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1. Full Text Reward, addiction, withdrawal to nicotine
by De Biasi, Mariella and Dani, John A
Annual review of neuroscience, ISSN 0147-006X, 07/2011, Volume 34, Issue 1, pp. 105 - 130
Nucleus accumbens | Dopamine | Interpeduncular nucleus | Ventral tegmental area | Habenula | Synaptic plasticity | Limbic System - pathology | Receptors, Nicotinic - metabolism | Substance Withdrawal Syndrome - etiology | Humans | Cerebral Cortex - pathology | Neuronal Plasticity - drug effects | Nicotine - adverse effects | Substance Withdrawal Syndrome - pathology | Animals | Neuronal Plasticity - physiology | Neurons - physiology | Reward | Behavior, Addictive - physiopathology | Substance Withdrawal Syndrome - psychology | Dopamine - metabolism | Psychological aspects | Physiological aspects | Health aspects | Nicotine | Tobacco habit | Addictions | Neurons | Index Medicus | interpeduncular nucleus | synaptic plasticity | nucleus accumbens | ventral tegmental area | habenula | dopamine
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2. Full Text Morphine withdrawal recruits lateral habenula cytokine signaling to reduce synaptic excitation and sociability
by Valentinova, Kristina and Tchenio, Anna and Trusel, Massimo and Clerke, Joseph A and Lalive, Arnaud L and Tzanoulinou, Stamatina and Matera, Alessandro and Moutkine, Imane and Maroteaux, Luc and Paolicelli, Rosa C and Volterra, Andrea and Bellone, Camilla and Mameli, Manuel
Nature neuroscience, ISSN 1097-6256, 07/2019, Volume 22, Issue 7, pp. 1053 - 1056
Neurosciences | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | Receptors, Glutamate - analysis | Naloxone - toxicity | Synaptic Transmission - physiology | Receptors, N-Methyl-D-Aspartate - analysis | Mice, Inbred C57BL | Male | Random Allocation | Receptors, Tumor Necrosis Factor, Type I - genetics | Cytokines - physiology | Animals | Microglia - physiology | Neuronal Plasticity | Receptors, Tumor Necrosis Factor, Type I - physiology | Social Behavior | Tumor Necrosis Factor-alpha - physiology | Female | Mice | Substance Withdrawal Syndrome - physiopathology | Substance Withdrawal Syndrome - psychology | Morphine - adverse effects | Adaptation, Psychological | Habenula - physiology | Neuroplasticity | Development and progression | Drug withdrawal symptoms | Cytokines | Health aspects | Analysis | Adaptations | Tumor necrosis factor receptors | Behavioral plasticity | Habenula | Synaptic plasticity | Morphine | Tumor necrosis factor-TNF | Inhibition (psychology) | Glutamatergic transmission | Tumor necrosis factor-α | Microglia | Index Medicus | Animal genetics | Neurons and Cognition | Neurobiology | Synaptic Transmission | Life Sciences | Genetics | Pulmonology and respiratory tract | Cardiology and cardiovascular system | Pharmaceutical sciences | Receptors, Glutamate | Receptors, Tumor Necrosis Factor, Type I | Biochemistry, Molecular Biology | Receptors, N-Methyl-D-Aspartate | Pharmacology | Substance Withdrawal Syndrome | Tumor Necrosis Factor-alpha | Psychiatrics and mental health | Human health and pathology | Naloxone | Molecular biology
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3. Full Text Is there an antiandrogen withdrawal syndrome with enzalutamide?
