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Biology subjects

Semelidou, O.

Publications and source records attributed to Semelidou, O..

3 recordsLinked to original sources

Altered cognitive processes shape tactile perception in autism.

Altered sensory perception is a hallmark of autism and shapes how individuals engage with their environment, with tactile perception playing a critical role in daily functioning and for social interactions. While sensory alterations are thought to contribute to cognitive differences in autism, the impact of cognition on sensory perception remains unclear. Here, we investigated how cognitive processes modulate tactile perception in the Fmr1-KO genetic mouse model of autism through a translational perceptual decision-making task. Our results revealed salience-dependent cognitive alterations that influenced sensory performance. During training, Fmr1-/y male mice distinguishing between a high- and a low-salience stimulus exhibited an increased choice consistency bias in low-salience trials. When tested across a continuum of intermediate stimulus intensities, these mice demonstrated enhanced tactile discrimination of low-salience stimuli but reduced discrimination facilitation for stimuli crossing category boundaries. These effects were accompanied by diminished integration of sensory history and were dissociable from the attention deficits that emerged under high cognitive load. Together, our findings reveal that tactile perceptual alterations reflect context-dependent weighting and integration of sensory information during decision-making rather than uniform sensory deficits or enhancements, supporting a shift beyond traditional sensory-cognitive dichotomies.

neuroscience↗

Homosensory and heterosensory dishabituation engage distinct circuits in Drosophila

Habituation adaptively filters repeated, inconsequential sensory input, while the response to such stimuli re-emerges upon appearance of novel or salient cues (dishabituation).However, the neural circuits underlying dishabituation remain poorly defined, particularly in the central nervous system. Using Drosophila olfactory habituation to the odorant 3-octanol (OCT), we dissect the circuit basis of intramodal (odor-odor) and cross-modal (footshock-odor) dishabituation. A brief yeast odor puff dishabituates intramodally, whereas footshock cross-modally and neither operate through sensitization. Genetic silencing and optogenetics demonstrate that Mushroom Body (MBs) output drives both dishabituation forms. {beta} and {gamma} Kenyon cells (KCs) mediate dishabituation, while '{beta}' Kenyon cells mediate habituation. Dopaminergic neurons encode and PAM neurons mediating appetitive and PPL1 neurons aversive dishabituation, including that triggered by footshock and OCT itself. GABAergic APL neurons and specific MB output neurons tune the balance between habituation and dishabituation, relaying signals via MBONs to the Lateral Horn, a proposed decision node. Connectomic analysis reveals inhibitory interactions supporting this balance. Collectively, we reveal a multi-node circuit that dynamically overrides, rather than erases, habituation findings offering insight into habituation deficits in intellectual disability, autism, and schizophrenia. SIGNIFICANCE STATEMENTThis study identifies a multi-node neural circuit spanning the Mushroom Bodies, dopaminergic and GABAergic modulatory neurons and the Lateral Horn, that governs intramodal and cross-modal dishabituation in Drosophila. Showing that dishabituation dynamically overrides rather than erases habituation and that distinct dopaminergic populations encode stimulus valence to bias this switch, the work reveals a general logic for how the brain flexibly regulates sensory filtering.

animal behavior and cognition↗

Disrupted stimulus encoding shapes tactile perception in autism.

Touch is essential for interacting with the world, and atypical tactile experience is a core feature of autism that profoundly affects daily life. However, we do not know the neural mechanisms of low-level tactile perception and their alterations in autism. Using a translational perceptual task, we recapitulate the multifaceted tactile features of autistic individuals in the Fmr1-/y mouse model of autism, showing tactile hyposensitivity, interindividual variability, and unreliable responses. We reveal that impaired detection decoding in Fmr1-/y-hyposensitive mice stems from diminished single-neuron signal-to-noise ratio in the primary somatosensory cortex that leads to weak population encoding of the tactile stimulus and its detection. This manifests as reduced stimulus-dependent neural recruitment, impaired response precision, and disrupted ensemble dynamics. Decreasing neuronal hyperexcitability strengthens sensory encoding and improves tactile perception. This work provides a translational framework for probing neuronal-perceptual changes in neurodevelopmental conditions, reveals inter-individual variability in preclinical models, and uncovers the neural basis of tactile hyposensitivity in autism.

neuroscience↗