ORCID Profile
0000-0001-8047-5871
Current Organisations
Oregon Health & Science University
,
Garvan Institute of Medical Research
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Publisher: Elsevier BV
Date: 08-2011
Publisher: Frontiers Media SA
Date: 28-08-2019
Publisher: Springer New York
Date: 07-10-2016
Publisher: Springer New York
Date: 2013
DOI: 10.1007/2506_2013_4
Publisher: eLife Sciences Publications, Ltd
Date: 08-06-2021
DOI: 10.7554/ELIFE.64911
Abstract: Precise and efficient insertion of large DNA fragments into somatic cells using gene editing technologies to label or modify endogenous proteins remains challenging. Non-specific insertions/deletions (INDELs) resulting from the non-homologous end joining pathway make the process error-prone. Further, the insert is not readily removable. Here, we describe a method called CRISP R-mediated i nsertion of e xon (CRISPIE) that can precisely and reversibly label endogenous proteins using CRISPR/Cas9-based editing. CRISPIE inserts a designer donor module, which consists of an exon encoding the protein sequence flanked by intron sequences, into an intronic location in the target gene. INDELs at the insertion junction will be spliced out, leaving mRNAs nearly error-free. We used CRISPIE to fluorescently label endogenous proteins in mammalian neurons in vivo with previously unachieved efficiency. We demonstrate that this method is broadly applicable, and that the insert can be readily removed later. CRISPIE permits protein sequence insertion with high fidelity, efficiency, and flexibility.
Publisher: Cold Spring Harbor Laboratory
Date: 23-10-2023
Publisher: eLife Sciences Publications, Ltd
Date: 07-05-2021
Publisher: Wiley
Date: 18-03-2013
DOI: 10.1002/CNE.23238
Publisher: MyJove Corporation
Date: 26-06-2012
DOI: 10.3791/3755
Publisher: Wiley
Date: 15-01-2014
DOI: 10.1002/CNE.23454
Publisher: Elsevier BV
Date: 2017
DOI: 10.1016/J.HEARES.2016.07.004
Abstract: Studies of congenital and early-onset deafness have demonstrated that an absence of peripheral sound-evoked activity in the auditory nerve causes pathological changes in central auditory structures. The aim of this study was to establish whether progressive acquired hearing loss could lead to similar brain changes that would degrade the precision of signal transmission. We used complementary physiologic hearing tests and microscopic techniques to study the combined effect of both magnitude and duration of hearing loss on one of the first auditory synapses in the brain, the endbulb of Held (EB), along with its bushy cell (BC) target in the anteroventral cochlear nucleus. We compared two hearing mouse strains (CBA/Ca and heterozygous shaker-2
Publisher: Cold Spring Harbor Laboratory
Date: 03-12-2020
DOI: 10.1101/2020.12.03.409417
Abstract: Precise and efficient insertion of large DNA fragments into somatic cells using gene editing technologies to label or modify endogenous proteins remains challenging. Non-specific insertions/deletions (INDELs) resulting from the non-homologous end joining pathway make the process error-prone. Further, the insert is not readily removable. Here, we describe a method called CRISPR -mediated insertion of e xon (CRISPIE) that can precisely and reversibly label endogenous proteins using CRISPR/Cas9-based editing. CRISPIE inserts a designer donor module, which consists of an exon encoding the protein sequence flanked by intron sequences, into an intronic location in the target gene. INDELs at the insertion junction will be spliced out, leaving mRNAs nearly error-free. We used CRISPIE to fluorescently label endogenous proteins in neurons in vivo with previously unachieved efficiency. We demonstrate that this method is broadly applicable, and that the insert can be readily removed later. CRISPIE permits protein sequence insertion with high fidelity, efficiency, and flexibility.
Publisher: Wiley
Date: 02-09-2016
DOI: 10.1002/CNE.24095
Abstract: Ascending projections of the dorsal cochlear nucleus (DCN) target primarily the contralateral inferior colliculus (IC). In turn, the IC sends bilateral descending projections back to the DCN. We sought to determine the nature of these descending axons in order to infer circuit mechanisms of signal processing at one of the earliest stages of the central auditory pathway. An anterograde tracer was injected in the IC of CBA/Ca mice to reveal terminal characteristics of the descending axons. Retrograde tracer deposits were made in the DCN of CBA/Ca and transgenic GAD67-EGFP mice to investigate the cells giving rise to these projections. A multiunit best frequency was determined for each injection site. Brains were processed by using standard histologic methods for visualization and examined by fluorescent, brightfield, and electron microscopy. Descending projections from the IC were inferred to be excitatory because the cell bodies of retrogradely labeled neurons did not colabel with EGFP expression in neurons of GAD67-EGFP mice. Furthermore, additional experiments yielded no glycinergic or cholinergic positive cells in the IC, and descending projections to the DCN were colabeled with antibodies against VGluT2, a glutamate transporter. Anterogradely labeled endings in the DCN formed asymmetric postsynaptic densities, a feature of excitatory neurotransmission. These descending projections to the DCN from the IC were topographic and suggest a feedback pathway that could underlie a frequency-specific enhancement of some acoustic signals and suppression of others. The involvement of this IC-DCN circuit is especially noteworthy when considering the gating of ascending signal streams for auditory processing. J. Comp. Neurol. 525:773-793, 2017. © 2016 Wiley Periodicals, Inc.
