Study Objectives: Brief sleep loss alters cognition and the activity and synaptic structures of both principal neurons and interneurons in hippocampus. However, although sleep-dependent coordination of activity between hippocampus and neocortex is essential for memory consolidation, much less is known about how sleep loss affects neocortical input to hippocampus, or excitatory-inhibitory balance within neocortical structures. We aimed to test how the synaptic structures of SST+ interneurons in lateral and medial entorhinal cortex (LEC and MEC), which are the major neocortical input to hippocampus, are affected by brief sleep disruption in the hours following learning.
View Article and Find Full Text PDFDuring the formation of the auditory system in mammals, spiral ganglion neurons (SGNs) form ribbon-type synapses with hair cells in the cochlea to establish the first "sensorineural" component of sound transduction. Ahead of synapse formation in the cochlea, the SGNs undergo migration and extension with developing Schwann and otic mesenchyme cells to form radial bundles, fasciculated groups of nerve fibers found between the SGN somata and hair cells. Thus far, reports have shown that Eph/Ephrin signaling is important for the formation of radial bundles.
View Article and Find Full Text PDFStudy Objectives: Brief sleep loss alters cognition and synaptic structures of principal neurons in the hippocampus and neocortex. However, while in vivo recording and bioinformatic data suggest that inhibitory interneurons are more strongly affected by sleep loss, it is unclear how sleep and sleep deprivation (SD) affect interneurons' synapses. Disruption of the somatostatin-expressing (SST+) interneuron population seems to be a critical early sign of neuropathology in Alzheimer's dementia, schizophrenia, and bipolar disorder-and the risk of developing all three is increased by habitual sleep loss.
View Article and Find Full Text PDFResearchers may implement magnetic resonance imaging (MRI) to evaluate neurophysiological metrics (e.g. connectivity) in athletes with sports-related concussion (SRC).
View Article and Find Full Text PDFStudy Objectives: Brief sleep loss alters cognition and synaptic structures of principal neurons in hippocampus and neocortex. However, while recording and bioinformatic data suggest that inhibitory interneurons are more strongly affected by sleep loss, it is unclear how sleep and sleep deprivation affect interneurons' synapses. Disruption of the SST+ interneuron population seems to be a critical early sign of neuropathology in Alzheimer's dementia, schizophrenia, and bipolar disorder - and the risk of developing all three is increased by habitual sleep loss.
View Article and Find Full Text PDFEpigenetic factors are critically important for embryonic and postnatal development. Over the past decade, substantial technological advancements have occurred that now permit the study of epigenetic mechanisms that govern all aspects of inner ear development, from otocyst patterning to maturation and maintenance of hair cell stereocilia. In this review, we highlight how three major classes of epigenetic regulation (DNA methylation, histone modification, and chromatin remodeling) are essential for the development of the inner ear.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
August 2021
Sleep loss disrupts consolidation of hippocampus-dependent memory. To characterize effects of learning and sleep loss, we quantified activity-dependent phosphorylation of ribosomal protein S6 (pS6) across the dorsal hippocampus of mice. We find that pS6 is enhanced in dentate gyrus (DG) following single-trial contextual fear conditioning (CFC) but is reduced throughout the hippocampus after brief sleep deprivation (SD; which disrupts contextual fear memory [CFM] consolidation).
View Article and Find Full Text PDFEpigenetic regulation of gene transcription by chromatin remodeling proteins has recently emerged as an important contributing factor in inner ear development. Pathogenic variants in CHD7, the gene encoding Chromodomain Helicase DNA binding protein 7, cause CHARGE syndrome, which presents with malformations in the developing ear. Chd7 is broadly expressed in the developing mouse otocyst and mature auditory epithelium, yet the pathogenic effects of Chd7 loss in the cochlea are not well understood.
View Article and Find Full Text PDF