Topic: dopaminergic neurotransmission

Schizophrenia presents as a complex psychiatric disorder characterized by a heterogeneous genetic and neurobiological background. Unfortunately, the prevailing mechanistic remains incompletely elucidated. A dopaminergic basis for schizophrenia has been proposed, implicating an upregulation in dopaminergic neurotransmission. This notion is supported by observations of behavioral hypersensitivity to dopamine receptor-activating drugs in individuals with schizophrenia, as well as postmortem analyses revealing elevated density of dopamine D2 receptors (D2R) in the striatum of schizophrenia patient

Dysfunctional dopaminergic neurotransmission is implicated in several pathologies, including movement disorders such as parkinsonism and psychiatric diseases, suggesting overlapping pathological mechanisms. The dopamine transporter (DAT) is a key regulator of dopamine signalling and rare disease-associated DAT variants can cause psychiatric diseases and early-onset parkinsonism. However, the pathobiological processes that link DAT dysfunction to both parkinsonism and psychiatric symptoms are unknown. To investigate this, we developed a novel mouse disease model that expresses two mutations in

Exposure to air pollution, and particularly to particulate matter (PM), has been associated with higher rates of Multiple Sclerosis (MS) relapses and increased neuroinflammation in MS patients, suggesting that PM exposure may contribute to MS exacerbation. To address this issue, we have combined the induction of MOG35-55-induced experimental autoimmune encephalomyelitis (EAE) in mice – the most used animal model of MS - with PM10 exposure. Mice were exposed to PM10 dosages relevant for human exposure before the immunization or during the pre-symptomatic phase. In both cases, PM10 exposures did