Topic: glutamate transmission

The endocannabinoid system (ECS) has gained attention as a potential target to treat Alzheimer’s disease (AD) due to its neuroprotective, antioxidant, and anti-inflammatory properties. Consequently, natural cannabinoids like delta9-tetrahydrocannabinol (THC) and cannabidiol (CBD) have emerged as potential drugs against AD. Previous findings from our research group demonstrated that a combination of non-psychoactive doses of THC and CBD mitigates cognitive decline in an AD murine model, the APP/PS1 mice. Cognitive decline in AD is linked to the dysregulation of glutamate transmission within the

Drug addiction is a psychiatric disorder defined as a compulsive pattern of drug-seeking/taking behaviors, with recurrent episodes of abstinence and relapse. Addictive drugs increase dopamine in the nucleus accumbens (NAc), where it persistently shapes excitatory glutamate transmission, thereby hijacking natural reward processing. Recently, we provide evidence, from mice to humans, that psychostimulants and opiates alter DA-glutamate signal integration in the NAc through a drug-evoked heteromerization (i.e direct physical interaction) of glutamate NMDA receptors (NMDAR) with D1R or D2R. Using

The ventral tegmental area (VTA) is a major site of opioid reward processing. Mu-opioid receptor (MOR) agonism inhibits GABAergic VTA interneurons, thereby disinhibiting dopamine release from nucleus accumbens-projecting VTA neurons. This GABA disinhibition circuit canonically drives opioid-induced reward and opioid-seeking in the VTA. However, we recently discovered MOR-expressing VTA neurons that release glutamate. In opposition to the classic GABA disinhibition model, MOR agonism on glutamatergic VTA neurons decreases activity in VTA dopamine neurons. Here, we investigated the role of GABA-