Peter C. Kind

The paper investigates how loss of FMRP in a rat model of FXS affects functional connectivity over development and whether early lovastatin treatment can normalize it.

This study shows astrocytes alter the transcriptomic and epigenetic landscape of developing cortical neurons, promoting intrinsic excitability and influencing disease-related pathways.

This study shows that LTP in sensory cortex is impaired in Fragile X mice, leading to hypoplasticity in layer 2/3 pyramidal neurons and altered somatosensory processing.

The paper tests for axon initial segment (AIS) structural plasticity in human, mouse, and rat cortical neurons across different conditions and finds no evidence of AIS length changes over short-term activity modulation.

This study characterizes a Grin2b heterozygous knockout rat model, revealing seizure and sleep-wake abnormalities, and tests the efficacy of two antiseizure drugs.

This study shows that reduced GluN2A expression in rat models decreases seizure-like activity in specific in vitro epilepsy models.

The paper identifies a common depression in activity-dependent bulk endocytosis across rodent models of autism spectrum disorders, suggesting it as a homeostatic response to hyperexcitability.

This study shows that noradrenergic modulation can restore visual discrimination in a SYNGAP1 mouse model by improving coding precision in the primary visual cortex.

This study investigates the role of FMRP in oligodendrocyte maturation and myelination in human and rat models, finding shared defects in morphology and function.

The paper shows that wild-type bone marrow-derived microglia-like cells reduce strain-dependent neuropathology in Csf1r mutant mice by preventing thalamic calcification.

This study shows that neurodevelopmental processes in the cortex and thalamus can occur normally without microglia, using a genetically modified mouse model.

This study shows that FMRP loss in microglia increases RAC1 signaling, leading to inflammation and neuronal hyperexcitability in FXS, which can be mitigated by RAC1 inhibition.

This study shows that CDKL5 deficiency impairs synaptic vesicle endocytosis in neurons, highlighting its presynaptic role in epilepsy.

This study shows that rats with Fragile X Syndrome exhibit impaired experience-dependent changes in hippocampal spatial activity and circuit function compared to wild-type rats.

This study analyzes EEG brain state distribution and connectivity in SYNGAP1 mutant rats, finding altered state dynamics and reduced connectivity during sleep spindles.

The paper examines flight-freeze response imbalances in Nlgn3-/y rats, finding hyperexcitability in periaqueductal grey neurons linked to altered fear behaviors.

This study investigates synaptic function in a Cdkl5 KO rat model of CDKL5 deficiency disorder, finding normal NMDA and AMPA receptor function but altered synaptic density and plasticity.

The paper identifies excessive ribosomal protein translation as a key factor in Fragile X Syndrome by showing its role in disrupting synaptic protein translation and LTD.

This study shows FMRP is essential for activity-dependent bulk endocytosis in neurons, and targeting this process may alleviate hyperexcitability in fragile X syndrome.

The paper identifies developing interneurons as a potential target for autism genetic risk factors by analyzing human and rodent neural data.

LAB-AID is an interactive web tool that visualizes and interrogates hierarchical biological experimental data to improve understanding and identify outliers and batch effects.

This study creates a rat model with SYNGAP enzymatic domain deletion, showing learning, social, and seizure deficits in heterozygous animals.

This paper investigates whether demyelination in multiple sclerosis leads to selective neurodegeneration of inhibitory interneurons and presents a rodent model to study this phenomenon.

The paper identifies rare CRE variants associated with X-linked intellectual disability by combining sequencing, functional assays in zebrafish and mice, and phenotypic analysis.

This study shows that loss of FMRP in a mouse model of Fragile X Syndrome leads to increased single-spine excitation and more multiply-innervated spines, contributing to circuit hyperexcitability.

The paper shows that synGAP heterozygosity leads to increased TARP levels in the PSD of female rodents but not males, indicating a sex difference in PSD adaptation.

The paper investigates how cellular and synaptic compensations in Fmr1-KO mice affect sensory processing in the barrel cortex, finding that despite compensatory mechanisms, sensory encoding precision is lost, leading to hypersensitivity.