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Razak, K.

Publications and source records attributed to Razak, K..

2 recordsLinked to original sources

Frontal Cortex Hyperactivation and Gamma Desynchrony in Fragile X Syndrome: Correlates of Auditory Hypersensitivity

Fragile X syndrome (FXS) is an X-linked disorder that often leads to intellectual disability, anxiety, and sensory hypersensitivity. While sound sensitivity (hyperacusis) is a distressing symptom in FXS, its neural basis is not well understood. It is postulated that hyperacusis may stem from temporal lobe hyperexcitability or dysregulation in top-down modulation. Studying the neural mechanisms underlying sound sensitivity in FXS using scalp electroencephalography (EEG) is challenging because the temporal and frontal regions have overlapping neural projections that are difficult to differentiate. To overcome this challenge, we conducted EEG source analysis on a group of 36 individuals with FXS and 39 matched healthy controls. Our goal was to characterize the spatial and temporal properties of the response to an auditory chirp stimulus. Our results showed that males with FXS exhibit excessive activation in the frontal cortex in response to the stimulus onset, which may reflect changes in top-down modulation of auditory processing. Additionally, during the chirp stimulus, individuals with FXS demonstrated a reduction in typical gamma phase synchrony, along with an increase in asynchronous gamma power, across multiple regions, most strongly in temporal cortex. Consistent with these findings, we observed a decrease in the signal-to-noise ratio, estimated by the ratio of synchronous to asynchronous gamma activity, in individuals with FXS. Furthermore, this ratio was highly correlated with performance in an auditory attention task. Compared to controls, males with FXS demonstrated elevated bidirectional frontotemporal information flow at chirp onset. The evidence indicates that both temporal lobe hyperexcitability and disruptions in top-down regulation play a role in auditory sensitivity disturbances in FXS. These findings have the potential to guide the development of therapeutic targets and back-translation strategies.

neuroscience↗

Astrocytes regulate inhibition in Fragile X Syndrome

Astrocytes control neural communications by influencing GABAergic transmission through uptake and synthesis of GABA. Impaired GABAergic signaling is thought to underlie cortical hyperexcitability in autism. Here we show that dysregulation of astrocyte GABA transport in Fragile X syndrome (FXS), a leading genetic cause of autism, contributes to circuit hyperexcitability. Human FXS astrocytes derived from patient-specific induced pluripotent stem cells and mouse Fmr1 knockout (KO) astrocytes display a significant increase in levels of GABA and GABA-synthesizing enzyme GAD65/67. Our astrocyte-specific Fmr1 KO (cKO) mouse model reveals reduced inhibitory connectivity and impaired cortical responses to sound. Reverse GABA transport in cortical astrocytes contributes to impaired fidelity of temporal processing and hyperactive behaviors in cKO mice. Blocking astrocyte GABA transport is sufficient to restore PV expression, cortical activity, EEG responses, and locomotor behavior. Our findings suggest astrocyte GABA transport plays a key role in regulating cortical inhibition, and contributes to autism-associated phenotypes. HighlightsO_LIFXS astrocytes show elevated levels of GABA and its synthesizing enzyme GAD65/67 C_LIO_LIFmr1 KO cortical astrocytes suppress PV expression leading to enhanced overall cell activity through reverse GABA transport C_LIO_LIAstrocyte-specific postnatal deletion of Fmr1 results in reduced inhibitory cortical connectivity, impaired fidelity of temporal processing and behavioral hyperactivity C_LIO_LIAcute blockade of astrocytic GABA transport is sufficient to restore cortical responses and correct hyperactive mouse behaviors C_LI Graphic Abstract O_FIG O_LINKSMALLFIG WIDTH=192 HEIGHT=200 SRC="FIGDIR/small/479618v5_ufig1.gif" ALT="Figure 1"> View larger version (55K): org.highwire.dtl.DTLVardef@1c84f4corg.highwire.dtl.DTLVardef@1ce0884org.highwire.dtl.DTLVardef@1913d17org.highwire.dtl.DTLVardef@41f061_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