The main goals of this study were to validate and characterize a new chronic animal model of post-traumatic stress disorder (PTSD), and to evaluate the effects of cannabidiol (CBD) and/or sertraline (SERT) on PTSD-like behavioral and neurochemical alter...

The herb Cannabis sativa (marijuana) and its active component, Δ9-tetrahydrocannabinol (Δ9-THC), induce feelings of “high” and euphoria by activating cannabinoid type 1 receptors (CB1Rs) in the brain. The membrane-lipid derivates arachydonoil ethanolamide (nicknamed anandamide, after “ananda

Exposure to Δ9-tetrahydrocannabinol (THC), the primary psychoactive compound in cannabis, is associated with psychotomimetic side-effects and an increased risk of serious neuropsychiatric disorders, such as schizophrenia. The nucleus accumbens shell (NA...

Marijuana’s analgesic action has been linked to allosteric positive modulation of glycine receptors (GlyRs) by Δ9-tetrahydrocannabinol (THC), a major psychoactive component in cannabis. GlyRs are the predominant inhibitory ligand-gated ion channels that...

Bioactive ingredients present in the marijuana plant, including Δ9-tetrahydrocannabinol (THC), cannabinol and cannabidiol, produce distinct biological effects. THC produces psychotropic effects by activating neuronal CB1 cannabinoid receptors, whereas the non-psychotropic ingredients cannabinol and cannbidiol reduce systemic inflammation by antagonizing the actions of endogenous cannabinoids (endocannabinoids). Individuals suffering from neuroinflammation, such as multiple sclerosis patients, report numerous benefits from smoking marijuana. However, the mechanistic basis of these effects is unclear. Neuroinflammation is associated with activation of microglial cells, the resident macrophages of the brain, which migrate towards inflammatory sites where they exacerbate cell damage. Here we show that pathophysiological stimulation of neurons and microglial cells increases endocannabinoid production. We also demonstrate that mouse microglial cells express cannabinoid CB2 receptors at the leading edges of their...

Glycine receptors (GlyRs) are inhibitory ligand-gated ion channels that regulate signal transduction in the central nervous system. They are important targets for many anesthetics and analgesics, including Δ9-tetrahydrocannabinol (THC). The undesirable ...

Exposure to cannabis and its primary psychoactive component delta-9-tetrahydrocannabinol (THC) may induce changes in neural circuitry that in turn lead to adverse consequences on behavior. Previous studies in rodents have shown that intraperitoneal or s...

Marijuana is the most common illicit drug used by pregnant women and is associated with offspring’s attention and learning deficits from early childhood until later in life. However, the impact of prenatal cannabis exposure (PCE) on maladaptive gene exp...

Temporal lobe epilepsy (TLE) is the most common form of refractory focal epilepsy and is usually regarded as a multifactorial polygenic disorder. Data from clinical studies suggest that cannabidiol and Δ9-tetrahydrocannabinol may be effective in the pre...

Although Δ9-tetrahydrocannabinol (THC) produces analgesia, its effects on nociceptive primary afferents are unknown. These neurons participate not only in pain signaling but also in the local response to tissue injury. Here, we show that THC and cannabinol induce a CB1/CB2 cannabinoid receptor-independent release of calcitonin gene-related peptide from capsaicin-sensitive perivascular sensory nerves. Other psychotropic cannabinoids cannot mimic this action. The vanilloid receptor antagonist ruthenium red abolishes the responses to THC and cannabinol. However, the effect of THC on sensory nerves is intact in vanilloid receptor subtype 1 gene knock-out mice. The THC response depends on extracellular calcium but does not involve known voltage-operated calcium channels, glutamate receptors, or protein kinases A and C. These results may indicate the presence of a novel cannabinoid receptor/ion channel in the pain pathway.