0000000000559029

AUTHOR

Günther Schütz

showing 4 related works from this author

Understanding Cannabinoid Psychoactivity with Mouse Genetic Models

2007

Marijuana and its main psychotropic ingredient Δ9-tetrahydrocannabinol (THC) exert a plethora of psychoactive effects through the activation of the neuronal cannabinoid receptor type 1 (CB1), which is expressed by different neuronal subpopulations in the central nervous system. The exact neuroanatomical substrates underlying each effect of THC are, however, not known. We tested locomotor, hypothermic, analgesic, and cataleptic effects of THC in conditional knockout mouse lines, which lack the expression of CB1 in different neuronal subpopulations, including principal brain neurons, GABAergic neurons (those that release γ aminobutyric acid), cortical glutamatergic neurons, and neurons expres…

MaleMESH: Body TemperatureCannabinoid receptormedicine.medical_treatmentGene ExpressionMESH: Receptor Cannabinoid CB1NeocortexMESH: gamma-Aminobutyric AcidMESH: CatalepsyPharmacologyHippocampusMESH: Mice KnockoutMESH: Corpus StriatumBody TemperatureMESH: Autonomic Nervous SystemMESH: NeocortexMice0302 clinical medicineReceptor Cannabinoid CB1MESH: Behavior AnimalCannabinoid receptor type 1MESH: AnimalsMESH: Gene SilencingDronabinolMESH: NociceptorsBiology (General)gamma-Aminobutyric AcidMice Knockout0303 health sciencesBehavior Animalmusculoskeletal neural and ocular physiologyGeneral NeuroscienceMESH: Pain ThresholdNociceptorsMESH: Glutamic AcidMESH: InterneuronsMESH: Motor Activity3. Good healthGABAergicMESH: TetrahydrocannabinolGeneral Agricultural and Biological SciencesResearch Articlemedicine.drugPain ThresholdMESH: Gene ExpressionMESH: Psychotropic DrugsQH301-705.5Glutamic AcidMotor ActivityBiologyAutonomic Nervous SystemGeneral Biochemistry Genetics and Molecular Biologygamma-Aminobutyric acid03 medical and health sciencesGlutamatergicDopamine receptor D1InterneuronsCannabinoid Receptor Modulatorsmental disorders[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologymedicineAnimalsGenetic Predisposition to Disease[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyGene SilencingTetrahydrocannabinolMESH: MiceAnesthesiology and Pain Management030304 developmental biologyPharmacologyCatalepsyPsychotropic DrugsModels GeneticGeneral Immunology and MicrobiologyCannabinoidsIllicit Drugsorganic chemicalsMESH: MaleCorpus StriatumPrimerDisease Models Animalnervous systemCannabinoidNervous System Diseases030217 neurology & neurosurgeryNeurosciencePLoS Biology
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CB1 Cannabinoid Receptors and On-Demand Defense Against Excitotoxicity

2003

Abnormally high spiking activity can damage neurons. Signaling systems to protect neurons from the consequences of abnormal discharge activity have been postulated. We generated conditional mutant mice that lack expression of the cannabinoid receptor type 1 in principal forebrain neurons but not in adjacent inhibitory interneurons. In mutant mice,the excitotoxin kainic acid (KA) induced excessive seizures in vivo. The threshold to KA-induced neuronal excitation in vitro was severely reduced in hippocampal pyramidal neurons of mutants. KA administration rapidly raised hippocampal levels of anandamide and induced protective mechanisms in wild-type principal hippocampal neurons. These protecti…

MaleCannabinoid receptorReceptors Drugmedicine.medical_treatment2-ArachidonoylglycerolExcitotoxicityHippocampal formationmedicine.disease_causeHippocampusMicechemistry.chemical_compoundPiperidinesCannabinoid receptor type 1Excitatory Amino Acid AgonistsReceptors Cannabinoidgamma-Aminobutyric AcidMice KnockoutNeuronsKainic AcidMultidisciplinaryBrainEndocannabinoid systemNeuroprotective AgentsMitogen-Activated Protein KinasesRimonabantSignal Transductionmedicine.medical_specialtyKainic acidPolyunsaturated AlkamidesGlutamic AcidMice TransgenicArachidonic AcidsIn Vitro TechniquesBiologyGlyceridesProsencephalonInternal medicinemedicineAnimalsFuransGenes Immediate-EarlyEpilepsyCannabinoidsBrain-Derived Neurotrophic FactorExcitatory Postsynaptic PotentialsMice Inbred C57BLEndocrinologyGene Expression Regulationnervous systemchemistryMutationPyrazolesCannabinoidNeuroscienceEndocannabinoidsScience
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An integrated genome research network for studying the genetics of alcohol addiction

2010

Alcohol drinking is highly prevalent in many cultures and contributes to the global burden of disease. In fact, it was shown that alcohol constitutes 3.2% of all worldwide deaths in the year 2006 and is linked to more than 60 diseases, including cancers, cardiovascular diseases, liver cirrhosis, neuropsychiatric disorders, injuries and foetal alcohol syndrome. Alcoholism, which has been proven to have a high genetic load, is one potentially fatal consequence of chronic heavy alcohol consumption, and may be regarded as one of the most prevalent neuropsychiatric diseases afflicting our society today. The aim of the integrated genome research network 'Genetics of Alcohol Addiction'-which is a …

PharmacologyGeneticsCandidate genemedicine.medical_specialtybusiness.industryImaging geneticsAddictionmedia_common.quotation_subjectMedicine (miscellaneous)Human factors and ergonomicsPoison controlSuicide preventionGenetic loadPsychiatry and Mental healthInjury preventionmedicinePsychiatrybusinessmedia_commonAddiction Biology
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Loss of the Ca2+/calmodulin-dependent protein kinase type IV in dopaminoceptive neurons enhances behavioral effects of cocaine.

2008

The persistent nature of addiction has been associated with activity-induced plasticity of neurons within the striatum and nucleus accumbens (NAc). To identify the molecular processes leading to these adaptations, we performed Cre/loxP-mediated genetic ablations of two key regulators of gene expression in response to activity, the Ca 2+ /calmodulin-dependent protein kinase IV (CaMKIV) and its postulated main target, the cAMP-responsive element binding protein (CREB). We found that acute cocaine-induced gene expression in the striatum was largely unaffected by the loss of CaMKIV. On the behavioral level, mice lacking CaMKIV in dopaminoceptive neurons displayed increased sensitivity to cocai…

AdultMalemedicine.medical_specialtymedia_common.quotation_subjectMice TransgenicStriatumBiologyNucleus accumbensCREBPolymorphism Single NucleotideCocaine-Related DisordersMiceInternal medicineGene expressionmedicineAnimalsHumansProtein kinase ACyclic AMP Response Element-Binding Proteinmedia_commonRegulation of gene expressionNeuronsAnalysis of VarianceMultidisciplinaryNeuronal PlasticityAddictionGene Expression ProfilingBiological SciencesMolecular biologyImmunohistochemistryConditioned place preferenceCorpus StriatumEndocrinologyGene Expression Regulationbiology.proteinFemaleBrazilCalcium-Calmodulin-Dependent Protein Kinase Type 4Gene DeletionProceedings of the National Academy of Sciences of the United States of America
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