Search

Your search keyword '"Yongling, Zhu"' showing total 4 results
Start Over Author "Yongling, Zhu" Search Limiters Peer Reviewed Topic synapses
4 results on '"Yongling, Zhu"'

1. Complete Disruption of the Kainate Receptor Gene Family Results in Corticostriatal Dysfunction in Mice

Author

Daniele Procissi, Yongling Zhu, Herman B. Fernandes, John Marshall, Bryan A. Copits, Geoffrey T. Swanson, Toshihiro Nomura, Jian Xu, Lei Wang, Anis Contractor, and Susumu Mori

Subjects
0301 basic medicine, Male, striatum, perseverative behavior, corticostriatal synapse, Kainate receptor, Striatum, Neurotransmission, Biology, Medium spiny neuron, Synaptic Transmission, General Biochemistry, Genetics and Molecular Biology, Article, 03 medical and health sciences, Mice, 0302 clinical medicine, Receptors, Kainic Acid, Cerebellar Diseases, Biological neural network, Animals, Receptor, lcsh:QH301-705.5, Cerebral Cortex, Mice, Knockout, Neurons, Glutamate receptor, Excitatory Postsynaptic Potentials, Anatomy, Corpus Striatum, 030104 developmental biology, kainate receptor, nervous system, lcsh:Biology (General), Knockout mouse, Synapses, Neuroscience, 030217 neurology & neurosurgery
Abstract

Summary Kainate receptors are members of the glutamate receptor family that regulate synaptic function in the brain. They modulate synaptic transmission and the excitability of neurons; however, their contributions to neural circuits that underlie behavior are unclear. To understand the net impact of kainate receptor signaling, we generated knockout mice in which all five kainate receptor subunits were ablated (5ko). These mice displayed compulsive and perseverative behaviors, including over-grooming, as well as motor problems, indicative of alterations in striatal circuits. There were deficits in corticostriatal input to spiny projection neurons (SPNs) in the dorsal striatum and correlated reductions in spine density. The behavioral alterations were not present in mice only lacking the primary receptor subunit expressed in adult striatum (GluK2 KO), suggesting that signaling through multiple receptor types is required for proper striatal function. This demonstrates that alterations in striatal function dominate the behavioral phenotype in mice without kainate receptors.

Published
2017

2. Na+ Occupancy and Mg2+ Block of the N-Methyl-d-Aspartate Receptor Channel

Author

Anthony Auerbach and Yongling Zhu

Subjects
inorganic chemicals, Physiology, Xenopus, Sodium, chemistry.chemical_element, magnesium, Receptors, N-Methyl-D-Aspartate, Dissociation (chemistry), channel blockade, Membrane Potentials, Reaction rate constant, Extracellular, Animals, ion binding sites, Membrane potential, Chromatography, selectivity, Electrophysiology, Dissociation constant, Kinetics, chemistry, Synapses, Oocytes, Biophysics, Ligand-gated ion channel, Original Article, permeation, Intracellular
Abstract

The effect of extracellular and intracellular Na(+) on the single-channel kinetics of Mg(2+) block was studied in recombinant NR1-NR2B NMDA receptor channels. Na(+) prevents Mg(2+) access to its blocking site by occupying two sites in the external portion of the permeation pathway. The occupancy of these sites by intracellular, but not extracellular, Na(+) is voltage-dependent. In the absence of competing ions, Mg(2+) binds rapidly (10(8) M(-1)s(-1), with no membrane potential) to a site that is located 0.60 through the electric field from the extracellular surface. Occupancy of one of the external sites by Na(+) may be sufficient to prevent Mg(2+) dissociation from the channel back to the extracellular compartment. With no membrane potential; and in the absence of competing ions, the Mg(2+) dissociation rate constant is10 times greater than the Mg(2+) permeation rate constant, and the Mg(2+) equilibrium dissociation constant is approximately 12 microM. Physiological concentrations of extracellular Na(+) reduce the Mg(2+) association rate constant approximately 40-fold but, because of the "lock-in" effect, reduce the Mg(2+) equilibrium dissociation constant only approximately 18-fold.

Published
2001

3. Hippocampal Metaplasticity Is Required for the Formation of Temporal Associative Memories.

Author

Jian Xu, Antion, Marcia D., Nomura, Toshihiro, Kraniotis, Stephen, Yongling Zhu, and Contractor, Anis

Subjects
HIPPOCAMPUS physiology, TEMPORAL lobe, MEMORY, NEUROPLASTICITY, SYNAPSES, GLUTAMATE receptors
Abstract

Metaplasticity regulates the threshold for modification of synaptic strength and is an important regulator of learning rules; however, it is not known whether these cellular mechanisms for homeostatic regulation of synapses contribute to particular forms of learning. Conditional ablation of mGluR5 in CAI pyramidal neurons resulted in the inability of low-frequency trains of afferent activation to prime synapses for subsequent theta burst potentiation. Priming-induced metaplasticity requires mGluR5-mediated mobilization of endocannabinoids during the priming train to induce long-term depression of inhibition (I-LTD). Mice lacking priming-induced plasticity had no deficit in spatial reference memory tasks, but were impaired in an associative task with a temporal component. Conversely, enhancing endocannabinoid signaling facilitated temporal associative memory acquisition and, after training animals in these tasks, ex vivo I-LTD was partially occluded and theta burst LTP was enhanced. Together, these results suggest a link between metaplasticity mechanisms in the hippocampus and the formation of temporal associative memories. [ABSTRACT FROM AUTHOR]

Published
2014
Full Text
View/download PDF

4. A C-Terminal Determinant of GluR6 Kainate Receptor Trafficking.

Author

Sheng Yan, Eng H., Sanders, James M., Jian Xu, Yongling Zhu, Contractor, Anis, and Swanson, Geoffrey T.

Subjects
PROTEINS, GREEN fluorescent protein, IMMUNOFLUORESCENCE, KIDNEYS, SYNAPSES
Abstract

Intracellular trafficking of ionotropic glutamate receptors is regulated predominantly by determinants in the cytoplasmic C-terminal domain of the subunit proteins. Although AMPA receptors are found at the vast majority of excitatory synapses, synaptic kainate receptors exhibit a much more restricted distribution, suggesting that specific mechanisms exist for selective trafficking of these receptor proteins. In this report, we define a critical forward trafficking motif that is necessary for surface expression of the glutamate receptor 6 (GluR6) kainate receptor as well as chimeric proteins containing only the GluR6 C-terminal domain. The trafficking determinant was identified by tracking surface expression of green fluorescent protein-tagged GluR6 receptors with confocal immunofluorescence in COS-7 cells and cultured neurons and patch-clamp electrophysiology in human embryonic kidney 293 cells. Serial truncation and alanine site mutagenesis of the GluR6 subunit C terminus localized the critical motif to a seven amino acid stretch of predominantly basic residues. Alanine mutation of the trafficking motif reduced kainate receptor current amplitudes by >90% and resulted in retention of the mutated receptors in the endoplasmic reticulum. This forward trafficking domain is the first such identified for kainate receptors. [ABSTRACT FROM AUTHOR]

Published
2004
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results