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1. Serotonin-dopamine interaction
: experimental evidence and therapeutic relevance
by Di Giovanni, Giuseppe and Di Matteo, Vincenzo and Esposito, Ennio
2008, Progress in brain research, ISBN 0444532358, Volume 172., xv, 665 p. [6] p. of plates
This book provides a unique and timely multidisciplinary synthesis of our current knowledge of the anatomy, pharmacology, physiology and behavioral data of the... 
Neurochemistry | Neurotransmitters | Dopamine | Serotonin | Neurochimie
Book
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2. Metabolic modifiers
: effects on the nutrient requirements of food-producing animals
National Research Council (U.S.). Subcommittee on Effects of Metabolic Modifiers on the Nutrient Requirements of Food-Producing Animals
1994, ISBN 9780309049979, xii, 79
Nutrition | Anabolic steroids in animal nutrition | Feed utilization efficiency | Livestock | Somatotropin in animal nutrition | Adrenergic beta agonists in animal nutrition | Metabolism | Requirements
Book
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3. Beta₂-agonists in asthma treatment
by Pauwels, Romain and O'Byrne, Paul M
1997, Lung biology in health and disease, ISBN 9780824794965, Volume 106., xvi, 443
Adrenergic beta agonists | Chemotherapy | Therapeutic use | Asthma
Book
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4. Pain control and drug policy
: a time for change
by Faguet, Guy B
2010, ISBN 9780313382802, xiv, 238
Book
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5. Opioid agonists, antagonists and mixed narcotic analgesics
: theoretical background and considerations for practical use
by Freye, Enno
1987, ISBN 9780387174716, ix, 108
Narcotics | Therapeutic use | Opioids
Book
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6. Full Text N-terminal guanidinylation of TIPP (Tyr-Tic-Phe-Phe) peptides results in major changes of the opioid activity profile
by Weltrowska, Grazyna and Nguyen, Thi M.-D and Chung, Nga N and Wilkes, Brian C and Schiller, Peter W
Bioorganic & Medicinal Chemistry Letters, ISSN 0960-894X, 09/2013, Volume 23, Issue 18, pp. 5082 - 5085
Derivatives of peptides of the TIPP (Tyr-Tic-Phe-Phe; Tic = 1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid) family containing a guanidino (Guan) function in... 
μ Opioid agonist/δ opioid antagonists | δ Partial opioid agonists | Peptide synthesis | Guanidinylated opioid peptides | δ Opioid antagonists | μ Opioid agonist/δ opioid agonists | Opioid agonist/δ opioid agonists | Opioid antagonists δ Partial opioid agonists μ | Guanidinylated opioid peptides δ | Opioid agonist/δ opioid antagonists μ | CHEMISTRY, MEDICINAL | mu Opioid agonist/delta opioid agonists | CHEMISTRY, ORGANIC | AGONISTS | mu Opioid agonist/delta opioid antagonists | RECEPTOR ANTAGONIST | DEPENDENCE | BRAIN-BARRIER PERMEABILITY | POTENT | TIPP | MORPHINE-TOLERANCE | delta Partial opioid agonists | MICE | delta Opioid antagonists | MODULATION | Dose-Response Relationship, Drug | Guanidines - chemistry | Receptors, Opioid, delta - metabolism | Oligopeptides - chemical synthesis | Tetrahydroisoquinolines - pharmacology | Tetrahydroisoquinolines - chemistry | Models, Molecular | Receptors, Opioid, delta - antagonists & inhibitors | Structure-Activity Relationship | Tetrahydroisoquinolines - chemical synthesis | Oligopeptides - pharmacology | Oligopeptides - chemistry | guanidinylated opioid peptides | μ opioid agonist | δ opioid agonists | δ opioid antagonists | δ partial opioid agonists
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7. Full Text Transcranial random noise stimulation-induced plasticity is NMDA-receptor independent but sodium-channel blocker and benzodiazepines sensitive
by Chaieb, Leila and Antal, Andrea and Paulus, Walter
Frontiers in Neuroscience, ISSN 1662-4548, 2015, Volume 9, p. 125
Background: Application of transcranial random noise stimulation (tRNS) between 0.1 and 640 Hz of the primary motor cortex (M1) for 10 min induces a persistent... 
