Graziella Madeo

TL;DR: An overview of the role of striatal cholinergic transmission in physiological and pathological conditions, in the context of the pathogenesis of movement disorders, is provided.

TL;DR: The aim of this review is to try to integrate different lines of evidence from both pathogenic and genetic animal models that suggest that early synaptic impairment may represent the key event in PD pathogenesis.

TL;DR: An abnormal time window for synaptic integration between thalamic intralaminar nuclei and corticostriatal inputs is demonstrated, which might alter the action selection process, thereby predisposing DYT1 gene mutation carriers to develop dystonic movements.

TL;DR: It is demonstrated that selective M1 muscarinic receptor antagonism offsets synaptic plasticity deficits in the striatum of mice with the DYT1 dystonia mutation, providing a potential mechanistic rationale for the development of improved antimuscarinic therapies for this movement disorder.

TL;DR: A selective impairment of corticostriatal synaptic plasticity in knock-in mice heterozygous for Δ-torsinA (Tor1a(+/Δgag) mice) as compared to controls is reported, confirming an imbalance between dopaminergic and cholinergic signaling in the striatum.