Proceedings of the National Academy of Sciences, ISSN 0027-8424, 10/2013, Volume 110, Issue 42, pp. E4016 - E4025
The pathological end-state of Parkinson disease is well described from postmortem tissue, but there remains a pressing need to define early functional changes...
In vivo electrophysiology | Voltammetry | Dopamine transmission | Neurodegeneration | Behavioral phenotyping | voltammetry | behavioral phenotyping | MULTIDISCIPLINARY SCIENCES | neurodegeneration | ALPHA-SYNUCLEIN | RELEASE | LOCUS TRIPLICATION | SUBSTANTIA-NIGRA | MICE LACKING | dopamine transmission | in vivo electrophysiology | GAMMA-SYNUCLEIN | CHOLINERGIC INTERNEURONS | DISEASE | MUTATION | PARS RETICULATA | Substantia Nigra - physiopathology | Parkinsonian Disorders - physiopathology | Corpus Striatum - physiopathology | Substantia Nigra - pathology | Dopaminergic Neurons - pathology | Humans | Substantia Nigra - metabolism | Corpus Striatum - metabolism | Synaptic Transmission | Aging - pathology | Chromosomes, Artificial, Bacterial - genetics | Parkinsonian Disorders - metabolism | Animals | Parkinsonian Disorders - pathology | alpha-Synuclein - biosynthesis | Chromosomes, Artificial, Bacterial - metabolism | Dopaminergic Neurons - metabolism | Parkinsonian Disorders - genetics | Mice | alpha-Synuclein - genetics | Corpus Striatum - pathology | Aging - metabolism | Biological Sciences | PNAS Plus
In vivo electrophysiology | Voltammetry | Dopamine transmission | Neurodegeneration | Behavioral phenotyping | voltammetry | behavioral phenotyping | MULTIDISCIPLINARY SCIENCES | neurodegeneration | ALPHA-SYNUCLEIN | RELEASE | LOCUS TRIPLICATION | SUBSTANTIA-NIGRA | MICE LACKING | dopamine transmission | in vivo electrophysiology | GAMMA-SYNUCLEIN | CHOLINERGIC INTERNEURONS | DISEASE | MUTATION | PARS RETICULATA | Substantia Nigra - physiopathology | Parkinsonian Disorders - physiopathology | Corpus Striatum - physiopathology | Substantia Nigra - pathology | Dopaminergic Neurons - pathology | Humans | Substantia Nigra - metabolism | Corpus Striatum - metabolism | Synaptic Transmission | Aging - pathology | Chromosomes, Artificial, Bacterial - genetics | Parkinsonian Disorders - metabolism | Animals | Parkinsonian Disorders - pathology | alpha-Synuclein - biosynthesis | Chromosomes, Artificial, Bacterial - metabolism | Dopaminergic Neurons - metabolism | Parkinsonian Disorders - genetics | Mice | alpha-Synuclein - genetics | Corpus Striatum - pathology | Aging - metabolism | Biological Sciences | PNAS Plus
Journal Article
PLoS ONE, ISSN 1932-6203, 11/2015, Volume 10, Issue 11, p. e0142838
Recent evidence points to a neuroprotective action of bee venom on nigral dopamine neurons in animal models of Parkinson's disease (PD). Here we examined...
