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of 890 results
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AbstractThis study determined whether the cannabis constituent cannabidiol attenuates the development of morphine reward in the conditioned place preference paradigm. Mice received either saline or morphine in combination with increasing doses of cannabidiol us...Nov 13, 2017
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Marijuana consumption elicits diverse physiological and psychological effects in humans, including memory loss. Here we report that Δ9-tetrahydrocannabinol (THC), the major psychoactive component of marijuana, is toxic for hippocampal neurons. Treatment of cultured neurons or hippocampal slices with THC caused shrinkage of neuronal cell bodies and nuclei as well as genomic DNA strand breaks, hallmarks of neuronal apoptosis. Neuron death induced by THC was inhibited by nonsteroidal anti-inflammatory drugs, including indomethacin and aspirin, as well as vitamin E and other antioxidants. Furthermore, treatment of neurons with THC stimulated a significant increase in the release of arachidonic acid. We hypothesize that THC neurotoxicity is attributable to activation of the prostanoid synthesis pathway and generation of free radicals by cyclooxygenase. These data suggest that some of the memory deficits caused by cannabinoids may be caused by THC neurotoxicity.Jul 15, 1998
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AbstractThe aim of this study was to evaluate the effects of cannabidiol (CBD) in alcohol reinforcement, motivation and relapse in C57BL/6J mice. To this purpose, the effects of CBD (60 mg/kg i.p.) and ethanol on rectal temperature (3 g/kg p.o.), ethanol-handli...
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Evidence suggests that the phytocannabinoids Δ-9-tetrahydrocannabinol (THC) and cannabidiol (CBD) differentially regulate salience attribution and psychiatric risk. The ventral hippocampus (vHipp) relays emotional salience via control of dopamine (DA) neuronal activity states, which are dysregulated in psychosis and schizophrenia. Using in vivo electrophysiology in male Sprague Dawley rats, we demonstrate that intra-vHipp THC strongly increases ventral tegmental area (VTA) DA neuronal frequency and bursting rates, decreases GABA frequency, and amplifies VTA beta, gamma and ε oscillatory magnitudes via modulation of local extracellular signal-regulated kinase phosphorylation (pERK1–2). Remarkably, whereas intra-vHipp THC also potentiates salience attribution in morphine place-preference and fear conditioning assays, CBD coadministration reverses these changes by downregulating pERK1–2 signaling, as pharmacological reactivation of pERK1–2 blocked the inhibitory properties of CBD. These results identify vHipp...Oct 30, 2019
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AbstractAnxiety disorders are becoming more prevalent every year, with almost 19% of the adult population suffering from some sort of anxiety disorder within the past year. Due to a variety of biological and social factors, females are more likely to be diagnos...Oct 21, 2019
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SfN News Advocacy Press ReleaseWeek of July 2, 2018: Read the Latest Advocacy and Science NewsJul 9, 2018
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AbstractCannabis is the most widely used illicit drug and its use is often associated with psychiatric disorders. THC is an agonist of cannabinoid 1 and 2 receptors (CB1R, CB2R), through which it acts on brain reward systems to increase dopamine (DA) neuron act...Nov 11, 2017
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AbstractThe present investigation assessed the neuroprotective efficacy of cannabidiol (CBD) in a kainic acid (KA) seizure model of temporal lobe epilepsy. Sixty-six male Sprague-Dawley rats were used. Each animal was housed individually in a clear polycarbonat...Oct 20, 2019
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AbstractChronic cannabinoid exposure results in tolerance to cannabinoid-induced locomotor effects which are mediated by the cannabinoid receptors (CB1R) located in motor control region, such as cerebellum. In cerebellar cortex, acute activation of presynaptic CB1R suppresses parallel fibers (PF) synaptic inputs to Purkinje cells (PC). Whole-cell patch-clamp recordings have been carried out in PC to analyze the properties of evoked excitatory synaptic transmission in mice chronically exposed to Δ9-THC or to its vehicle. Paired-pulse facilitation (PPF) was used to analyze PF-PC short-term synaptic plasticity. We observed a decreased PPF in mice chronically treated with THC, indicating an increased release probability after prolonged cannabinoid exposure. In addition, inhibition of PF-PC synaptic transmission induced by the selective CB1R agonist CP55940 is decreased in THC-treated mice. This suggests that, following chronic THC treatment, functional tolerance to the CB1R agonist occurs at cerebellar PF-PC synapses,...Nov 14, 2005
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AbstractIntroduction: Limited therapeutic effects of current Alzheimer (AD) treatments highlight the need for new research approaches. Thereby drugs that target different aspects of AD pathology simultaneously could provide therapeutic benefits compared to more...Nov 6, 2018