Sentences with phrase «controlling synaptic»

We will explore the function of these genes in controlling synaptic homeostasis, develop novel imaging approaches to visualize homeostatic changes in real time, and systematically screen genes implicated in aging and longevity for roles in homeostatic plasticity.

In this publication, under the title of «Membrane - Derived Phospholipids Control Synaptic Neurotransmission and Plasticity», the Cadiz scientists have reflected the work of years that has led them to identify a molecule, Lysophosphatidic acid (LPA), as a possible element implicated in the link between the metabolic state of an organism and its cerebral function.

Nguyen plans on applying IM - LARIAT technology to a living brain, where she would be able to control synaptic vesicle transmission and communication between neurons.

A presynaptic endosomal trafficking pathway controls synaptic growth signaling.

LIM Kinase1 controls synaptic stability downstream of the type II BMP receptor.

A recent study has demonstrated that PSD95 and PSD93 jointly control the synaptic targetting of AMPA receptors in mature synapses (Elias 2006).

Not exact matches

Slow - acting neurotransmitters control the efficacy of fast synaptic transmission by regulating the efficiency of neurotransmitter release from presynaptic terminals and by regulating the efficiency with which fast - acting neurotransmitters produce their effects on postsynaptic receptors.

The model is able to learn, due to synaptic plasticity, to control the signals that open and close the neural gates, so as to control the flow of information among different areas.

The synaptic vesicle protein that mediates membrane fusion during exocytosis also regulates the rate and extent of this process by controlling vesicle tethering.

Researchers in Guoping Feng's lab at MIT hypothesized that a mutation in Shank3 differentially affects synaptic development in two neural pathways that contribute to motor control.

In this study, the authors were able to show that TGF β1 triggers N - methyl - D - aspartate receptor (NMDA), a molecule controlling memory formation and maintenance through synaptic plasticity.

«There is mounting evidence that the cellular machinery that controls cell death also controls the strength and number of synaptic connections,» Overstreet - Wadiche said.

They control the strength and duration of the synaptic signal.

This regulation is spectacularly apparent in the exquisite speed and precision of synaptic exocytosis, where synaptotagmin (the calcium - ion sensor for fusion) cooperates with complexin (the clamp activator) to control the precisely timed release of neurotransmitters that initiates synaptic transmission and underlies brain function.

With the combined use of genetics and pharmacology, the investigators altered the production of proteins controlled by eIF2α in adult mice, essentially converting them into adolescents by making them more susceptible to cocaine - induced changes in synaptic strength and behavior.

«There is mounting evidence that the cellular machinery that controls cell death also controls the strength and number of synaptic connections»

The next major advance which moved this analysis from a cell physiological to a molecular level was accomplished by Scheller and Südhof who made overlapping contributions that characterized the proteins that controlled the two key steps of transmitter release: 1) They showed the mechanism by which the vesicle is mobilized to the release sites of the presynaptic terminal, where the synaptic vesicle first fuses with the membrane of the sending neuron and then leaves the cell, and 2) they also discovered how Ca2 + drives the vesicle to release its contents.

«It is a sort of shepherding effect by alpha - synuclein that occurs away from the synapse itself, and controls the number of synaptic vesicles used in each transmission,» Fusco said.

We also conduct electrophysiological, biochemical, imaging, antd behavioral studies with various knockout and transgenic mice to determine how precise genetic manipulations that either activate or abolish specific translational control mechanisms alter synaptic function and behavior.

The work combines remote control of action potential firing and synaptic signaling combined with imaging of activity with genetically encoded calcium and voltage sensors and electrophysiology.

We also study how molecular signaling, translational control, synaptic plasticity, and behavior are altered in mouse models of developmental disability, autism, aging, and Alzheimer's disease.

Detailed biochemical and sophisticated imaging experiments are employed to delineate the molecular signaling cascades that couple receptors to the translational apparatus during long - lasting synaptic plasticity in the hippocampus, amygdala, cortex, and striatum, and whether these types of translational control are required for memory formation, social behaviors, and behavioral flexibility.

We use a number of experimental approaches to gain a greater understanding of translational control mechanisms necessary for maintaining long - lasting changes in synaptic strength and memory.

Ubiquitin ligase TRIM3 controls hippocampal plasticity and learning by regulating synaptic?

Homeostatic control of synaptic function has been demonstrated in diverse organisms, including flies, rodents, and humans, yet the genes and molecular mechanisms governing these processes remain unclear.

