Neural Comput - Deficient GABAergic gliotransmission may cause broader sensory tuning in schizophrenia.


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We examined how the depression of intracortical inhibition due to a reduction in ambient GABA concentration impairs perceptual information processing in schizophrenia. A neural network model with a gliotransmission-mediated ambient GABA regulatory mechanism was simulated. In the network, interneuron-to-glial-cell and principal-cell-to-glial-cell synaptic contacts were made. The former hyperpolarized glial cells and let their transporters import (remove) GABA from the extracellular space, thereby lowering ambient GABA concentration, reducing extrasynaptic GABAa receptor-mediated tonic inhibitory current, and thus exciting principal cells. In contrast, the latter depolarized the glial cells and let the transporters export GABA into the extracellular space, thereby elevating the ambient GABA concentration and thus inhibiting the principal cells. A reduction in ambient GABA concentration was assumed for a schizophrenia network. Multiple dynamic cell assemblies were organized as sensory feature columns. Each cell assembly responded to one specific feature stimulus. The tuning performance of the network to an applied feature stimulus was evaluated in relation to the level of ambient GABA. Transporter-deficient glial cells caused a deficit in GABAergic gliotransmission and reduced ambient GABA concentration, which markedly deteriorated the tuning performance of the network, broadening the sensory tuning. Interestingly, the GABAergic gliotransmission mechanism could regulate local ambient GABA levels: it augmented ambient GABA around stimulus-irrelevant principal cells, while reducing ambient GABA around stimulus-relevant principal cells, thereby ensuring their selective responsiveness to the applied stimulus. We suggest that a deficit in GABAergic gliotransmission may cause a reduction in ambient GABA concentration, leading to a broadening of sensory tuning in schizophrenia. The GABAergic gliotransmission mechanism proposed here may have an important role in the regulation of local ambient GABA levels, thereby improving the sensory tuning performance of the cortex.

Resumo Limpo

examin depress intracort inhibit due reduct ambient gaba concentr impair perceptu inform process schizophrenia neural network model gliotransmissionmedi ambient gaba regulatori mechan simul network interneurontoglialcel principalcelltoglialcel synapt contact made former hyperpolar glial cell let transport import remov gaba extracellular space therebi lower ambient gaba concentr reduc extrasynapt gabaa receptormedi tonic inhibitori current thus excit princip cell contrast latter depolar glial cell let transport export gaba extracellular space therebi elev ambient gaba concentr thus inhibit princip cell reduct ambient gaba concentr assum schizophrenia network multipl dynam cell assembl organ sensori featur column cell assembl respond one specif featur stimulus tune perform network appli featur stimulus evalu relat level ambient gaba transporterdefici glial cell caus deficit gabaerg gliotransmiss reduc ambient gaba concentr mark deterior tune perform network broaden sensori tune interest gabaerg gliotransmiss mechan regul local ambient gaba level augment ambient gaba around stimulusirrelev princip cell reduc ambient gaba around stimulusrelev princip cell therebi ensur select respons appli stimulus suggest deficit gabaerg gliotransmiss may caus reduct ambient gaba concentr lead broaden sensori tune schizophrenia gabaerg gliotransmiss mechan propos may import role regul local ambient gaba level therebi improv sensori tune perform cortex

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