0000000000518966

AUTHOR

Maria Tattoli

0000-0002-4970-264x

showing 2 related works from this author

Prenatal exposure to the CB1 receptor agonist WIN 55,212-2 causes learning disruption associated with impaired cortical NMDA receptor function and em…

2005

The aim of this study was to investigate whether prenatal exposure to the cannabinoid CB1 receptor agonist WIN 55,212-2 (WIN) at a daily dose devoid of overt signs of toxicity and/or gross malformations (0.5 mg/kg, gestation days 5-20), influences cortical glutamatergic neurotransmission, learning and emotional reactivity in rat offspring. Basal and K+-evoked extracellular glutamate levels were significantly lower in cortical cell cultures obtained from pups exposed to WIN during gestation with respect to those measured in cultures obtained from neonates born from vehicle-treated dams. The addition of NMDA to cortical cell cultures from neonates born from vehicle-treated dams concentration-…

MaleMarijuana AbuseCannabinoid receptoractive avoidance behaviour; basal and K+-evoked glutamate levels; cortical cell cultures; homing behaviour; maternal marijuana consumption; ultrasonic vocalizationEmotionsReceptor Cannabinoid CB1Pregnancyactive avoidance behaviourWIN 55212-2Cells CulturedCerebral CortexBehavior AnimalGlutamate receptorBraincortical cell culturesCalcium Channel Blockersactive avoidance behaviour; basal and k plus -evoked glutamate levels; basal and k+-evoked glutamate levels; cortical cell cultures; homing behaviour; maternal marijuana consumption; ultrasonic vocalizationPrenatal Exposure Delayed EffectsChloratesNMDA receptorbasal and K+-evoked glutamate levelsFemaleMicrotubule-Associated Proteinsmedicine.drugAgonistmedicine.medical_specialtyOffspringmedicine.drug_classCognitive NeuroscienceMorpholinesGlutamic Acidmaternal marijuana consumptionNeurotransmissionBiologyNaphthalenesReceptors N-Methyl-D-AspartateCellular and Molecular NeuroscienceGlutamatergicInternal medicinemedicineAvoidance LearningAnimalsRats WistarBenzoxazinesRatsultrasonic vocalizationEndocrinologyAnimals Newbornhoming behaviourVocalization AnimalExtracellular SpaceNeuroscience
researchProduct

Prenatal low-level exposure to CO alters postnatal development of hippocampal nitric oxide synthase and haem-oxygenase activities in rats.

2001

The effects of prenatal CO exposure (150 ppm from days 0 to 20 of pregnancy) on the postnatal development of hippocampal neuronal NO synthase (nNOS) and haem-oxygenase (HO-2) isoform activities in 15-, 30- and 90-d-old rats were investigated. Unlike HO-2, hippocampal nNOS activity increased from postnatal days 15-90 in controls. Prenatal CO produced a long-lasting decrease in either nNOS or HO-2. The results suggest that the altered developmental profile of hippocampal nNOS and HO-2 activities could be involved in cognitive deficits and long-term potentiation dysfunction exhibited by rats prenatally exposed to CO levels resulting in carboxyhaemoglobin (HbCO) levels equivalent to those obser…

Gene isoformmedicine.medical_specialtyNitric Oxide Synthase Type IHippocampal formationHippocampusCarbon monoxide; haem-oxygenase; hippocampus; nitric oxide synthase; prenatal exposure.HemoglobinsPregnancyInternal medicinemedicineAnimalsPharmacology (medical)Rats WistarPharmacologyDevelopmental profilePregnancyCarbon MonoxidebiologyChemistryLong-term potentiationLow level exposuremedicine.diseaseHaem OxygenaseRatsNitric oxide synthaseIsoenzymesPsychiatry and Mental healthEndocrinologyPrenatal Exposure Delayed EffectsHeme Oxygenase (Decyclizing)biology.proteinFemaleNitric Oxide SynthaseThe international journal of neuropsychopharmacology
researchProduct