Sentences with phrase «in normal neurons»

«It appears that in normal neurons, caspase - 2 and RhoA form an inactive complex outside the dendritic spines,» said Dr. Lefort.

There are several reasons why nobody before Shatz had found genes coding for MHCI in normal neurons.

Not exact matches

And, perhaps most strikingly, a team at a gaggle of New York research institutions published a paper showing how they'd used hPSCs to cook up — in just days, rather than several months — cortical neurons (critical central nervous system cells) that had normal electrophysiological signaling properties.

In animal models, exposure to cigarette smoke or nicotine during fetal development alters the expression of the nicotinic acetylcholine receptor in areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDIn animal models, exposure to cigarette smoke or nicotine during fetal development alters the expression of the nicotinic acetylcholine receptor in areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDIn human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDS.

Reporting in The Journal of Neuroscience, they showed that neurons of the mouse forebrain depend heavily on NAD in normal cognitive function.

«To our surprise, the neurons were normal,» said Vatine, a postdoctoral scientist in Svendsen's laboratory and first author of the study.

His lab differentiates iPSCs from autistic patients into neurons and glial cells, which they suspect may be releasing cytokines at levels higher than normal in autistic patients.

Under a microscope these are the very regions that accumulate tangled clumps of tau, a normal protein found mostly in neurons.

The extent of proteasome accumulation was such that the ability of the remaining proteasomes within the neuron to perform their normal housekeeping functions was likely to be impaired, potentially explaining the neuronal pathologies observed in ALS.

During normal brain development in the first weeks of life, precursor cells in the SVZ in the piglets give birth to neurons that migrate primarily to the prefrontal cortex, the team reports today in Science Translational Medicine.

By examining the brains of these mice, the researchers observed a substantial decrease in inhibitory CA2 neurons, as compared to a control group of normal, healthy mice — a change remarkably similar to that previously observed in postmortem examinations of people with schizophrenia.

In a study published October 30 in Neuron, the scientists show that mice genetically altered so they don't produce serotonin didn't scratch as much as normal mice when exposed to irritantIn a study published October 30 in Neuron, the scientists show that mice genetically altered so they don't produce serotonin didn't scratch as much as normal mice when exposed to irritantin Neuron, the scientists show that mice genetically altered so they don't produce serotonin didn't scratch as much as normal mice when exposed to irritants.

Normal patterns of brain firing are seemingly chaotic, but during a seizure, neurons synchronize and fire convulsively in parallel.

IBM developed a technique for making carbon nanotubes emit light, paving the way for new fiber optics; Harvard scientists figured out how to deposit tiny wires on glass or plastic, opening the door for the development of supercheap computers; and at the University of Central Florida, neuroscientist Beverly Rzigalinski discovered a nanomolecular fountain of youth effect: When Rzigalinski applied cerium oxide nanoparticles to rat neurons in a petri dish, the particles seemed to strip out the free radicals that make tissues age and kept the neurons alive and functioning up to six times their normal life span.

The researchers found that mutant mice lacking Del - 1 had more severe attacks of the EAE than normal mice, with more damage to myelin, the fatty sheath that coats neurons and helps in the transmission of signals along the cell.

Stress - susceptible animals that behaved as if they were depressed or anxious were restored to relatively normal behavior by tweaking the system, according to a study appearing in the July 20 issue of Neuron.

To solve this problem, the authors developed a genetic system to generate small patches of neurons lacking dati in an otherwise normal brain.

«It was particularly exciting to see plasticity in the neurons impaired by mHTT,» said Davidson, noting that in the HD mice, brain areas that had begun to atrophy recovered volume and permitted better motor function after the researchers restored mTORC1 activity to more normal levels.

The investigators are now looking for approaches that might turn the «volume» back down to normal levels in the peripheral sensory neurons, including both genetic and pharmaceutical approaches.

The authors suggest that the intricate balance between the signaling of neurons in these three brain regions may be crucial for normal social behavior in humans, and that disruption may contribute to various psychiatric conditions, including autistic spectrum disorders.

In the study, scientists examined basal forebrain cholinergic neurons to try to understand why they are damaged early and are among the first to die in normal aging and in Alzheimer'In the study, scientists examined basal forebrain cholinergic neurons to try to understand why they are damaged early and are among the first to die in normal aging and in Alzheimer'in normal aging and in Alzheimer'in Alzheimer's.

«Yifan's thesis research, however, found that TIA - 1 does not influence COX - 2 expression in neurons, nor play a role in seizure control in the normal brain.»

When the mice died at 31 weeks, their brains had 20 % fewer neurons than normal mouse brains in regions that Huntington's strikes in people.

We'll assume that each model is valid for all neurons of that type in all normal brain, much as we assume that all resistors behave the same way in any electronic device.

Furthermore, we assumed above that all neurons of one type behave in the same way in all normal brains, just as all polar bears hunt seals under normal circumstances.