by Rodriguez‐Vida, Alejo and Bianchini, Diletta and Van Hemelrijck, Mieke and Hughes, Simon and Malik, Zafar and Powles, Thomas and Bahl, Amit and Rudman, Sarah and Payne, Heather and Bono, Johann and Chowdhury, Simon
BJU international, ISSN 1464-4096, 03/2015, Volume 115, Issue 3, pp. 373 - 380
castration‐resistant prostate cancer | androgen receptor targeting | hormone therapy | androgen receptor gene F876L mutation | enzalutamide | antiandrogen withdrawal syndrome | castration-resistant prostate cancer | Life Sciences & Biomedicine | Urology & Nephrology | Science & Technology | Phenylthiohydantoin - adverse effects | Phenylthiohydantoin - therapeutic use | Substance Withdrawal Syndrome - etiology | Prostatic Neoplasms, Castration-Resistant - blood | Humans | Middle Aged | Kaplan-Meier Estimate | Male | Antineoplastic Agents - therapeutic use | Prostatic Neoplasms, Castration-Resistant - drug therapy | Phenylthiohydantoin - analogs & derivatives | Prostate-Specific Antigen - blood | Prostatic Neoplasms, Castration-Resistant - pathology | Antineoplastic Agents - adverse effects | Substance Withdrawal Syndrome - blood | Aged, 80 and over | Androgen Antagonists - therapeutic use | Aged | Kallikreins - blood | Retrospective Studies | Androgen Antagonists - adverse effects | Prostate cancer | Analysis | Medical research | Metastasis | Index Medicus
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4. Full Text Inactivation of a CRF-dependent amygdalofugal pathway reverses addiction-like behaviors in alcohol-dependent rats
by de Guglielmo, Giordano and Kallupi, Marsida and Pomrenze, Matthew B and Crawford, Elena and Simpson, Sierra and Schweitzer, Paul and Koob, George F and Messing, Robert O and George, Olivier
Nature communications, ISSN 2041-1723, 12/2019, Volume 10, Issue 1, pp. 1238 - 1238
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Humans | Septal Nuclei - pathology | Male | Optogenetics | Septal Nuclei - cytology | Substance Withdrawal Syndrome - pathology | Behavior, Animal | Septal Nuclei - metabolism | Substance Withdrawal Syndrome - metabolism | Central Amygdaloid Nucleus - physiopathology | Corticotropin-Releasing Hormone - genetics | Neurons - metabolism | Neural Pathways - physiopathology | Septal Nuclei - physiopathology | Alcoholism - physiopathology | Behavior, Addictive - physiopathology | Disease Models, Animal | Alcoholism - pathology | Central Amygdaloid Nucleus - cytology | Rats | Corticotropin-Releasing Hormone - metabolism | Central Amygdaloid Nucleus - pathology | Animals | Neural Pathways - metabolism | Central Amygdaloid Nucleus - metabolism | Substance Withdrawal Syndrome - physiopathology | Substance Withdrawal Syndrome - psychology | Drug addiction | Deactivation | Amygdala | Neurons | Drinking behavior | Withdrawal | Stria terminalis | Inactivation | Corticotropin-releasing hormone | Alcohol use | Alcohols | Addiction | Inhibition | Index Medicus
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5. Full Text Immune reconstitution inflammatory syndrome after withdrawal of natalizumab?
