2 edition of Role of versican in the regulation of glutamatergic synaptic transmission. found in the catalog.
Role of versican in the regulation of glutamatergic synaptic transmission.
Written in English
Extracellular matrix (ECM) molecules and their cleavage products critically regulate the growth and arborization of neurites of neuronal cells. Versican is one of the major ECM molecules in the brain and versican G3-containing fragments are found in human astrocytoma. In addition, versican G3 peptides promote the growth of various non-neuronal cells. I hypothesized that the versican G3 domain regulates central synaptic formation and transmission. I found that: (1) versican G3 domain, but not a G3 mutant that lacks two epithelial growth factor (EGF) motifs, enhanced neurite outgrowth, glutamate-evoked currents, and miniature excitatory postsynaptic currents, as well as the surface expression and total protein levels of glutamate receptors in cultured hippocampal neurons; and (2) the effects of G3 on neurite growth and glutamate-currents were significantly reduced by blocking the EGF receptor. I conclude that the versican G3 domain regulates glutamatergic synaptic formation and transmission, possibly via an EGF receptor-mediated signaling pathway.
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Because Glu can cause neuronal degeneration, there are two major therapeutic approaches for neurological diseases: prevent the degeneration of neurons by controlling excitotoxicity, and modulate glutamatergic synaptic transmission and function in the surviving neurons by positive or negative regulation of glutamate receptors (GluRs). October –September Fatty acid binding proteins and the regulation of synaptic transmission and plasticity in monoaminergic neurons SUNY REACH Role: Principal Investigator $20, March –August Regulation of social reward in rat valproic acid model of autism Research Institute on Addictions Role: Co-Investigator $22,
Glutamatergic neurons represent the largest neuronal class in the brain and are responsible for the bulk of excitatory synaptic transmission and plasticity. Abnormalities in glutamatergic neurons are linked to several brain disorders and their modulation represents a potential opportunity for emerging bioelectronic medicine (BEM) approaches. Synaptic vesicles (SVs) store neurotransmitters and release them by exocytosis. The vesicular neurotransmitter transporters discriminate which transmitter will be sequestered and stored by the vesicles. However, it is unclear whether the neurotransmitter phenotype of SVs is solely defined by the transporters or whether it is associated with additional proteins.
Glutamate receptors are synaptic and non synaptic receptors located primarily on the membranes of neuronal and glial cells. Glutamate (the conjugate base of glutamic acid) is abundant in the human body, but particularly in the nervous system and especially prominent in the human brain where it is the body's most prominent neurotransmitter, the brain's main excitatory neurotransmitter, and also. Long-Lasting Enhancement of Glutamatergic Synaptic Transmission by Acetylcholine Contrasts with Response Adaptation after Exposure to Low-Level Nicotine Romain Girod, Lorna W. Role Journal of Neuroscience 15 July , 21 (14) ; DOI: /JNEUROSCI
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In neuroscience, glutamate refers to the anion of glutamic acid in its role as a neurotransmitter: a chemical that nerve cells use to send signals to other is by a wide margin the most abundant excitatory neurotransmitter in the vertebrate nervous system.
It is used by every major excitatory function in the vertebrate brain, accounting in total for well over 90% of the synaptic Receptors: NMDA, AMPA, kainate, mGluR. General overview of glutamate transmission.
Glutamate is the major excitatory neurotransmitter in the mammalian brain and accounts for approximately 70% of synaptic transmission in the central nervous system (Nicholls, ; Niciu et al., ).The actions of glutamate are mediated by both fast-acting ligand-gated ion channels, commonly referred to as ionotropic glutamate receptors, Cited by: Glutamatergic transmission in the vertebrate brain requires the involvement of glia cells, in a continuous molecular dialogue.
Glial glutamate receptors and transporters are key molecules that sense synaptic activity and by these means modify their physiology in the short and long by: At glutamatergic synapses, excitatory amino acid (EAA) transporters are involved in the removal of the neurotransmitter glutamate (Glu) from the synaptic cleft to stop intercellular signaling following the release of the neurotransmitter and action on receptors (Figure 1).EAAs are major brain neurotransmitters.
They are primarily involved in the so-called excitatory ‘fast signaling,’ which. Further complexity in the regulation of ionotropic glutamatergic neurotransmission is provided by molecular variability at the transcriptional and post-transcriptional level.
RNA editing of AMPA and kainate receptor subunits (Higuchi et al., ) and alternative splicing of mRNA transcripts (Sommer et al., ) modulate second messenger Cited by: To understand the interactive role of the 5-HT and NE systems in glutamatergic transmission, we recorded AMPAR-EPSC in PFC slices.
Reuptake inhibitors fluoxetine and desipramine were used to elevate the synaptic concentration of endogenous 5-HT and NE, respectively. Glutamate (Glu) is the major mediator of excitatory synaptic transmission in the mammalian brain Under normal conditions, Glu plays a prominent role in synaptic plasticity, learning, and memory, but in pathological conditions it is known to be a potent neuronal excitotoxin, triggering either rapid or.
