Topic: excitation/inhibition imbalance

Autism spectrum disorder (ASD) is a term used to describe a wide variety of neurodevelopmental disorders that share manifestations and symptoms including intellectual disabilities, social impairments, delayed speech development and repetitive behaviors. Different animal models of ASD share similar electrophysiological and morphological aberrations at the neuronal level. In particular, previous studies have shown that the developmental maturation of GABAergic circuitry appears altered leading to an excitation/inhibition imbalance in the adult. During neurotransmission, the polarity of the GABAe

Multiple studies suggest that inhibitory neurons are involved in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). ALS and FTD are two devastating, frequently co-occurring neurodegenerative disorders. While ALS primarily affects motor neurons, causing rapid progressive paralysis and premature death, FTD affects frontal and temporal lobes, leading to severe changes in personality, behaviour, or language skills. To characterise the contribution of inhibitory neurons to these phenotypes, we generated a mouse model based on the expression of mutant Fused in Sarcoma (FUS) selec

Although the aetiology of schizophrenia is still not thoroughly understood, post-mortem studies of patients have consistently revealed alterations of GABAergic interneurons, particularly lower levels of GAD67 and parvalbumin in cortical parvalbumin interneurons (PVs). A deficient maturation of PVs could relate to the neurodevelopmental aspect of schizophrenia since normal wiring of cortical circuits relies on this process. We have previously shown that mice with an early postnatal NMDA receptor ablation in corticolimbic GABAergic interneurons –predominantly PVs– present schizophrenia-like phen