by Lenhard, T and Biller, A and Mueller, W and Metz, I and Schönberger, J and Wildemann, B
Neurology, ISSN 0028-3878, 08/2010, Volume 75, Issue 9, pp. 831 - 833
Clinical Neurology | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | Neurology | Biological and medical sciences | Malformations of the nervous system | Medical sciences | Multiple Sclerosis, Relapsing-Remitting - pathology | Immune Reconstitution Inflammatory Syndrome - etiology | Natalizumab | Substance Withdrawal Syndrome - etiology | Immune Reconstitution Inflammatory Syndrome - diagnosis | Multiple Sclerosis, Relapsing-Remitting - drug therapy | Humans | Antibodies, Monoclonal - adverse effects | Substance Withdrawal Syndrome - pathology | Immune Reconstitution Inflammatory Syndrome - pathology | Antibodies, Monoclonal, Humanized | Antibodies, Monoclonal - administration & dosage | Adult | Female | Substance Withdrawal Syndrome - diagnosis | Index Medicus | Abridged Index Medicus
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6. Full Text Cannabinoid Type 1 Receptor (CB1) Ligands with Therapeutic Potential for Withdrawal Syndrome in Chemical Dependents of Cannabis sativa
by Ferreira, Jaderson V and Chaves, Gisele A and Marino, Bianca L. B and Sousa, Kessia P. A and Souza, Lucilene R and Brito, Maiara F. B and Teixeira, Hueldem R. C and da Silva, Carlos H. T. P and Santos, Cleydson B. R and Hage‐Melim, Lorane I. S
ChemMedChem, ISSN 1860-7179, 08/2017, Volume 12, Issue 16, pp. 1408 - 1416
structural similarity | Cannabis sativa | virtual screening | computational chemistry | medicinal chemistry | Caco-2 Cells | Resorcinols - pharmacokinetics | Receptor, Cannabinoid, CB2 - agonists | Humans | Half-Life | Substance Withdrawal Syndrome - drug therapy | Cannabis - metabolism | Blood-Brain Barrier - drug effects | Resorcinols - therapeutic use | Blood-Brain Barrier - metabolism | Substance Withdrawal Syndrome - pathology | Resorcinols - pharmacology | Receptor, Cannabinoid, CB1 - metabolism | Receptor, Cannabinoid, CB2 - metabolism | Cannabis - chemistry | Animals | Receptor, Cannabinoid, CB1 - agonists | Substance Withdrawal Syndrome - metabolism | Resorcinols - chemistry | Cell Membrane Permeability - drug effects | Drug Design | Ligands | Mice | Marijuana | Health aspects | Index Medicus
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7. Full Text Neonatal withdrawal syndrome after chronic maternal consumption of 4-methylethcathinone
by Pichini, Simona and Rotolo, Maria Concetta and García, Jordi and Girona, Noelia and Leal, Lorna and García-Algar, Oscar and Pacifici, Roberta
Forensic science international, ISSN 0379-0738, 2014, Volume 245, pp. e33 - e35
Pathology | Meconium | Hair testing | Neonatal withdrawal syndrome | 4-Methylethcathinone | Life Sciences & Biomedicine | Medicine, Legal | Legal Medicine | Science & Technology | Pregnancy | Propiophenones - adverse effects | Maternal-Fetal Exchange | Humans | Designer Drugs - adverse effects | Amphetamines - adverse effects | Female | Neonatal Abstinence Syndrome - etiology | Infant, Newborn | Substance-Related Disorders - complications | Mephedrone | Birth defects | Research | Maternal-fetal exchange | Hypertension | Hair | Ecstasy | Urine | Consumption | Cardiac arrhythmia | Dopamine | Medical treatment | Methamphetamine | Hepatitis | Drug dosages | Heroin | Drugs | Websites | Segments | Markets | Liquid chromatography | Exposure | Index Medicus
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8. Full Text Spinal microglial P2X4 receptor–brain-derived neurotrophic factor signaling regulates nicotine withdrawal-induced hyperalgesia
by Zhang, Xiaodi and Xu, Pengcheng and Li, Chengbao and Zhu, Wenchao and Wu, Shanshan and Yu, Ailan and Ding, Yonghong and Wang, Qinghe and Zhang, Zongwang
Neuroreport, ISSN 0959-4965, 04/2017, Volume 28, Issue 6, pp. 339 - 347