Pathological hallmarks of AD, including plaques and loss of synaptic markers, are readily apparent at nine months of age in huAPP / PS1 mice along with clear deficits in spatial memory when compared to wild type controls [7, 10, 11, 31].

The molecular mechanisms that control this «synaptic plasticity» are poorly understood.

mThy1 - AS mice administered only control IgG1 suffered dendritic atrophy (as suggested by reduced staining with MAP2) and synaptic loss (evaluated with postsynaptic density - 95 (PSD - 95) and synaptophysin) across several regions of the brain, but this neurodegenerative damage was substantially prevented in mice administered 1H7, 5C1, or 9E4.

In order to analyze the function of individual proteins in neuronal circuits or synaptic remodeling, researchers combine the Cre and FLP recombinases to control both knockout of a target gene and expression of a separate gene.

The findings, reported in the Oct. 5 issue of Current Biology, define a gene expression program that controls the timing of synaptic remodeling.

We continue to focus our efforts on understanding the distinct roles of the various types of translational control in long - lasting synaptic plasticity and memory using pharmacological and genetic approaches in various brain regions, including the hippocampus, amygdala, and prefrontal cortex.

He also studies how dysregulated translational control contributes to altered synaptic function and aberrant behaviors in developmental brain disorders and neurodegenerative disease.

Discovered that the persistent sodium current, INaP, paradoxically amplifies afterhyperpolarizations and reduces the frequency (f / I) gain, and strongly modulates spike timing (Vervaeke et al., Neuron 2006); that Kv7 / M / KCNQ - type K + channels but not SK channels are essential for excitability control in hippocampal neurons (Gu et al., J Physiol, 2005); that Kv7 / M / KCNQ - type K + channels are essential for spatial learning and prevention of epilepsy (Nature Neuroscience 8: 51 - 60, 2005), that KCa1 / BK - type K + channels are essential for cerebellar learning and motor control (Proc Natl Acad Sci USA 101: 0474 - 8, 2004), the role of postsynaptic voltage-gated K + channels in regulation of synaptic plasticity (LTP) and integration (Proc Natl Acad Sci USA 99:10144, 2002); that Kv7 / M / KCNQ - type K + channels are essential for intrinsic theta resonance in hippocampal neurons (J Physiol 545:783, 2002).

Klann, E. and Richter, J.D. (2007) Translational control of synaptic plasticity and learning and memory.

In 2012, Haghighi's team published a paper showing synaptic homeostasis was controlled by an enzyme, the target of rapamycin (TOR), which plays a critical role in regulating lifespan in a wide range of organisms from yeast to mice.

YanGang Sun, Juan Pita - Almenar, Chia - Shan Wu, John J Renger, Victor N. Uebele, Hui - Chen Lu, Michael Beierlein (2013) «Biphasic cholinergic synaptic transmission controls action potential activity in thalamic reticular nucleus neurons», Journal of Neuroscience 33: 2048 - 59.

YanGang Sun, Chia - Shan Wu, Hui - Chen Lu, Michael Beierlein «Target - dependent control of synaptic inhibition by endocannabinoids in the thalamus» (2011), Journal of Neuroscience, 31:9222 - 30.

Notably, we have found that prolonged activation of these pathways results in altered translational control, which contributes to synaptic dysfunction and memory deficits in AD model mice.

Costa - Mattioli, M., Sonenberg, N., and Klann, E. (2008) Translational control mechanisms in synaptic plasticity and memory.

By default, twist - to - rotate is disabled; in order to activate it, you must open the Synaptics tab in the Mouse control panel, select Rotating, then press the gear icon to the right and enable TwistRotate.

If you don't have a precision touchpad in your PC, you'll have to use a manufacturer - provided tool like the Synaptic control panel available at Control Panel > Hardware and Sound > Mouse > Clickpad Secontrol panel available at Control Panel > Hardware and Sound > Mouse > Clickpad SeControl Panel > Hardware and Sound > Mouse > Clickpad Settings.

HP claim that Synaptics allow for more control over the different options their trackpads offers, but at the end of the day, Precision is just better.

If you already have, we recommend heading to Control Panel > Uninstall a Program and uninstalling the Synaptics or ELAN drivers that appear here.

After Windows 10 was installed, there was a new icon for the Synaptics TouchPad in the systray, which allowed full control.