Transcranial magnetic stimulation (TMS) | D-cycloserine (D-CYC: partial NMDA receptor agonist) | Dextromethorphan (DMO: NMDA receptor antagonist) | transcranial random noise stimulation (tRNS) | Carbamazepine (CBZ: sodium channel blocker) | Lorazepam (LOR: GABA A receptor agonist) | Ropinirole (ROP: D 2 /D 3 receptor agonist) | Transcranial direct current stimulation (tDCS) | carbamazepine (CBZ: sodium channel blocker) | CELLS | ACTIVATION | EXCITATION | NEUROPLASTICITY | HUMANS | NEUROSCIENCES | CORTICAL EXCITABILITY | HUMAN MOTOR CORTEX | CONSOLIDATION | ropinirole (ROP: D-2/D-3 receptor agonist) | transcranial magnetic stimulation (TMS) | NONINVASIVE BRAIN-STIMULATION | dextromethorphan (DMO: NMDA receptor antagonist) | transcranial direct current stimulation (tDCS) | MODULATION | lorazepam (LOR: GABA(A) receptor agonist) | Dopamine | Transcranial magnetic stimulation | γ-Aminobutyric acid A receptors | Glutamic acid receptors (ionotropic) | Noise | Cortex | Dopamine D3 receptors | Excitability | N-Methyl-D-aspartic acid receptors | Dextromethorphan | Cortex (motor) | Cycloserine | Benzodiazepines | Carbamazepine | Neurophysiology | Electrical currents | Electrodes | Morphology | Agonists | Lorazepam | Magnetic fields | Electric fields | ropinirole (ROP: D2/D3 receptor agonist) | lorazepam (LOR: GABAA receptor agonist)
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8. Full Text Clonidine and Dexmedetomidine Increase the Pressor Response to Norepinephrine in Experimental Sepsis: A Pilot Study
by Geloen, A and Chapelier, K and Cividjian, A and Dantony, E and Rabilloud, M and May, C N and Quintin, L
Critical Care Medicine, ISSN 0090-3493, 12/2013, Volume 41, Issue 12, pp. e431 - e438
OBJECTIVE:During septic shock, vasopressors are a cornerstone of therapy. In septic shock, very high doses of vasopressors sometimes have to be used due to... 
A-1 agonist | Escherichia coli | A-2 agonist | Septic shock | Pressor response | Endotoxin | A-1 adrenergic agonist | A-2 adrenergic agonist | Vascular reactivity | Dexmedetomidine | Lipopolysaccharide | Sepsis | Clonidine | Norepinephrine | Endotoxemia | norepinephrine | SURGERY | MORTALITY | REQUIREMENTS | dexmedetomidine | septic shock | endotoxemia | vascular reactivity | RATS | alpha-2 adrenergic agonist | alpha-1 adrenergic agonist | alpha-1 agonist | alpha-2 agonist | CRITICAL CARE MEDICINE | INFLAMMATORY RESPONSES | clonidine | pressor response | ENDOTOXIN-INDUCED SHOCK | ROSTRAL VENTROLATERAL MEDULLA | SYMPATHETIC-NERVE ACTIVITY | ESSENTIAL-HYPERTENSION | lipopolysaccharide | sepsis | endotoxin | Vasoconstrictor Agents - therapeutic use | Norepinephrine - therapeutic use | Dexmedetomidine - therapeutic use | Shock, Septic - chemically induced | Rats | Shock, Septic - complications | Male | Shock, Septic - physiopathology | Clonidine - therapeutic use | Random Allocation | Rats, Sprague-Dawley | Lipopolysaccharides | Hypotension - drug therapy | Pilot Projects | Adrenergic alpha-2 Receptor Agonists - therapeutic use | Animals | Hypotension - physiopathology | Arterial Pressure - drug effects | Hypotension - etiology
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9. Full Text AM-251 and rimonabant act as direct antagonists at mu-opioid receptors: Implications for opioid/cannabinoid interaction studies
by Seely, Kathryn A and Brents, Lisa K and Franks, Lirit N and Rajasekaran, Maheswari and Zimmerman, Sarah M and Fantegrossi, William E and Prather, Paul L
Neuropharmacology, ISSN 0028-3908, 10/2012, Volume 63, Issue 5, pp. 905 - 915
Mu-opioid and CB1-cannabinoid agonists produce analgesia; however, adverse effects limit use of drugs in both classes. Additive or synergistic effects... 