SUBTHALAMIC NUCLEUS | POTASSIUM CHANNELS | MULTIDISCIPLINARY SCIENCES | ANTIPSYCHOTIC-DRUGS | SK3 | HIGH-FREQUENCY STIMULATION | DOPAMINERGIC-NEURONS | NIGRA PARS RETICULATA | RECEPTORS | SUBSTANTIA-NIGRA | SMALL-CONDUCTANCE | Bee Venoms - therapeutic use | Substantia Nigra - physiopathology | Catalepsy - drug therapy | Electric Stimulation | Rats, Wistar | Motor Activity - drug effects | Male | Bee Venoms - administration & dosage | Motor Cortex - drug effects | Parkinson Disease - drug therapy | Haloperidol | Oxidopamine | Catalepsy - physiopathology | Action Potentials - drug effects | Disease Models, Animal | Parkinson Disease - complications | Catalepsy - complications | Basal Ganglia - physiopathology | Receptors, Dopamine - metabolism | Bee Venoms - pharmacology | Motor Cortex - physiopathology | Parkinson Disease - physiopathology | Substantia Nigra - drug effects | Animals | Dopamine Antagonists - pharmacology | Basal Ganglia - drug effects | Care and treatment | Parkinson's disease | Venom | Patient outcomes | Development and progression | Research | Health aspects | Life Sciences | Neurons and Cognition | Neurobiology
SUBTHALAMIC NUCLEUS | POTASSIUM CHANNELS | MULTIDISCIPLINARY SCIENCES | ANTIPSYCHOTIC-DRUGS | SK3 | HIGH-FREQUENCY STIMULATION | DOPAMINERGIC-NEURONS | NIGRA PARS RETICULATA | RECEPTORS | SUBSTANTIA-NIGRA | SMALL-CONDUCTANCE | Bee Venoms - therapeutic use | Substantia Nigra - physiopathology | Catalepsy - drug therapy | Electric Stimulation | Rats, Wistar | Motor Activity - drug effects | Male | Bee Venoms - administration & dosage | Motor Cortex - drug effects | Parkinson Disease - drug therapy | Haloperidol | Oxidopamine | Catalepsy - physiopathology | Action Potentials - drug effects | Disease Models, Animal | Parkinson Disease - complications | Catalepsy - complications | Basal Ganglia - physiopathology | Receptors, Dopamine - metabolism | Bee Venoms - pharmacology | Motor Cortex - physiopathology | Parkinson Disease - physiopathology | Substantia Nigra - drug effects | Animals | Dopamine Antagonists - pharmacology | Basal Ganglia - drug effects | Care and treatment | Parkinson's disease | Venom | Patient outcomes | Development and progression | Research | Health aspects | Life Sciences | Neurons and Cognition | Neurobiology
Journal Article
PLOS ONE, ISSN 1932-6203, 11/2015, Volume 10, Issue 11, p. e0142838
Recent evidence points to a neuroprotective action of bee venom on nigral dopamine neurons in animal models of Parkinson’s disease (PD). Here we examined...
Neuroprotection | Basal ganglia | Animal models | Parkinson's disease | Disease | Circuits | Substantia nigra | Catalepsy | Potassium conductance | Cortex (motor) | Haloperidol | Channels | Potassium channels (calcium-gated) | Psychotropic drugs | Discharge frequency | Rodents | Drug therapy | Movement disorders | Calcium channels | Firing pattern | Dopamine | Neurodegenerative diseases | Akinesia | Neurons | Medical treatment | Cortex | 6-Hydroxydopamine | Central nervous system diseases | Pharmacology | Injection | Ganglia | Apomorphine | Resistance | Calcium conductance | Venom | Conductance | Potassium | Calcium ions | Life Sciences | Neurons and Cognition | Pharmaceutical sciences | Neurobiology
Neuroprotection | Basal ganglia | Animal models | Parkinson's disease | Disease | Circuits | Substantia nigra | Catalepsy | Potassium conductance | Cortex (motor) | Haloperidol | Channels | Potassium channels (calcium-gated) | Psychotropic drugs | Discharge frequency | Rodents | Drug therapy | Movement disorders | Calcium channels | Firing pattern | Dopamine | Neurodegenerative diseases | Akinesia | Neurons | Medical treatment | Cortex | 6-Hydroxydopamine | Central nervous system diseases | Pharmacology | Injection | Ganglia | Apomorphine | Resistance | Calcium conductance | Venom | Conductance | Potassium | Calcium ions | Life Sciences | Neurons and Cognition | Pharmaceutical sciences | Neurobiology
Journal Article
Cell Reports, ISSN 2211-1247, 10/2019, Volume 29, Issue 4, pp. 920 - 931.e7
Parkinson’s disease (PD) is characterized by the death of dopamine neurons in the substantia nigra pars compacta (SNc) and accumulation of α-synuclein....
mouse models | autophagy | pathology | neurotransmission | behavior | dopamine | Parkinson’s disease | LRRK2 | DISEASE | ALPHA-SYNUCLEIN | AUTOPHAGY | RELEASE | DEFICITS | SUBSTANTIA-NIGRA | MICE LACKING | DEGENERATION | CELL BIOLOGY
mouse models | autophagy | pathology | neurotransmission | behavior | dopamine | Parkinson’s disease | LRRK2 | DISEASE | ALPHA-SYNUCLEIN | AUTOPHAGY | RELEASE | DEFICITS | SUBSTANTIA-NIGRA | MICE LACKING | DEGENERATION | CELL BIOLOGY
Journal Article
International Journal of Neuropsychopharmacology, ISSN 1461-1457, 03/2014, Volume 17, Issue 8, pp. 1295 - 1306
Parkinson's disease has traditionally been viewed as a motor disorder caused by the loss of dopamine (DA) neurons. However, emotional and cognitive syndromes...