The release of the endotoxin lipopolysaccharides (LPS) from gram-negative bacteria is key in the induction of the downstream cytokine release from cells targeting cells throughout the body.
However, LPS itself has direct effects on cellular activity and can alter synaptic transmission. Animals experiencing septicemia are generally in a critical state and are often treated with various.
Our results indicate that IL potentiates synaptic activity in a dose- and time-dependent manner exerting both presynaptic (short-term exposure) and postsynaptic (long-term exposure) action. Obtained results demonstrate involvement of IL in the regulation of basal glutamatergic synaptic transmission and plasticity at normal conditions.
Yan Dong's 30 research works with citations and 1, reads, including: A Critical Role of Basolateral Amygdala to Nucleus Accumbens Projection in Sleep Regulation of Reward Seeking. The astrocytic glutamine (Gln)‐glutamate (Glu) cycle (GGC) supplies Gln for the regulation of glutamatergic synaptic transmission (GST) in the adult hippocampus.
Increased synaptic Glu release in the perinatal ventrolateral ventromedial nucleus of the hypothalamus (vlVMH) modulates sexual differentiation, however, whether GGC regulates GST in. Impaired synaptic plasticity and dendritic loss in excitatory glutamatergic synapses are early events in Alzheimer disease (AD).
These synaptic abnormalities are triggered by accumulation of soluble fibrillary β-amyloid (Aβ) oligomers, which bind to several postsynaptic and presynaptic partners. Many of the synaptic effects of Aβ oligomers involve NMDA receptors (NMDARs) and type 1. Glutamatergic transmission is the major excitatory transmission of the mammalian brain and is increasingly believed to play a role in the generation of sleep homeostasis through changes in cortical synaptic plasticity, 79 although a more general mechanism needs be involved to explain data across all species.
80 Not surprisingly, therefore. Overview of Synaptic Neurotransmission: Glutamatergic Excitation Glutamate receptors (GluRs), the major excitatory receptor in the brain, are characterized as ionotropic or metabotropic. Ionotropic GluRs are tetrameric ligand-gated cation channels that induce depolarization of the postsynaptic membrane following the presynaptic release of.
Both glutamatergic and GABAergic neurons are highly diversified in the central nervous system (CNS). More than half a century after the discovery of the effects of GABA, it is now established that in mature neurons, neuronal excitability is characterized by a balance between glutamatergic excitatory input and GABAergic inhibitory transmission.
Glutamatergic transmission in the vertebrate brain requires the involvement of glia cells, in a continuous molecular dialogue. Glial glutamate receptors and transporters are key molecules that sense synaptic activity and by these means modify their physiology in the short and long term.
Posttranslational modifications that regulate protein-protein interactions and modulate transmitter removal. They have been implicated in problems with learn- ing and memory, addiction, motor regulation, and Fragile X syndrome (Niswender and Conn, ).
Group II metabotropic receptors are situated not only on post-synaptic cells, but also on pre-synaptic cells, possibly to suppress glutamate transmission (Swanson et al., ). The process of synaptic transmission generates or inhibits electrical impulses in a network of neurons for the processing of information.
Glutamate is the primary excitatory neurotransmitter in the brain, while GABA is the principal inhibitory neurotransmitter. The balance of glutamatergic and GABAergic tone is crucial to normal neurologic. In addition to affecting rapid transmission at glutamatergic synapses, there will be effects on long-term synaptic changes, the direction – long-term potentiation (LTP) or long-term depression (LTD) – and magnitude of which depend on the number of activated NMDA receptors.
These phenomena are clearly illustrated by the glial changes in the SON. John A. Payne, in Physiology and Pathology of Chloride Transporters and Channels in the Nervous System, 3.
Role of KCC2 in Development of the Nervous System. GABAergic transmission exhibits many unique features that permit it to serve important roles during the life of a neuron – from controlling the maturation of neurons and neuronal networks during development to operating as the.
glutamatergic drive to inhibitory circuits that regulate DMV activity in a murine model of type 1 diabetes. It was hypoth-esized that glutamate would prominently alter GABAergic, inhibitory synaptic transmission to DMV neurons from mice after chronic hyperglycemia and hypoinsulinemia.
Synaptic.Stephen D. Meriney, Erika E. Fanselow, in Synaptic Transmission, Associative Long-Term Potentiation. A type of long-term synaptic plasticity called “associative LTP” was identified at the thousands of synapses formed between the Schaffer collateral pathway and the CA1 pyramidal cells.
These synapses are studied experimentally by stimulating the fiber tract (Schaffer collaterals) that.The Role of Dopamine in Retinal Function. Abstract. Dopamine (DA) is the major catecholamine in all vertebrate retinas including man.
All vertebrates have dopaminergic neurons identified as amacrine cells (ACs) and interplexiform cells (IPCs), with great variations among different species.