Autoantibodies directed against the GluA3 subunit (anti-GluA3 hIgGs) of AMPA receptors have been identified in 20%-25% of patients with frontotemporal lobar degeneration (FTLD). Data from patients and in vitro/ex vivo pre-clinical studies indicate that anti-GluA3 hIgGs negatively affect glutamatergic neurotransmission. However, whether and how the chronic presence of anti-GluA3 hIgGs triggers synaptic dysfunctions and the appearance of FTLD-related neuropathological and behavioural signature has not been clarified yet.
View Article and Find Full Text PDFBackground And Purpose: Cognitive and motor functions are modulated by dopaminergic signalling, which is shaped by several genetic factors. The biological effects of single genetic variants might differ depending on epistatic interactions that can be functionally multi-directional and non-linear.
Experimental Approach: We performed behavioural and neurochemical assessments in genetically modified mice and behavioural assessments and genetic screening in human patients with 22q11.
Front Mol Neurosci
December 2022
Social decision-making requires the ability to balance both the interests of the self and the interests of others to survive in social environments. Empathy is essential to the regulation of this type of interaction, and it often sustains relevant prosocial behaviors such as altruism and helping behavior. In the last decade, our capacity to assess affective and empathy-like behaviors in rodents has expanded our understanding of the neurobiological substrates that underly social decision-making processes such as prosocial behaviors.
View Article and Find Full Text PDFDecisions that favor one's own interest versus the interest of another individual depend on context and the relationships between individuals. The neurobiology underlying selfish choices or choices that benefit others is not understood. We developed a two-choice social decision-making task in which mice can decide whether to share a reward with their conspecifics.
View Article and Find Full Text PDFToxic aggregates of α-synuclein (αsyn) are considered key drivers of Parkinson's disease (PD) pathology. In early PD, αsyn induces synaptic dysfunction also modulating the glutamatergic neurotransmission. However, a more detailed understanding of the molecular mechanisms underlying αsyn-triggered synaptic failure is required to design novel therapeutic interventions.
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