Basal ganglia | Parkinson's disease | SK channels (KCa | dopamine | non-motor symptoms | ) | PSYCHIATRY | FIRING PATTERN | CA2+-ACTIVATED K+ CHANNELS | OLFACTORY DISCRIMINATION | SK channels (KCa2) | NEUROSCIENCES | CLINICAL NEUROLOGY | APAMIN | SUBTHALAMIC NUCLEUS | NEURONS | PHARMACOLOGY & PHARMACY | ACTIVATED POTASSIUM CHANNEL | SMALL-CONDUCTANCE | BRAIN | PARKINSONS-DISEASE | Tyrosine 3-Monooxygenase - metabolism | Motor Activity - drug effects | Potassium Channel Blockers - therapeutic use | Rats | Male | Substantia Nigra - metabolism | Apamin - pharmacology | Cognition - drug effects | Corpus Striatum - metabolism | Small-Conductance Calcium-Activated Potassium Channels - metabolism | Small-Conductance Calcium-Activated Potassium Channels - antagonists & inhibitors | Dose-Response Relationship, Drug | Oxidopamine - toxicity | Substantia Nigra - drug effects | Animals | Parkinson Disease, Secondary - drug therapy | Parkinson Disease, Secondary - psychology | Corpus Striatum - drug effects | Behavior, Animal - drug effects | Apamin - therapeutic use | Parkinson Disease, Secondary - chemically induced | Parkinson Disease, Secondary - complications | Dopamine - metabolism | Potassium Channel Blockers - pharmacology | Neuroscience | Cognitive science
Basal ganglia | Parkinson's disease | SK channels (KCa | dopamine | non-motor symptoms | ) | PSYCHIATRY | FIRING PATTERN | CA2+-ACTIVATED K+ CHANNELS | OLFACTORY DISCRIMINATION | SK channels (KCa2) | NEUROSCIENCES | CLINICAL NEUROLOGY | APAMIN | SUBTHALAMIC NUCLEUS | NEURONS | PHARMACOLOGY & PHARMACY | ACTIVATED POTASSIUM CHANNEL | SMALL-CONDUCTANCE | BRAIN | PARKINSONS-DISEASE | Tyrosine 3-Monooxygenase - metabolism | Motor Activity - drug effects | Potassium Channel Blockers - therapeutic use | Rats | Male | Substantia Nigra - metabolism | Apamin - pharmacology | Cognition - drug effects | Corpus Striatum - metabolism | Small-Conductance Calcium-Activated Potassium Channels - metabolism | Small-Conductance Calcium-Activated Potassium Channels - antagonists & inhibitors | Dose-Response Relationship, Drug | Oxidopamine - toxicity | Substantia Nigra - drug effects | Animals | Parkinson Disease, Secondary - drug therapy | Parkinson Disease, Secondary - psychology | Corpus Striatum - drug effects | Behavior, Animal - drug effects | Apamin - therapeutic use | Parkinson Disease, Secondary - chemically induced | Parkinson Disease, Secondary - complications | Dopamine - metabolism | Potassium Channel Blockers - pharmacology | Neuroscience | Cognitive science
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 10/2008, Volume 105, Issue 41, pp. 15991 - 15996
Acetylcholine (ACh) is a known modulator of the activity of dopaminergic (DAergic) neurons through the stimulation of nicotinic ACh receptors (nAChRs). Yet,...