Analgesia | Morphine | Marijuana | G-protein | Adenylyl cyclase | CB1 receptors | AGONIST MORPHINE | ACTIVATION | PROTEIN-KINASE | CB1 CANNABINOID RECEPTOR | SYNERGISTIC INTERACTIONS | NEUROSCIENCES | INHIBITION | KAPPA | FULL AGONIST | ADENYLYL-CYCLASE | PHARMACOLOGY & PHARMACY | RAT-BRAIN | Pyrazoles - therapeutic use | Receptor, Cannabinoid, CB2 - agonists | Humans | Analgesics, Opioid - pharmacology | Receptors, Opioid, mu - agonists | Piperidines - pharmacology | Cannabinoid Receptor Agonists - therapeutic use | Recombinant Proteins - antagonists & inhibitors | Piperidines - metabolism | Receptors, Opioid, mu - metabolism | Morpholines - metabolism | Analgesics, Non-Narcotic - metabolism | Drug Inverse Agonism | Mice | Analgesics, Opioid - metabolism | Kinetics | Receptor, Cannabinoid, CB1 - antagonists & inhibitors | Analgesics, Opioid - antagonists & inhibitors | Cannabinoid Receptor Agonists - metabolism | Cricetulus | Analgesics, Non-Narcotic - pharmacology | Cannabinoid Receptor Agonists - pharmacology | Receptor, Cannabinoid, CB2 - genetics | Analgesics, Opioid - adverse effects | Narcotic Antagonists - metabolism | Receptor, Cannabinoid, CB1 - agonists | Analgesics, Non-Narcotic - adverse effects | Cannabinoid Receptor Agonists - adverse effects | Morpholines - adverse effects | CHO Cells | Pyrazoles - adverse effects | Pyrazoles - pharmacology | Binding, Competitive | Recombinant Proteins - metabolism | Cricetinae | Morpholines - pharmacology | Narcotic Antagonists - adverse effects | Recombinant Proteins - agonists | Analgesics, Non-Narcotic - therapeutic use | Pyrazoles - metabolism | Mice, Inbred Strains | Receptors, Opioid, mu - antagonists & inhibitors | Receptor, Cannabinoid, CB1 - metabolism | Receptor, Cannabinoid, CB2 - metabolism | Animals | Narcotic Antagonists - therapeutic use | Piperidines - therapeutic use | Narcotic Antagonists - pharmacology | Piperidines - adverse effects | Receptors, Opioid, mu - genetics | Index Medicus | Drugs | Pain perception | Opioid receptors | Cyclic AMP | Opioid receptors (type mu) | Antagonists | Cannabinoid CB1 receptors | Guanine nucleotide-binding protein | Antagonism | Cell activation | Side effects | Inverse agonists | CB1 Receptors | Adenylyl Cyclase
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10. Full Text Novel Dopamine Therapeutics for Cognitive Deficits in Schizophrenia
by Arnsten, Amy F.T and Girgis, Ragy R and Gray, David I and Mailman, Richard B
Biological Psychiatry, ISSN 0006-3223, 2016, Volume 81, Issue 1, pp. 67 - 77
Abstract Schizophrenia is characterized by profound cognitive deficits that are not alleviated by currently available medications. Many of these cognitive... 
