Search results for "Catalepsy"

showing 5 items of 5 documents

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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The gamma(2)-MSH peptide mediates a central analgesic effect via a GABA-ergic mechanism that is independent from activation of melanocortin receptors.

2001

Using the latency for tail-flick after thermal stimulation we have assessed the effects of alpha-, gamma(1)- and gamma(2)-MSH on nociceptive threshold in the mice. Intracisternal injections of gamma(2)-MSH induced a distinct analgesia, while gamma(1)-MSH in the same doses gave only a minor analgesia. Intracisternal alpha-MSH instead gave a short-term hyperalgesia. The effect of gamma(2)-MSH was not blocked by any of the MC(4)/MC(3)receptor antagonist HS014, naloxone or by the prior intracisternal administrations of gamma(1)-MSH. However, the gamma(2)-MSH analgesic response was completely attenuated by treating animals with the GABA(A)antagonist bicuculline. The gamma(2)-MSH analgesic effect…

MaleNarcotic Antagonists(+)-NaloxonePharmacologyGABA Antagonistschemistry.chemical_compoundMiceEndocrinologyDrug Interactionsgamma-Aminobutyric AcidAnalgesicsMice Inbred BALB Cintegumentary systemMuscimolNaloxoneReceptors MelanocortinNociceptorsGeneral MedicineReceptor antagonistNeurologyHyperalgesiamedicine.symptomhormones hormone substitutes and hormone antagonistsmedicine.drugPain ThresholdTailendocrine systemmedicine.medical_specialtyanimal structuresmedicine.drug_classCatalepsyBicucullinePeptides CyclicCellular and Molecular Neurosciencegamma-MSHMelanocortin receptorInternal medicinemedicineAnimalsGABA ModulatorsGABA AgonistsCatalepsyDiazepamEthanolEndocrine and Autonomic SystemsAntagonistCentral Nervous System DepressantsBicucullinemedicine.diseaseEndocrinologyMuscimolchemistryReceptors Corticotropinalpha-MSHNeuropeptides
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Lack of Specific Effects of Selective D1 and D2 Dopamine Antagonists vs. Risperidone on Morphine-Induced Hyperactivity

2000

Abstract RODRIGUEZ-ARIAS, M., I. BROSETA, M. A. AGUILAR AND J. MINARRO. Lack of specific effects of selective D 1 and D 2 dopamine antagonists on morphine-induced hyperactivity. PHARMACOL BIOCHEM BEHAV 66 (1) 189–197, 2000.—In the present study, three different dopamine antagonists were challenged in order to counteract hyperactivity induced by 50 mg/kg of morphine. A wide range of doses of morphine (50, 25, 12.5, 6.25, or 3.12 mg/kg) were evaluated on spontaneous locomotor activity. A significant increase was observed only with the two higher doses tested (25 and 50 mg/kg). No decrease was found with any of the doses used at any period of time. After analyzing doses of SCH 23390 (0.5, 0.1,…

MaleNarcoticsmedicine.medical_specialtyClinical BiochemistryMotor ActivityPharmacologyCatalepsyToxicologyBiochemistryMiceBehavioral Neurosciencechemistry.chemical_compoundDopamineInternal medicinemedicineAnimalsBiological PsychiatryPharmacologyRacloprideCatalepsySCH-23390RisperidoneMorphineChemistryReceptors Dopamine D1AntagonistDopamine antagonistBenzazepinesRisperidonemedicine.diseaseDopamine D2 Receptor AntagonistsEndocrinologyRacloprideMorphineDopamine Antagonistsmedicine.drugPharmacology Biochemistry and Behavior
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Lunasin-induced behavioural effects in mice: Focus on the dopaminergic system

2013

The present study for the first time is devoted to identify central effects of synthetic lunasin, a 43 amino acid peptide. A markedly expressed neuroleptic/cataleptic effect was observed at low (0.1-10 nmol/mouse) centrally administered doses in male C57Bl/6 mice. Lunasin considerably reduced the amphetamine hyperlocomotion but weakly apomorphine climbing behaviour. No influence on ketamine and bicuculline effects was observed. Binding assay studies demonstrated modest affinity of lunasin for the dopamine D₁ receptor (Ki=60 ± 15 μM). In a functional assay of cAMP accumulation on live cells lunasin antagonised apomorphine effect on D₁ receptor activation (pEC₅₀=6.1 ± 0.3), but had no effect …

Malemedicine.medical_specialtyApomorphineDopamine AgentsMotor ActivityPharmacologyBicucullineLunasinBehavioral NeuroscienceDopamine receptor D1SeizuresDopamineInternal medicineCyclic AMPmedicineAnimalsHumansGABA-A Receptor AntagonistsAmphetamineReceptorCatalepsyReceptors Dopamine D2ChemistryReceptors Dopamine D1DopaminergicBrainMice Inbred C57BLApomorphineAmphetamineHEK293 CellsEndocrinologyDopamine receptorSoybean ProteinsKetamineExcitatory Amino Acid AntagonistsCentral Nervous System Agentsmedicine.drugBehavioural Brain Research
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Rotarod impairment: catalepsy-like screening test for antipsychotic side effects.

2009

Extrapyramidal motoric symptoms are casual side effects under antipsychotic medication. New generation antipsychotics are expected to have a reduced risk due to different receptor affinities. Here, haloperidol and the new generation antipsychotics, risperidone, amisulpride, and aripiprazole, were examined with both catalepsy test and rotarod performance test to screen for their usability in mice. Mice treated with haloperidol, risperidone, and aripiprazole showed dose and time-dependent impairment. Amisulpride-treated mice showed no signs of catalepsy. Catalepsy test and rotarod performance test were useful methods to detect side effects of both generation antipsychotics. Catalepsy test pro…

Malemedicine.medical_specialtyTime FactorsScreening testmedicine.medical_treatmentStatistics as TopicDrug Evaluation PreclinicalCatalepsyPharmacologyMotor ActivityRotarod performance testMiceBasal Ganglia DiseasesmedicineHaloperidolAnimalsAmisulprideAntipsychoticPsychiatryFreezing Reaction CatalepticRisperidoneDose-Response Relationship DrugGeneral NeuroscienceGeneral Medicinemedicine.diseaseDisease Models AnimalRotarod Performance TestAripiprazolePsychologymedicine.drugAntipsychotic AgentsThe International journal of neuroscience
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