Cholinergics | Locomotion | Neurons | Hyperactivity | Mice | Gene expression regulation | Nicotinic receptors | Cholinergic receptors | Behavioral neuroscience | Ventral tegmental area | Dopaminergic systems | Lentiviral vector | RNAi | Gene rescue | Biological Sciences | gene rescue | lentiviral vector | dopaminergic systems
Cholinergics | Locomotion | Neurons | Hyperactivity | Mice | Gene expression regulation | Nicotinic receptors | Cholinergic receptors | Behavioral neuroscience | Ventral tegmental area | Dopaminergic systems | Lentiviral vector | RNAi | Gene rescue | Biological Sciences | gene rescue | lentiviral vector | dopaminergic systems
Journal Article
Current Neuropharmacology, ISSN 1570-159X, 2014, Volume 12, Issue 1, pp. 13 - 14
Journal Article
Neuropharmacology, ISSN 0028-3908, 2017, Volume 113, Part A, pp. 519 - 532
Parkinson's disease (PD) is a progressive neurodegenerative disease originating from the loss of dopa-mine (DA) neurons in the substantia nigra pars compacta...
Life Sciences | Neurons and Cognition | Neurobiology
Life Sciences | Neurons and Cognition | Neurobiology
Journal Article
Neuropharmacology, ISSN 0028-3908, 02/2017, Volume 113, Issue Pt A, pp. 519 - 532
Parkinson's disease (PD) is a progressive neurodegenerative disease originating from the loss of dopamine (DA) neurons in the substantia nigra pars compacta...
Homeostasis | Reaction time | Apamin | Parkinson's disease | Calcium-activated potassium channel | ATP CHANNELS | REFERENCE GENES | FIRING PATTERN | CA2+-ACTIVATED K+ CHANNELS | SUBTHALAMIC NUCLEUS NEURONS | SUBSTANTIA-NIGRA | NEUROSCIENCES | REAL-TIME PCR | PHARMACOLOGY & PHARMACY | ACTIVATED POTASSIUM CHANNEL | SMALL-CONDUCTANCE | PARKINSONS-DISEASE | Gene Expression | Small-Conductance Calcium-Activated Potassium Channels - genetics | Rats, Wistar | Small-Conductance Calcium-Activated Potassium Channels - biosynthesis | Basal Ganglia - metabolism | Rats | Male | Reaction Time - physiology | Substantia Nigra - metabolism | Corpus Striatum - metabolism | Parkinsonian Disorders - metabolism | Oxidopamine - toxicity | Substantia Nigra - drug effects | Animals | Apamin - toxicity | Reaction Time - drug effects | Corpus Striatum - drug effects | Parkinsonian Disorders - genetics | Dopamine - metabolism | Basal Ganglia - drug effects | Physiological aspects | Phenols | Nervous system diseases | RNA | Neurons | Life Sciences | Neurons and Cognition
Homeostasis | Reaction time | Apamin | Parkinson's disease | Calcium-activated potassium channel | ATP CHANNELS | REFERENCE GENES | FIRING PATTERN | CA2+-ACTIVATED K+ CHANNELS | SUBTHALAMIC NUCLEUS NEURONS | SUBSTANTIA-NIGRA | NEUROSCIENCES | REAL-TIME PCR | PHARMACOLOGY & PHARMACY | ACTIVATED POTASSIUM CHANNEL | SMALL-CONDUCTANCE | PARKINSONS-DISEASE | Gene Expression | Small-Conductance Calcium-Activated Potassium Channels - genetics | Rats, Wistar | Small-Conductance Calcium-Activated Potassium Channels - biosynthesis | Basal Ganglia - metabolism | Rats | Male | Reaction Time - physiology | Substantia Nigra - metabolism | Corpus Striatum - metabolism | Parkinsonian Disorders - metabolism | Oxidopamine - toxicity | Substantia Nigra - drug effects | Animals | Apamin - toxicity | Reaction Time - drug effects | Corpus Striatum - drug effects | Parkinsonian Disorders - genetics | Dopamine - metabolism | Basal Ganglia - drug effects | Physiological aspects | Phenols | Nervous system diseases | RNA | Neurons | Life Sciences | Neurons and Cognition
Journal Article
FASEB Journal, ISSN 0892-6638, 04/2012, Volume 26, Issue 4, pp. 1682 - 1693
Metabotropic glutamate (mGlu) receptors are promising targets to treat numerous brain disorders. So far, allosteric modulators are the only subtype selective...
