Dustin J. Hines

ORCID: 0000-0003-2952-9824
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Sleep and Wakefulness Research
  • Memory and Neural Mechanisms
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Genetics and Neurodevelopmental Disorders
  • Neural dynamics and brain function
  • Psychedelics and Drug Studies
  • Amino Acid Enzymes and Metabolism
  • Tryptophan and brain disorders
  • Neuroscience and Neural Engineering
  • Receptor Mechanisms and Signaling
  • Neurotransmitter Receptor Influence on Behavior
  • EEG and Brain-Computer Interfaces
  • Cellular transport and secretion
  • Immune Response and Inflammation
  • Photoreceptor and optogenetics research
  • Olfactory and Sensory Function Studies
  • Ubiquitin and proteasome pathways
  • Epilepsy research and treatment
  • Mitochondrial Function and Pathology
  • Neurogenesis and neuroplasticity mechanisms
  • Adenosine and Purinergic Signaling
  • Ion Channels and Receptors
  • Neurological disorders and treatments
  • Zebrafish Biomedical Research Applications

University of Nevada, Las Vegas
2018-2024

Tufts University
2012-2018

University of British Columbia
2005-2013

Western University
2008

University of Lethbridge
2001-2005

Pannexin-1 (Px1) is expressed at postsynaptic sites in pyramidal neurons, suggesting that these hemichannels contribute to dendritic signals associated with synaptic function. We found that, N-methyl-d-aspartate receptor (NMDAR) activation induced a secondary prolonged current and dye flux were blocked specific inhibitory peptide against Px1 hemichannels; knockdown of by RNA interference the cultured neurons. Enhancing endogenous NMDAR brain slices removing external magnesium ions (Mg2+)...

10.1126/science.1165209 article EN Science 2008-12-04

Abstract Microglia cells exhibit two forms of motility, constant movement filopodia probing surrounding brain tissue, and outgrowth larger processes in response to nearby damage. The mechanisms functions sensing process are not well characterized but likely critical for normal immune function the brain. Using photon laser scanning microscopy we investigated microglia damage, explored relationship between movement. Further, examined roles Cl − or K + channel activation, as actin...

10.1002/glia.20874 article EN Glia 2009-04-20

The level of excitation in the brain is kept under control through inhibitory signals mainly exerted by GABA neurons. However, molecular machinery that regulates balance between and inhibition (E/I) remains unclear. Candidate molecules implicated this process are neuroligin (NL) adhesion molecules, which differentially enriched at either excitatory or contacts. In study, we use transgenic mouse models expressing NL1 NL2 to examine whether enhanced expression specific NLs results synaptic...

10.1523/jneurosci.0032-08.2008 article EN Journal of Neuroscience 2008-06-11

Major depressive disorder is a debilitating condition with lifetime risk of ten percent. Most treatments take several weeks to achieve clinical efficacy, limiting the ability bring instant relief needed in psychiatric emergencies. One intervention that rapidly alleviates symptoms sleep deprivation; however, its mechanism action unknown. Astrocytes regulate responses deprivation, raising possibility glial signaling mediates antidepressive-like actions deprivation. Here, we found astrocytic...

10.1038/tp.2012.136 article EN cc-by Translational Psychiatry 2013-01-15

Abstract Trans‐synaptic cell‐adhesion molecules have been implicated in regulating CNS synaptogenesis. Among these, the Neuroligin (NL) family (NLs 1–4) of postsynaptic adhesion proteins has shown to promote development and specification excitatory versus inhibitory synapses. NLs form a heterophilic complex with presynaptic transmembrane protein Neurexin (NRX). A differential association scaffolding NRX isoforms suggested regulate ratio synapses ( E/I ratio). Using transgenic mice, we tested...

10.1002/hipo.20630 article EN Hippocampus 2009-05-12

The innate immune receptor Toll-like 4 (TLR4) is the activated by lipopolysaccharide (LPS), and TLR4-LPS interaction well known to induce an response, triggering sickness behavior. Within brain, TLR4 highly expressed in brain microglia, excessive inflammation resulting from activation of this pathway has been implicated depressive disorders neurodegenerative pathologies. We hypothesized that blocking LPS-induced would prevent downstream signaling suppress induction used interfering peptides...

10.1371/journal.pone.0060388 article EN cc-by PLoS ONE 2013-03-28

Dead reckoning is an on-line form of spatial navigation used by animal to identify its present location and return directly a starting location, even after circuitous outward trips. At present, it not known which several self-movement cues (efferent copy from movement commands, proprioceptive information, sensory flow, or vestibular information) are compute homeward trajectories. To determine whether information important for dead reckoning, the impact chemical labyrinthectomy was evaluated...

10.1523/jneurosci.22-22-10009.2002 article EN Journal of Neuroscience 2002-11-15

Myosin V motors mediate cargo transport; however, the identity of neuronal molecules transported by these proteins remains unknown. Here we show that myosin Vb is expressed in several populations and associates with alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate-type glutamate receptor subunit GluR1. In developing hippocampal neurons, expression tail domain Vb, but not Va, enhanced GluR1 accumulation soma reduced its surface expression. These changes were accompanied clustering...