Publisher: Springer Science and Business Media LLC
Date: 09-11-2022
DOI: 10.1038/S41586-022-05407-4
Abstract: The canonical model of striatal function predicts that animal locomotion is associated with the opposing regulation of protein kinase A (PKA) in direct and indirect pathway striatal spiny projection neurons (SPNs) by dopamine
Publisher: Elsevier BV
Date: 07-2018
DOI: 10.1016/J.HEARES.2018.03.021
Abstract: Reductions in sound-evoked activity in the auditory nerve due to hearing loss have been shown to cause pathological changes in central auditory structures. Hearing loss due strictly to the aging process are less well documented. In this study of CBA/CaH mice, we provide evidence for age-related pathology in the endbulb of Held, a large axosomatic ending arising from myelinated auditory nerve fibers. Endbulbs are known to be involved in the processing of temporal cues used for sound localization and speech comprehension. Hearing thresholds as measured by auditory brainstem response (ABR) thresholds remained stable up to one year, whereas suprathreshold litudes of early ABR waves decreased by up to 50% in older mice, similar to that reported for age-related cochlear synaptopathy (Sergeyenko et al., 2013). The reduction of ABR response magnitude with age correlated closely in time with the gradual atrophy of endbulbs of Held, and is consistent with the hypothesis that endbulb integrity is dependent upon normal levels of spike activity in the auditory nerve. These results indicate that central auditory pathologies emerge as consequence of so-called "hidden" hearing loss and suggest that such brain changes require consideration when devising therapeutic interventions.
Publisher: Society for Neuroscience
Date: 24-10-2007
DOI: 10.1523/JNEUROSCI.1486-07.2007
Abstract: How specific aspects of a stimulus are encoded at different stages of neural processing is a critical question in sensory neuroscience. In the present study, we investigated the neural code underlying the perception of stimulus intensity in the somatosensory system. We first characterized the responses of SA1 (slowly adapting type 1), RA (rapidly adapting), and PC (Pacinian) afferents of macaque monkeys to sinusoidal, diharmonic, and bandpass noise stimuli. We then had human subjects rate the perceived intensity of a subset of these stimuli. On the basis of these neurophysiological and psychophysical measurements, we evaluated a series of hypotheses about which aspect(s) of the neural activity evoked at the somatosensory periphery account for perception. We evaluated three types of neural codes. The first consisted of population codes based on the firing rate of neurons located directly under the probe. The second included population codes based on the firing rate of the entire population of active neurons. The third included codes based on the number of active afferents. We found that the response evoked in the localized population is logarithmic with stimulus litude (given a constant frequency composition), whereas the population response across all neurons is linear with stimulus litude. We conclude that stimulus intensity is best accounted for by the firing rate evoked in afferents located under or near the locus of stimulation, weighted by afferent type.
Publisher: Society for Neuroscience
Date: 07-2018
DOI: 10.1523/ENEURO.0250-18.2018
Abstract: Noise exposure is one of the most common causes of hearing loss and peripheral damage to the auditory system. A growing literature suggests that the auditory system can compensate for peripheral loss through increased central neural activity. The current study sought to investigate the link between noise exposure, increases in central gain, synaptic reorganization, and auditory function. All axons of the auditory nerve project to the cochlear nucleus, making it a requisite nucleus for sound detection. As the first synapse in the central auditory system, the cochlear nucleus is well positioned to respond plastically to loss of peripheral input. To investigate noise-induced compensation in the central auditory system, we measured auditory brainstem responses (ABRs) and auditory perception and collected tissue from mice exposed to broadband noise. Noise-exposed mice showed elevated ABR thresholds, reduced ABR wave 1 litudes, and spiral ganglion neuron loss. Despite peripheral damage, noise-exposed mice were hyperreactive to loud sounds and showed nearly normal behavioral sound detection thresholds. Ratios of late ABR peaks (2–4) relative to the first ABR peak indicated that brainstem pathways were hyperactive in noise-exposed mice, while anatomical analysis indicated there was an imbalance between expression of excitatory and inhibitory proteins in the ventral cochlear nucleus. The results of the current study suggest that a reorganization of excitation and inhibition in the ventral cochlear nucleus may drive hyperactivity in the central auditory system. This increase in central gain can compensate for peripheral loss to restore some aspects of auditory function.
Location: United States of America
No related grants have been discovered for Michael Muniak.