Drug development | mGluR | Parkinson's disease | POSITIVE ALLOSTERIC MODULATION | SITE | ACTIVATION | ACID | RECOGNITION | DOCKING | BIOCHEMISTRY & MOLECULAR BIOLOGY | drug development | BINDING DOMAIN | MOLECULAR DETERMINANTS | CELL BIOLOGY | MGLUR4 | BIOLOGY | CHARMM | Antiparkinson Agents - pharmacology | Rats, Wistar | Humans | Male | Structure-Activity Relationship | Dose-Response Relationship, Drug | Receptors, Metabotropic Glutamate - genetics | HEK293 Cells | Antiparkinson Agents - chemistry | Synaptic Transmission - drug effects | Molecular Structure | Receptors, Metabotropic Glutamate - chemistry | Binding Sites | Recombinant Proteins - metabolism | Excitatory Amino Acid Agonists - metabolism | Mutagenesis, Site-Directed | Phosphinic Acids - chemistry | Rats | Excitatory Amino Acid Agonists - pharmacology | Recombinant Proteins - genetics | Mice, Knockout | Patch-Clamp Techniques | Animals | Phosphinic Acids - pharmacology | Phosphinic Acids - metabolism | Ligands | Mice | Receptors, Metabotropic Glutamate - agonists | Antiparkinson Agents - metabolism | Excitatory Amino Acid Agonists - chemistry | Excitatory Amino Acid Agonists | Neurons and Cognition | Neurobiology | Recombinant Proteins | Synaptic Transmission | Life Sciences | Phosphinic Acids | Psychology and behavior | Antiparkinson Agents | Receptors, Metabotropic Glutamate | Cognitive Sciences
Drug development | mGluR | Parkinson's disease | POSITIVE ALLOSTERIC MODULATION | SITE | ACTIVATION | ACID | RECOGNITION | DOCKING | BIOCHEMISTRY & MOLECULAR BIOLOGY | drug development | BINDING DOMAIN | MOLECULAR DETERMINANTS | CELL BIOLOGY | MGLUR4 | BIOLOGY | CHARMM | Antiparkinson Agents - pharmacology | Rats, Wistar | Humans | Male | Structure-Activity Relationship | Dose-Response Relationship, Drug | Receptors, Metabotropic Glutamate - genetics | HEK293 Cells | Antiparkinson Agents - chemistry | Synaptic Transmission - drug effects | Molecular Structure | Receptors, Metabotropic Glutamate - chemistry | Binding Sites | Recombinant Proteins - metabolism | Excitatory Amino Acid Agonists - metabolism | Mutagenesis, Site-Directed | Phosphinic Acids - chemistry | Rats | Excitatory Amino Acid Agonists - pharmacology | Recombinant Proteins - genetics | Mice, Knockout | Patch-Clamp Techniques | Animals | Phosphinic Acids - pharmacology | Phosphinic Acids - metabolism | Ligands | Mice | Receptors, Metabotropic Glutamate - agonists | Antiparkinson Agents - metabolism | Excitatory Amino Acid Agonists - chemistry | Excitatory Amino Acid Agonists | Neurons and Cognition | Neurobiology | Recombinant Proteins | Synaptic Transmission | Life Sciences | Phosphinic Acids | Psychology and behavior | Antiparkinson Agents | Receptors, Metabotropic Glutamate | Cognitive Sciences
Journal Article
The International Journal of Neuropsychopharmacology, ISSN 1461-1457, 8/2009, Volume 12, Issue 7, pp. 905 - 915
Preclinical data support the view that brain-derived neurotrophic factor (BDNF) and serotonergic systems regulate circuits involved in affective disorders. The...
