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Canault, M.

Publications and source records attributed to Canault, M..

2 recordsLinked to original sources

Decoding Phonetic Features: Somatotopic and Sensorimotor Representations in Native and Non-native Consonant Perception

Speech perception relies on the integration of auditory and articulatory information, yet the precise role of motor regions remains debated. We combined behavioral measures and fMRI with multivariate pattern analyses to investigate cortical representations of native French and non-native Mandarin consonant perception under clear and noisy conditions. Cross-modal classification analysis showed that articulatory features of perceived degraded native bilabial and dental consonants are mapped somatotopically in right lip and tongue motor areas, which are also engaged in consonant production. These representations may support phoneme categorization by compensating for degraded input. Representational similarity analysis further revealed that a network encompassing bilateral temporal and frontal motor regions encodes phonetic features of native and non-native consonants, including place and manner of articulation. Our findings highlight that speech perception relies on embodied sensorimotor representations, which contribute to decoding phonetic features both within and across languages.

neuroscience↗

Mutations in CalDAG-GEFI Lead to Striatal Signaling Deficits and Psychomotor Symptoms in Multiple Species Including Human

Syndromes caused by mutations in Ras-MAP kinase signaling molecules are known as RASopathies and share features such as developmental delay, autistic traits, and cancer. Syndromic features of Rap-MAP kinase signaling defects remain undefined. CalDAG-GEFI is a calcium-responsive Rap-GTPase activator that is enriched in the matrix of the sensorimotor striatum and down-regulated in Huntingtons disease. We show here that CalDAG-GEFI mutations, including striatum-specific deletions and spontaneous mutations in the enzymatic domain, are associated with psychomotor phenotypes in humans, dogs and mice. The identification of these neural mutants was guided by the overt bleeding phenotype in CalDAG-GEFI knockout mice, and then in humans and other species with conserved platelet signaling deficits. Knockout mice exhibit loss of striatal long-term potentiation and deficits in dopamine, acetylcholine and glutamate signaling, along with delayed motor learning and drug-induced perseverative behaviors. Thus, loss of CalDAG-GEFI signaling produces an evolutionarily conserved syndrome characterized by bleeding and psychomotor dysfunction.

neuroscience↗