Psychiatry | Schizophrenia | D2 receptors | D1 agonist | Executive function | Prefrontal cortex | Working memory | agonist | receptors | LOW-DOSE HALOPERIDOL | RECEPTOR AGONIST DIHYDREXIDINE | PSYCHIATRY | FULL DOPAMINE | SCHIZOTYPAL PERSONALITY-DISORDER | NEUROSCIENCES | D-2 receptors | TREATMENT-RESISTANT SCHIZOPHRENIA | FUNCTIONAL SELECTIVITY | D-1 agonist | C-FOS EXPRESSION | PARKINSONS-DISEASE | WORKING-MEMORY | Receptors, Dopamine D1 - antagonists & inhibitors | Phenanthridines - therapeutic use | Humans | Prefrontal Cortex - physiopathology | Receptors, Dopamine D2 - agonists | Dopamine Agonists - therapeutic use | Dopamine Antagonists - therapeutic use | Schizophrenic Psychology | Dopamine Antagonists - administration & dosage | Phenanthridines - administration & dosage | Animals | Prefrontal Cortex - drug effects | Dopamine - physiology | Receptors, Dopamine D1 - physiology | Schizophrenia - physiopathology | Dopamine Agonists - administration & dosage | Receptors, Dopamine D1 - agonists | Receptors, Dopamine D2 - physiology | Schizophrenia - drug therapy | Receptors, Dopamine - physiology | Brain | Medical colleges | Dopamine | Neurons | Medical societies | Primates | Phenols | Pharmaceutical industry | Neurophysiology | schizophrenia | working memory | prefrontal cortex | executive function
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11. Full Text Targeting the endocannabinoid system with cannabinoid receptor agonists: pharmacological strategies and therapeutic possibilities
by Roger G. Pertwee
Philosophical Transactions: Biological Sciences, ISSN 0962-8436, 12/2012, Volume 367, Issue 1607, pp. 3353 - 3363
Human tissues express cannabinoid CB₁ and CB₂ receptors that can be activated by endogenously released 'endocannabinoids' or exogenously administered compounds... 
Receptors | Cannabinoids | Animal models | Pain | Medical treatment | Agonists | Morphine | Drug design | Endocannabinoids | Cannabinoid receptors | And CB2 | Blood-brain barrier | Cannabinoid receptor agonists | Δ9-tetrahydrocannabinol | Cannabinoid CB1 | Therapeutic applications and strategies | blood-brain barrier | Delta-tetrahydrocannabinol | cannabinoid CB1 and CB2 receptors | CB2 RECEPTOR | LIVER-DISEASES | AMYOTROPHIC-LATERAL-SCLEROSIS | ANXIETY-LIKE BEHAVIOR | MU-OPIOID RECEPTOR | RAT FORMALIN TEST | therapeutic applications and strategies | cannabinoid receptor agonists | NEUROPATHIC PAIN | MOUSE MODEL | BIOLOGY | PENTYLENETETRAZOLE-INDUCED SEIZURE | CENTRAL-NERVOUS-SYSTEM | Endocannabinoids - metabolism | Analgesics - pharmacology | Receptor, Cannabinoid, CB2 - agonists | Cardiovascular Diseases - drug therapy | Humans | Cannabinoid Receptor Agonists - pharmacology | Neurodegenerative Diseases - drug therapy | Pain - metabolism | Receptor, Cannabinoid, CB1 - agonists | Pain - drug therapy | Cannabinoid Receptor Agonists - therapeutic use | Dronabinol - pharmacology | Analgesics - therapeutic use | Cardiovascular Diseases - metabolism | Risk Assessment | Analgesics - administration & dosage | Clinical Trials as Topic | Neurodegenerative Diseases - metabolism | Blood-Brain Barrier - drug effects | Cannabinoid Receptor Agonists - administration & dosage | Drug Discovery | Blood-Brain Barrier - metabolism | Receptor, Cannabinoid, CB1 - metabolism | Receptor, Cannabinoid, CB2 - metabolism | Animals | Dronabinol - therapeutic use | Review
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12. Full Text Update on ultra-long-acting β agonists in chronic obstructive pulmonary disease
by Zafar, Muhammad Ahsan and Droege, Christopher and Foertsch, Madeline and Panos, Ralph J
Expert Opinion on Investigational Drugs, ISSN 1354-3784, 12/2014, Volume 23, Issue 12, pp. 1687 - 1701
Introduction: For the last two decades, long-acting β agonists (LABAs) have been a cornerstone in the management of chronic obstructive pulmonary disease... 