Microdialysis | Behaviour | 5-HT | Antidepressants | BDNF | RECEPTOR ANTAGONISTS | PSYCHIATRY | DEFICIENT MICE | KNOCKOUT MICE | NEUROSCIENCES | CLINICAL NEUROLOGY | CHRONIC FLUOXETINE | TRKB | microdialysis | SEROTONIN NEUROTRANSMISSION | IN-VIVO | PHARMACOLOGY & PHARMACY | behaviour | RAT-BRAIN | FACTOR BDNF | EXPRESSION | Depression - physiopathology | Motor Activity - drug effects | Male | Anxiety - prevention & control | Receptor, trkB - genetics | Hippocampus - drug effects | RNA, Messenger - metabolism | Paroxetine - administration & dosage | Depression - drug therapy | Depression - metabolism | In Situ Hybridization | Time Factors | Behavior, Animal - drug effects | Receptor, trkB - drug effects | Anxiety - metabolism | Disease Models, Animal | Microinjections | Anxiety - psychology | Drug Synergism | Brain-Derived Neurotrophic Factor - administration & dosage | Hippocampus - metabolism | Brain-Derived Neurotrophic Factor - toxicity | Animals | Citalopram - administration & dosage | Analysis of Variance | Serotonin Uptake Inhibitors - administration & dosage | Serotonin - metabolism | Depression - psychology | Antidepressive Agents - administration & dosage | Anxiety - chemically induced | Mice | Hippocampus - physiopathology
Microdialysis | Behaviour | 5-HT | Antidepressants | BDNF | RECEPTOR ANTAGONISTS | PSYCHIATRY | DEFICIENT MICE | KNOCKOUT MICE | NEUROSCIENCES | CLINICAL NEUROLOGY | CHRONIC FLUOXETINE | TRKB | microdialysis | SEROTONIN NEUROTRANSMISSION | IN-VIVO | PHARMACOLOGY & PHARMACY | behaviour | RAT-BRAIN | FACTOR BDNF | EXPRESSION | Depression - physiopathology | Motor Activity - drug effects | Male | Anxiety - prevention & control | Receptor, trkB - genetics | Hippocampus - drug effects | RNA, Messenger - metabolism | Paroxetine - administration & dosage | Depression - drug therapy | Depression - metabolism | In Situ Hybridization | Time Factors | Behavior, Animal - drug effects | Receptor, trkB - drug effects | Anxiety - metabolism | Disease Models, Animal | Microinjections | Anxiety - psychology | Drug Synergism | Brain-Derived Neurotrophic Factor - administration & dosage | Hippocampus - metabolism | Brain-Derived Neurotrophic Factor - toxicity | Animals | Citalopram - administration & dosage | Analysis of Variance | Serotonin Uptake Inhibitors - administration & dosage | Serotonin - metabolism | Depression - psychology | Antidepressive Agents - administration & dosage | Anxiety - chemically induced | Mice | Hippocampus - physiopathology
Journal Article
Human Molecular Genetics, ISSN 0964-6906, 03/2016, Volume 25, Issue 5, pp. 951 - 963
Mutations in leucine-rich repeat kinase 2 (LRRK2) lead to late-onset, autosomal dominant Parkinson's disease, characterized by the degeneration of dopamine...
COGNITIVE DYSFUNCTION | BIOCHEMISTRY & MOLECULAR BIOLOGY | IN-VIVO | GENETICS & HEREDITY | NEURONS | RECEPTOR ACTIVATION | G2019S | MICE | RELEASE | SUBSTANTIA-NIGRA | EXPRESSION | PARKINSONS-DISEASE | Antiparkinson Agents - pharmacology | Substantia Nigra - pathology | Dopaminergic Neurons - pathology | Humans | Male | Parkinson Disease - drug therapy | Substantia Nigra - metabolism | Corpus Striatum - metabolism | Action Potentials | Cell Death - genetics | Chromosomes, Artificial, Bacterial - chemistry | Chromosomes, Artificial, Bacterial - metabolism | Dopaminergic Neurons - metabolism | Dopaminergic Neurons - drug effects | Protein Domains | Female | Parkinson Disease - metabolism | Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 - metabolism | Corpus Striatum - pathology | Disease Models, Animal | Levodopa - pharmacology | Promoter Regions, Genetic | Parkinson Disease - pathology | Rats, Transgenic | Rats | Parkinson Disease - genetics | Aging - pathology | Substantia Nigra - drug effects | Animals | Corpus Striatum - drug effects | Mutation | Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 - genetics | Aging - metabolism | Amino Acid Substitution
COGNITIVE DYSFUNCTION | BIOCHEMISTRY & MOLECULAR BIOLOGY | IN-VIVO | GENETICS & HEREDITY | NEURONS | RECEPTOR ACTIVATION | G2019S | MICE | RELEASE | SUBSTANTIA-NIGRA | EXPRESSION | PARKINSONS-DISEASE | Antiparkinson Agents - pharmacology | Substantia Nigra - pathology | Dopaminergic Neurons - pathology | Humans | Male | Parkinson Disease - drug therapy | Substantia Nigra - metabolism | Corpus Striatum - metabolism | Action Potentials | Cell Death - genetics | Chromosomes, Artificial, Bacterial - chemistry | Chromosomes, Artificial, Bacterial - metabolism | Dopaminergic Neurons - metabolism | Dopaminergic Neurons - drug effects | Protein Domains | Female | Parkinson Disease - metabolism | Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 - metabolism | Corpus Striatum - pathology | Disease Models, Animal | Levodopa - pharmacology | Promoter Regions, Genetic | Parkinson Disease - pathology | Rats, Transgenic | Rats | Parkinson Disease - genetics | Aging - pathology | Substantia Nigra - drug effects | Animals | Corpus Striatum - drug effects | Mutation | Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 - genetics | Aging - metabolism | Amino Acid Substitution
Journal Article
The International Journal of Neuropsychopharmacology, ISSN 1461-1457, 2/2008, Volume 11, Issue 1, pp. 79 - 92
Growing evidence supports the involvement of brain-derived neurotrophic factor (BDNF) in mood disorders and the mechanism of action of antidepressant drugs....