thermal hyperalgesia | ionized calcium-binding adapter molecule 1 | brain-derived neurotrophic factor | minocycline | pain hypersensitivity | P2X4 receptor | Neurosciences | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | Hyperalgesia - chemically induced | Microglia - metabolism | Pain Threshold - physiology | Spinal Cord - drug effects | Spinal Cord - metabolism | Minocycline - pharmacology | Analgesics, Non-Narcotic - pharmacology | Substance Withdrawal Syndrome - drug therapy | Male | Hyperalgesia - pathology | Substance Withdrawal Syndrome - pathology | Substance Withdrawal Syndrome - metabolism | Spinal Cord - pathology | Microglia - pathology | Pain Threshold - drug effects | Brain-Derived Neurotrophic Factor - metabolism | Microfilament Proteins - metabolism | Nicotinic Agonists - toxicity | Disease Models, Animal | Calcium-Binding Proteins - metabolism | Hyperalgesia - metabolism | Microglia - drug effects | Hot Temperature | Nicotine - toxicity | Rats, Sprague-Dawley | Animals | Hyperalgesia - drug therapy | Receptors, Purinergic P2X4 - metabolism | Index Medicus
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9. Full Text Morphine Withdrawal Increases Brain-Derived Neurotrophic Factor Precursor
by Bachis, Alessia and Campbell, Lee A and Jenkins, Kierra and Wenzel, Erin and Mocchetti, Italo
Neurotoxicity research, ISSN 1029-8428, 10/2017, Volume 32, Issue 3, pp. 509 - 517
Neurochemistry | Neurology | Neurosciences | Biomedicine | BDNF | Tissue plasminogen activator | Neurobiology | Furin | proBDNF | Pharmacology/Toxicology | Opioid abuse | Cell Biology | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | Neurons - pathology | Frontal Lobe - metabolism | Tissue Plasminogen Activator - metabolism | Male | Morphine - toxicity | Corpus Striatum - metabolism | Substance Withdrawal Syndrome - pathology | Substance Withdrawal Syndrome - metabolism | Matrix Metalloproteinase 7 - metabolism | Brain-Derived Neurotrophic Factor - metabolism | Neurons - metabolism | Neurons - drug effects | Corpus Striatum - pathology | Furin - metabolism | Cells, Cultured | Matrix Metalloproteinase 3 - metabolism | Rats, Sprague-Dawley | Protein Precursors - metabolism | Morphine Dependence - metabolism | Morphine Dependence - pathology | Animals | Frontal Lobe - drug effects | Corpus Striatum - drug effects | Narcotics - toxicity | Frontal Lobe - pathology | Morphine | Proteases | Neurons | Analysis | Neurophysiology | Index Medicus | opioid abuse | tissue plasminogen activator | furin
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10. Full Text Methamphetamine abstinence induces changes in μ-opioid receptor, oxytocin and CRF systems: Association with an anxiogenic phenotype
by Georgiou, Polymnia and Zanos, Panos and Garcia-Carmona, Juan-Antonio and Hourani, Susanna and Kitchen, Ian and Laorden, Maria-Luisa and Bailey, Alexis
Neuropharmacology, ISSN 0028-3908, 06/2016, Volume 105, pp. 520 - 532
Methamphetamine withdrawal | Anxiety | Oxytocin | CRF | μ-opioid receptor | Pharmacology & Pharmacy | Neurosciences | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | Neurons - pathology | Amygdala - drug effects | Methamphetamine - adverse effects | Male | Amphetamine-Related Disorders - pathology | Receptors, Dopamine D2 - metabolism | Corpus Striatum - metabolism | Substance Withdrawal Syndrome - pathology | Substance Withdrawal Syndrome - metabolism | Central Nervous System Stimulants - adverse effects | Septum of Brain - pathology | Neurons - metabolism | Corticosterone - blood | Neurons - drug effects | Anxiety - metabolism | Corpus Striatum - pathology | Amphetamine-Related Disorders - metabolism | Disease Models, Animal | Receptors, Opioid, mu - metabolism | Mice, Inbred C57BL | Amygdala - metabolism | Proto-Oncogene Proteins c-fos - metabolism | Septum of Brain - metabolism | Septum of Brain - drug effects | Random Allocation | Amygdala - pathology | Corticotropin-Releasing Hormone - metabolism | Anxiety - pathology | Receptors, Oxytocin - metabolism | Animals | Methamphetamine - administration & dosage | Corpus Striatum - drug effects | Amphetamine-Related Disorders - complications | Central Nervous System Stimulants - administration & dosage | Substance Withdrawal Syndrome - psychology | Anxiety - etiology | Index Medicus
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