The study supports the importance of the serotonin which is specified and maintained by a specific gene, the Pet - 1 gene — for normal functioning of the neurons, synapses and networks in the cortex, as well as proper development of brain circuitry.

The result: In the planning phase of the movement, the activity of most neurons did not differ between the normal and the reversed - view hand movement.

More broadly, the research suggests a new framework for exploring how the mutated proteins interfere with normal processes for neuron survival in other neurodegenerative diseases.

The serums of some patients with subacute spongiform encephalopathies contain an autoantibody in higher titer against a normal fibrillar protein within the axon of mature central neurons in culture.

Normal mice with p16 had fewer neural stem cells in one part of the brain and fewer new neurons in the olfactory bulb, again demonstrating p16's ability to inhibit regeneration.

Chen and colleagues report online today in Science that mice without GRPR neurons scratched significantly less than normal mice did — about 80 % less in each case.

«When we stimulated D1 neurons in normal mice, we did not improve their timing»» he adds.

Last November he reported the first results: On average, autistic brains had many more neurons in some regions than normal brains.

«We hope that in the future, by fully understanding how this gene affects signaling in the brain, we may be able to identify drugs to restore the normal signaling balance in neurons and improve cognitive and social function in patients,» says lead author Dr. M. Chiara Manzini.

In normal German cockroaches, glucose elicits activity in sugar gustatory receptor neurons, which react when exposed to sugars like glucose and fructose — components of corn syrup, a common roach - bait ingredienIn normal German cockroaches, glucose elicits activity in sugar gustatory receptor neurons, which react when exposed to sugars like glucose and fructose — components of corn syrup, a common roach - bait ingredienin sugar gustatory receptor neurons, which react when exposed to sugars like glucose and fructose — components of corn syrup, a common roach - bait ingredient.

Working with the brains of six normal children and seven autistic children ages 2 to 16, most of whom died of drowning, Courchesne has studied neurons under the microscope and even counted the number of neural cells in different tissue samples.

In normal mice, these neurons — a subset of nerve cells that release the neurotransmitter gamma - amino butyric acid (GABA), and so are called GABAergic neurons — are most active during waking periods when the mice are eating or grooming, two highly pleasurable activities.

So normal movement requires that CPG neurons in the spinal cord connect to and control when motor neurons fire.

Working with Bhaduri, who has a background in statistics and bioinformatics, Pollen and Nowakowski began exploring how specific classes of neurons and stem cells in the developing brain contribute to normal brain growth as well as to neurodevelopmental disease, and have begun to build a comprehensive, open - source atlas of gene expression across the developing brain, which they hope will serve as a resource for other scientists.

«Following on the work of TSRI Professor Ardem Patapoutian, who has identified many of the genes that endow these neurons with selective responses to temperature, pain and pressure, we have found a way to produce induced sensory neurons from humans where these genes can be expressed in their «normal» cellular environment,» said Associate Professor Kristin K. Baldwin, an investigator in TSRI's Dorris Neuroscience Center.

Molecular profiling of PI cells identified the fly version of DH44 as a circadian molecule that is specifically expressed by PI neurons and required for normal rest / activity rhythms in flies.

These results collectively suggest that neural stem cells need MSI1 to generate enough neurons for normal brain size, but the presence of MSI1 also increases the vulnerability of these cells to Zika infection, leading to the death of the population which ultimately results in microcephaly.

The brains of the mice were smaller than normal and had fewer neurons in areas that controlled the affected behaviors.

The cells with the normal gene grew significantly longer dendrites — the portions of the cell that reach out to receive nerve impulses — than did neurons with the mutated gene, the team reports 14 October in Science.

To see what was happening in the brains of these ankyrin - G mutant mice, the researchers analyzed the cell components in inhibitory synapses connecting with pyramidal neurons, finding that two proteins known as GAT1 and GAD67 — responsible for making the neurochemical GABA that dials back nerve impulses — were at much lower levels in the synapses on pyramidal neurons in ankyrin - G mutant mice than in normal mice.

In a normal brain, the neurons of the central thalamus crackle with electrical activity when we struggle to pay attention to the world around us, and they accelerate their action as we emerge from sleep.

«We hypothesized that toxins would change the typical way microtubules are chemically modified in neurons and that a drug like tubacin could restore those modifications to normal, thereby treating the disease.»

«Within 3 weeks after expression of the NeuroD1 protein, we saw in the microscope that human glial cells were reinventing themselves: they changed their shape from flat sheet - like glial cells into normal - looking neurons with axon and dendritic branches,» Chen said.

In the new study, the researchers said the converted motor neurons compared favorably to normal mouse motor neurons, in terms of the genes that are turned on and off and how they functioIn the new study, the researchers said the converted motor neurons compared favorably to normal mouse motor neurons, in terms of the genes that are turned on and off and how they functioin terms of the genes that are turned on and off and how they function.

A region of the gene that produces the PACAP38 protein has held nearly constant, even in humans, presumably because the protein plays diverse roles in neuron communication and is essential for normal development of the cerebellum, affecting brain cell migration, for example.