Brain-derived neurotrophic factor | Serotonin transporter | receptors | 5-HT | Dorsal raphe nucleus | Hippocampus | hippocampus | BDNF | PSYCHIATRY | 8-OH-DPAT-INDUCED HYPOTHERMIA | REDUCED SEROTONIN TRANSPORTER | ANTIDEPRESSANT DRUGS | NEUROSCIENCES | CLINICAL NEUROLOGY | dorsal raphe nucleus | MESSENGER-RNA | serotonin transporter | RECEPTOR KNOCKOUT MICE | IN-VIVO | PHARMACOLOGY & PHARMACY | brain-derived neurotrophic factor | RAT-BRAIN | 5-HT1A receptors | 5-HT1B RECEPTORS | Brain Chemistry - drug effects | Brain-Derived Neurotrophic Factor - genetics | Synaptic Transmission - physiology | Synaptic Transmission - genetics | Electrophysiology | Male | Hippocampus - drug effects | Raphe Nuclei - metabolism | Citalopram | Serotonin Receptor Agonists - pharmacology | Brain-Derived Neurotrophic Factor - deficiency | Dose-Response Relationship, Drug | Receptor, Serotonin, 5-HT1A - metabolism | Paroxetine | 8-Hydroxy-2-(di-n-propylamino)tetralin - pharmacology | Mice, Knockout | Receptor, Serotonin, 5-HT1A - drug effects | Serotonin Plasma Membrane Transport Proteins - metabolism | Autoradiography | Hippocampus - metabolism | Phenotype | Animals | Microdialysis | Raphe Nuclei - drug effects | Serotonin - metabolism | Mice | Serotonin Uptake Inhibitors | Studies | Changes | Brain | Temperature | Gene loci
Brain-derived neurotrophic factor | Serotonin transporter | receptors | 5-HT | Dorsal raphe nucleus | Hippocampus | hippocampus | BDNF | PSYCHIATRY | 8-OH-DPAT-INDUCED HYPOTHERMIA | REDUCED SEROTONIN TRANSPORTER | ANTIDEPRESSANT DRUGS | NEUROSCIENCES | CLINICAL NEUROLOGY | dorsal raphe nucleus | MESSENGER-RNA | serotonin transporter | RECEPTOR KNOCKOUT MICE | IN-VIVO | PHARMACOLOGY & PHARMACY | brain-derived neurotrophic factor | RAT-BRAIN | 5-HT1A receptors | 5-HT1B RECEPTORS | Brain Chemistry - drug effects | Brain-Derived Neurotrophic Factor - genetics | Synaptic Transmission - physiology | Synaptic Transmission - genetics | Electrophysiology | Male | Hippocampus - drug effects | Raphe Nuclei - metabolism | Citalopram | Serotonin Receptor Agonists - pharmacology | Brain-Derived Neurotrophic Factor - deficiency | Dose-Response Relationship, Drug | Receptor, Serotonin, 5-HT1A - metabolism | Paroxetine | 8-Hydroxy-2-(di-n-propylamino)tetralin - pharmacology | Mice, Knockout | Receptor, Serotonin, 5-HT1A - drug effects | Serotonin Plasma Membrane Transport Proteins - metabolism | Autoradiography | Hippocampus - metabolism | Phenotype | Animals | Microdialysis | Raphe Nuclei - drug effects | Serotonin - metabolism | Mice | Serotonin Uptake Inhibitors | Studies | Changes | Brain | Temperature | Gene loci
Journal Article
Neurobiology of Disease, ISSN 0969-9961, 2013, Volume 62, Issue 100, pp. 193 - 207
Abstract Parkinson's disease (PD) is a neurodegenerative disorder classically characterized by the death of dopamine (DA) neurons in the substantia nigra pars...
