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Item type:Publication, Influence of E/I balance and pruning in peri-personal space differences in schizophrenia: a computational approach(Elsevier, 2021-09-09)The encoding of the space close to the body, named peri-personal space (PPS), is thought to play a crucial role in the unusual experiences of the self observed in schizophrenia (SCZ). However, it is unclear why SCZ patients and high schizotypal (H-SPQ) individuals present a narrower PPS and why the boundaries of the PPS are more sharply defined in patients. We hypothesise that the unusual PPS representation observed in SCZ is caused by an imbalance of excitation and inhibition (E/I) in recurrent synapses of unisensory neurons or an impairment of bottom-up and top-down connectivity between unisensory and multisensory neurons. These hypotheses were tested computationally by manipulating the effects of E/I imbalance, feedback weights and synaptic density in the network. Using simulations we explored the effects of such impairments in the PPS representation generated by the network and fitted the model to behavioural data. We found that increased excitation of sensory neurons could account for the smaller PPS observed in SCZ and H-SPQ, whereas a decrease of synaptic density caused the sharp definition of the PPS observed in SCZ. We propose a novel conceptual model of PPS representation in the SCZ spectrum that can account for alterations in self-world demarcation, failures in tactile discrimination and symptoms observed in patients. - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Reduced synaptic plasticity and E/I imbalance drive peripersonal space boundaries expansion in schizophrenia(Cold Spring Harbor Laboratory, 2024-07-23)Abnormal encoding of peripersonal space (PPS) is believed to affect bodily self disruptions in schizophrenia (SCZ). Empirical studies show that SCZ patients exhibit a narrower PPS than controls but maintain its plasticity. Computational research links this smaller PPS to increased excitation of sensory neurons and reduced feedforward synaptic density. However, it is unclear how such differences influence learning during the expansion of PPS boundaries. We hypothesise that Hebbian plasticity can account for PPS expansion after active tool use training. To explore the effect of such mechanisms on PPS plasticity, we developed a SCZ network model which was fit to behavioural data before and after tool manipulation. We found that PPS expansion occurs in spite of E/I imbalance or reduced synaptic density, but does not match the post-training PPS representation of patients. A better fit was obtained after altering plasticity by either reducing the learning rate, increasing the forgetting rate or increasing the plasticity threshold. We discuss our findings in terms of dysfunctional plasticity in SCZ and highlight the key challenges in identifying the neurobiological correlates of reduced plasticity within PPS networks. Because current empirical data supports multiple viable mechanisms, we propose experiments to distinguish between the proposed plasticity accounts and clarify mixed findings on PPS representation in SCZ. Graphical Highlights Using a peripersonal space network model, we found that PPS expansion after tool-use occurs in spite of E/I imbalance or reduced synaptic density. Reduced feedforward synaptic plasticity is required to match the post-training PPS representation of patients. Such reduction of synaptic plasticity could be achieved by either reducing the learning rate, increasing the forgetting rate or increasing the plasticity threshold relative to a healthy control model. Our model predicts that measuring PPS at intermediate time points during a longer stimulation protocol would help distinguish between these plasticity differences. - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Increased excitation enhances the sound-induced flash illusion by impairing multisensory causal inference in the schizophrenia spectrum(Cold Spring Harbor Laboratory, 2024-05-31)The spectrum of schizophrenia is characterised by an altered sense of self with known impairments in tactile sensitivity, proprioception, body-self boundaries, and self-recognition. These are thought to be produced by failures in multisensory integration mechanisms, commonly observed as enlarged temporal binding windows during audiovisual illusion tasks. To our knowledge, there is an absence of computational explanations for multisensory integration deficits in patients with schizophrenia and individuals with high schizotypy, particularly at the neurobiological level. We implemented a multisensory causal inference network to reproduce the responses of individuals who scored low in schizotypy in a simulated double flash illusion task. Next, we explored the effects of recurrent excitation, cross-modal and feedback weights, and synaptic density on the visual illusory responses of the network. Using quantitative fitting to empirical data, we found that an increase in the weights of the recurrent excitatory connectivity in the network enlarges the temporal binding window and increases the overall proneness to experience the illusion, matching the responses of individuals scoring high in schizotypy. Moreover, we found that an increase in excitation increases the probability of inferring a common cause from the stimuli. We propose an E/I imbalance account of reduced temporal discrimination in the SCZ spectrum and discuss possible links with Bayesian theories of schizophrenia. We highlight the importance of adopting a multisensory causal inference perspective to address body-related symptomatology of schizophrenia.