β agonist | ultra-long-acting β agonist | long-acting β agonist | chronic obstructive pulmonary disease | Chronic obstructive pulmonary disease | Ultra-long-acting β agonist | Long-acting β agonist | INHALED BETA-ADRENOCEPTOR AGONIST | ultra-long-acting beta agonist | PHARMACOLOGICAL CHARACTERIZATION | MU-G | COMBINATION THERAPY | beta agonist | FLUTICASONE PROPIONATE | ONCE-DAILY INDACATEROL | TWICE-DAILY SALMETEROL | DOUBLE-BLIND | PHARMACOLOGY & PHARMACY | long-acting beta agonist | CLINICALLY IMPORTANT DIFFERENCE | AIRWAY SMOOTH-MUSCLE | Bronchodilator Agents - therapeutic use | Animals | Adrenergic beta-2 Receptor Agonists - adverse effects | Humans | Adrenergic beta-2 Receptor Agonists - therapeutic use | Bronchodilator Agents - pharmacology | Treatment Outcome | Pulmonary Disease, Chronic Obstructive - metabolism | Bronchodilator Agents - adverse effects | Adrenergic beta-2 Receptor Agonists - pharmacology | Pulmonary Disease, Chronic Obstructive - drug therapy
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13. Full Text Efficacy and Tolerability of Mirabegron, a β3 -Adrenoceptor Agonist, in Patients with Overactive Bladder: Results from a Randomised European–Australian Phase 3 Trial
by Khullar, Vik and Amarenco, Gerard and Angulo, Javier C and Cambronero, Javier and Høye, Kjetil and Milsom, Ian and Radziszewski, Piotr and Rechberger, Tomasz and Boerrigter, Peter and Drogendijk, Ted and Wooning, Marianne and Chapple, Christopher
European Urology, ISSN 0302-2838, 2012, Volume 63, Issue 2, pp. 283 - 295
Abstract Background Mirabegron, a β3 -adrenoceptor agonist, has been developed for the treatment of overactive bladder (OAB). Objective To assess the efficacy... 
Urology | Mirabegron | β3-Adrenoceptor agonist | Overactive bladder (OAB) | Adrenoceptor agonist
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14. Full Text Pharmacology and therapeutics of bronchodilators
by Cazzola, Mario and Page, Clive P and Calzetta, Luigino and Matera, M. Gabriella
Pharmacological Reviews, ISSN 0031-6997, 2012, Volume 64, Issue 3, pp. 450 - 504
Bronchodilators are central in the treatment of of airways disorders. They are the mainstay of the current management of chronic obstructive pulmonary disease... 
BETA-ADRENOCEPTOR AGONISTS | RANDOMIZED CONTROLLED-TRIALS | OBSTRUCTIVE PULMONARY-DISEASE | METHACHOLINE-INDUCED BRONCHOCONSTRICTION | LONG-ACTING BETA-AGONISTS | ATRIAL-NATRIURETIC-PEPTIDE | INHALED BETA-ADRENOCEPTOR AGONIST | EXERCISE-INDUCED BRONCHOCONSTRICTION | PHARMACOLOGY & PHARMACY | AIRWAY SMOOTH-MUSCLE | GUINEA-PIG TRACHEA | Bronchodilator Agents - therapeutic use | Asthma - metabolism | Xanthines - adverse effects | Humans | Muscarinic Antagonists - adverse effects | Adrenergic beta-Agonists - pharmacology | Bronchodilator Agents - pharmacology | Muscarinic Antagonists - therapeutic use | Xanthines - therapeutic use | Xanthines - pharmacology | Asthma - drug therapy | Drug Discovery | Asthma - genetics | Animals | Muscarinic Antagonists - pharmacology | Adrenergic beta-Agonists - therapeutic use | Pulmonary Disease, Chronic Obstructive - metabolism | Bronchodilator Agents - adverse effects | Adrenergic beta-Agonists - adverse effects | Drug Combinations | Pulmonary Disease, Chronic Obstructive - drug therapy | Pulmonary Disease, Chronic Obstructive - genetics
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