Neurology | α-Synuclein | Voltammetry | Norepinephrine | Parkinson's disease | Dopamine | Behavior | IMMUNOCHEMICAL ANALYSIS | RELEASE | KNOCKOUT MICE | SUBSTANTIA-NIGRA | NEUROSCIENCES | MICE LACKING | VENTRAL TEGMENTAL AREA | ALLELIC VARIATION | GENE | alpha-Synudein | PRIMATE STRIATUM | PARKINSONS-DISEASE | Age Factors | Humans | Mice, Inbred C57BL | Basal Ganglia - metabolism | Male | Mice, Transgenic | Septal Nuclei - metabolism | Animals | Norepinephrine - metabolism | Dopaminergic Neurons - metabolism | Chromosomes, Artificial, Bacterial | Female | Mice | alpha-Synuclein - genetics | alpha-Synuclein - metabolism | Dopamine - metabolism | Disease Models, Animal
Neurology | α-Synuclein | Voltammetry | Norepinephrine | Parkinson's disease | Dopamine | Behavior | IMMUNOCHEMICAL ANALYSIS | RELEASE | KNOCKOUT MICE | SUBSTANTIA-NIGRA | NEUROSCIENCES | MICE LACKING | VENTRAL TEGMENTAL AREA | ALLELIC VARIATION | GENE | alpha-Synudein | PRIMATE STRIATUM | PARKINSONS-DISEASE | Age Factors | Humans | Mice, Inbred C57BL | Basal Ganglia - metabolism | Male | Mice, Transgenic | Septal Nuclei - metabolism | Animals | Norepinephrine - metabolism | Dopaminergic Neurons - metabolism | Chromosomes, Artificial, Bacterial | Female | Mice | alpha-Synuclein - genetics | alpha-Synuclein - metabolism | Dopamine - metabolism | Disease Models, Animal
Journal Article
Current Neuropharmacology, ISSN 1570-159X, 2011, Volume 9, Issue 1, pp. 14 - 15
Journal Article
16.
Full Text
Characterization of 5-HT1A/1B−/− mice: An animal model sensitive to anxiolytic treatments
Neuropharmacology, ISSN 0028-3908, 09/2011, Volume 61, Issue 3, pp. 478 - 488
Selective serotonin (5-HT) re-uptake inhibitors (SSRIs) are commonly used in the treatment of generalized anxiety disorder in Humans. However, because only few...
Neurochemistry | SSRI | Paroxetine | KO mice | 5-HT1B receptor | Electrophysiology | Depression | Anxiety | Behavior | 5-HT1A receptor | receptor | 5-HT | IN-VIVO MICRODIALYSIS | GENERALIZED ANXIETY DISORDER | FRONTAL-CORTEX | NEUROSCIENCES | CHRONIC FLUOXETINE | SEROTONIN REUPTAKE INHIBITORS | RECEPTOR KNOCKOUT MICE | PHARMACOLOGY & PHARMACY | DORSAL RAPHE NUCLEUS | OUT MICE | STRESS-INDUCED HYPERTHERMIA
Neurochemistry | SSRI | Paroxetine | KO mice | 5-HT1B receptor | Electrophysiology | Depression | Anxiety | Behavior | 5-HT1A receptor | receptor | 5-HT | IN-VIVO MICRODIALYSIS | GENERALIZED ANXIETY DISORDER | FRONTAL-CORTEX | NEUROSCIENCES | CHRONIC FLUOXETINE | SEROTONIN REUPTAKE INHIBITORS | RECEPTOR KNOCKOUT MICE | PHARMACOLOGY & PHARMACY | DORSAL RAPHE NUCLEUS | OUT MICE | STRESS-INDUCED HYPERTHERMIA
Journal Article