10.1074/jbc.m511725200 article EN cc-by Journal of Biological Chemistry 2005-12-08

Significance Temporal lobe epilepsy (TLE) is a chronic brain disorder characterized by the occurrence of spontaneous recurrent seizures. Much our knowledge based on how neurons contribute to this disorder. Here we provide view in which glial cells (astrocytes) progressive development TLE. We have combined model that more closely mimics complex features seizures epileptic patients, with astrocyte-specific molecular genetics identify astrocytes modulate TLE, including seizure occurrence,...

10.1073/pnas.1311967110 article EN Proceedings of the National Academy of Sciences 2013-10-07

Abstract In cultured hippocampal neurons, transient receptor potential 5 (TRPC5) channels are translocated and inserted into plasma membranes of neurons to generate nonselective cation (NSC) currents. We investigated whether TRPC5 channel translocation also contributes the generation NSC currents underlying afterdepolarizations plateau potentials (PPs) in pyramidal cells that induced by muscarinic activation. Using a biotinylation assay quantify change surface membrane proteins acute slices,...

10.1002/hipo.20807 article EN Hippocampus 2010-06-02

In mice, disrupting circadian rhythms with social jet lag for 6 wk caused significant weight gain, higher fasting blood glucose, and impaired glucose tolerance compared control. Voluntary exercise in mice experiencing prevented though the still experienced increased performance trained not lag. Social seems to be a potent rhythm disruptor that impacts exercise-induced training adaptations.

10.1152/japplphysiol.00632.2023 article EN Journal of Applied Physiology 2024-03-07

A strong body of research has defined the role excitotoxic glutamate in animal models brain ischemia and stroke; however, clinical trials receptor antagonists have demonstrated their limited capacity to prevent damage following ischemia. We propose that astrocyte–neuron signaling represents an important modulatory target may be useful mediating stroke. To assess impact astrocyte on stroke, we used astrocyte-specific dominant-negative SNARE mouse model (dnSNARE). Recent findings shown...

10.1523/jneurosci.5495-12.2013 article EN cc-by-nc-sa Journal of Neuroscience 2013-03-06

Brain-derived neurotrophic factor (BDNF) is a potent regulator of neuronal activity, neurogenesis, and depressive-like behaviors; however, downstream effectors by which BDNF exerts these varying actions remain to be determined. Here we reveal that induces long-lasting enhancements in the efficacy synaptic inhibition stabilizing γ2 subunit-containing GABA A receptors (GABA Rs) at cell surface, leading persistent reductions excitability. This effect dependent upon enhanced phosphorylation...

10.1523/jneurosci.1845-13.2013 article EN cc-by-nc-sa Journal of Neuroscience 2013-09-25

Spatial theory proposes that the hippocampus contributes to exploratory behavior allowing animals acquire information about their environment. In present study, movements of control rats, bulbectomized (anosmic) rats and hippocampectomized using neurotoxin N-methyl-D-aspartate (NMDA) were monitored on a large circular table without walls around which visual cues manipulated. The displayed organized spatial in they developed home bases, one or more places operationally defined as those spent...

10.1111/j.1460-9568.2005.04412.x article EN European Journal of Neuroscience 2005-11-01

Significance Schizophrenia is a condition characterized by interrelated symptoms including psychosis and hallucinations, decreased emotional expression motivation, cognitive impairments. Recent studies have shown that γ-aminobutyric acid (GABA), the principal inhibitory neurotransmitter in brain, contributes to of schizophrenia. However, details this alteration are not understood. GABA signaling can exert powerful control on groups neurons, acting as regulated on–off switches for brain...

10.1073/pnas.1308706110 article EN Proceedings of the National Academy of Sciences 2013-09-16

The diversity of inhibitory interneurons allows for the coordination and modulation excitatory principal cell firing. Interneurons that release GABA (γ-aminobutyric acid) onto soma axon exert powerful control by virtue proximity to site action potential generation at initial segment (AIS). Here we review examine cellular molecular regulation targeting GABAergic synapses in cortex hippocampus. We also describe their role controlling network activity normal pathological states. Recent studies...

10.3389/fnmol.2019.00154 article EN cc-by Frontiers in Molecular Neuroscience 2019-06-26

Intellectual disability (ID) is a common neurodevelopmental disorder that can arise from genetic mutations ranging trisomy to single nucleotide polymorphism. Mutations in growing number of genes have been identified as causative ID, including ARHGEF9. Evaluation 41 ARHGEF9 patient reports shows ubiquitous inclusion along with other frequently reported symptoms epilepsy, abnormal baseline EEG activity, behavioral symptoms, and sleep disturbances. codes for the Cdc42 Guanine Nucleotide...

10.1038/s41380-022-01468-z article EN cc-by Molecular Psychiatry 2022-02-15
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