animals | Signal Transduction - drug effects | Depression - psychology | Cholinergic Neurons - pathology | Acetylcholinesterase - metabolism | Stress, Psychological - complications | RNA, Small Interfering - metabolism | Physiological aspects | Hippocampus (Brain) | Stress (Psychology) | Depression, Mental | Biological Sciences
Journal Article
Molecular Psychiatry, ISSN 1359-4184, 05/2009, Volume 14, Issue 5, pp. 511 - 522
Although elevated activity of the tryptophan-degrading enzyme indoleamine 2,3-dioxygenase (IDO) has been proposed to mediate comorbid depression in... 
Kynurenine | Minocycline | Tryptophan | 1-methyltryptophan | Forced-swim test | Tail suspension test | tail suspension test | RHEUMATOID-ARTHRITIS | forced-swim test | DENDRITIC CELLS | KYNURENINE PATHWAY | PSYCHIATRY | BIOCHEMISTRY & MOLECULAR BIOLOGY | kynurenine | NECROSIS-FACTOR-ALPHA | PROINFLAMMATORY CYTOKINES | NEUROSCIENCES | INTERFERON-ALPHA | QUINOLINIC ACID | CANCER-PATIENTS | minocycline | INDUCED SICKNESS BEHAVIOR | TRYPTOPHAN DEGRADATION | tryptophan | Indoleamine-Pyrrole 2,3,-Dioxygenase - genetics | Indoleamine-Pyrrole 2,3,-Dioxygenase - metabolism | Minocycline - pharmacology | Kynurenine - adverse effects | Motor Activity - drug effects | Male | Chromatography, High Pressure Liquid | Dose-Response Relationship, Drug | Kynurenine - blood | Tryptophan - blood | Time Factors | Minocycline - therapeutic use | Tryptophan - analogs & derivatives | Depression - chemically induced | Behavior, Animal - drug effects | Swimming | Disease Models, Animal | Enzyme Inhibitors - pharmacology | Enzyme Activation - drug effects | Hindlimb Suspension - methods | Enzyme Inhibitors - therapeutic use | Mice, Inbred ICR | Gene Expression Regulation - drug effects | Animals | Lipopolysaccharides - pharmacology | Cytokinins - metabolism | Mice | Tryptophan - pharmacology | Tryptophan - therapeutic use | Indoleamine-Pyrrole 2,3,-Dioxygenase - antagonists & inhibitors | Depression - blood | Mediators | Depression, Mental | Indole | Physiological aspects | Development and progression | Inflammation | Research | Enzyme activation | serotonin | interferon-γ | tumor necrosis factor-α | depression | interleukin-1β | forced swim test
Journal Article