Sentences with phrase «normal mouse brains»

But when they looked at the activity in the bad NMDA channels, they found more in HD mouse brains than normal mouse brains.
The researchers measured 40 % more of the enzyme PDE4A5 in the brains of sleep - deprived mice than in normal mouse brains.
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.

Not exact matches

These mice performed better than their normal counterparts on learning tests well into old age, and their brains did not exhibit the decline in neurogenesis typically seen in aged mice.
The behavioral tests used here modeled one dimension of the disease — an inability to experience pleasure from normal activities — but not others, such as stress and anxiety, and probably tap into different brain mechanisms in mice than in humans, he says.
«Mice that don't have these molecules seem to be able to change their brain circuits with experience much more rapidly than normal mice,» Shatz sMice that don't have these molecules seem to be able to change their brain circuits with experience much more rapidly than normal mice,» Shatz smice,» Shatz says.
When they next measured responses in the auditory regions of the brain, a more sensitive test, the mice responded to much quieter sounds: 19 of 25 mice heard sounds quieter than 80 decibels, and a few could heard sounds as soft as 25 - 30 decibels, like normal mice.
The researchers discovered that in brain regions involved in regulating anxiety — the amygdala and prefrontal cortex — microbe - free mice had an overabundance of some types of microRNA and a shortage of others compared with normal mice.
Alzheimer's mice with normal BACE1 levels experienced a steady increase in plaques, clearly seen in samples of their brains.
But the customary setup in such experiments — fiber - optic cables implanted in the brain and a heavy helmet linked to a laser — is invasive and cumbersome for mice, the usual subjects, severely hampering researchers» ability to observe normal activity and social behavior.
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.
If one eye is deprived of sight, they rapidly rewire their brains to compensate, then beat normal one - eyed mice on tests of visual acuity.
To investigate the longer - term effects of higher - than - normal acetylcholine levels on the brain, Hermona Soreq of the Hebrew University of Jerusalem and her colleagues first induced high levels of acetylcholine by forcing 26 mice to swim, an activity stressful to mice.
The normal mice's brain plaques seemed to be built from human A-beta protein, and the only source of that was the blood of the mutated partner mouse.
But these plaques were also inside the brains of the normal mice in the joined pairs.
He and colleagues at the University of California, San Francisco, injected the brains of mice with prions they had created in the lab by misfolding normal prion protein, known as PrP.
Removing a single gene from the brains of mice and zebrafish causes these animals to become more anxious than normal.
The brains of mice genetically modified to lack normal prion proteins had significantly higher beta - amyloid levels.
«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.
Post mortems showed that brain connections lost in the untreated mice remained healthy, and completely normal protein production had resumed in the treated animals, even though the prions continued to accumulate.
Song says the amyloid - beta traveled from the genetically - modified mice to the brains of their normal partners, where it accumulated and began to inflict damage.
Not only did the normal mice develop plaques, but also a pathology similar to «tangles» — twisted protein strands that form inside brain cells, disrupting their function and eventually killing them from the inside - out.
As a final test to see whether parasites could directly access the brain from the blood, the researchers infected mice with a mixture of normal parasites and mutants that was unable to reproduce, each labeled in different colors.
To understand how DIXDC1 mutations put normal brain function at risk, Cheyette's team turned to mutant mice that lacked a functioning copy of the gene.
The researchers were surprised to find that the brains of mice lacking the BAI1 gene looked normal anatomically.
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.
The investigators reached this conclusion by comparing the integrity and development of the blood - brain barrier between two groups of mice: the first group was raised in an environment where they were exposed to normal bacteria, and the second (called germ - free mice) was kept in a sterile environment without any bacteria.
With thoughts of a jolt fresh in their brain, mice with normal levels of α - CaMKII froze up when they returned to the chamber an hour later, while mice with boosted levels remained calm.
As the mice developed, Verma's team found that the rodents» brains were only a third of their normal size, with particularly striking reductions in brain areas involved in learning and memory.
The drug restored in the mice normal levels of serotonin, a neurotransmitter communicating messages between nerve cells in the brain.
In mice with A-T, the cerebellum appears normal and they do not exhibit the obvious degeneration seen in the human brain.
At the same time, the rodents had an even greater response to social defeat stress than normal mice do, suggesting their brains also are more susceptible to a depressive - like state.
The brains of the mice were smaller than normal and had fewer neurons in areas that controlled the affected behaviors.
But he adds that the study does not show that human astrocytes are genetically normal when engrafted into the mouse brain, and it does not rule out the idea that the improved learning and memory «could be due to the persisting progenitor cells.»
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.
Indeed, those mice in Schwarzchild's study that were pretreated with caffeine retained near - normal dopamine levels when exposed to a chemical known to induce Parkinson's - like symptoms by decreasing brain dopamine.
In normal mice, ginkgo halved the volume of brain tissue injured after a stroke, but it had little effect on mutant mice that lacked heme oxygenase.
Treatment of the mice with insulin, either by normal injection or injection into the fluid surrounding the brain, reversed the process.
Using a new class of mathematical models that do not make many assumptions about how behavior is organized, we will deconstruct the mouse's normal behavior into motifs, or syllables, and correlate those with brain activity.
They observed a significant decrease in the number of proliferating stem cells in the brains of HIV / gp120 - mice compared with similar tissue from normal, wild - type mice.
Finally, we generate new tools and mouse models to study the role of de novo protein synthesis in normal brain function and in pathophysiology associated with neurodevelopmental and neurodegenerative disease.
Mice with a single missing gene have brains that are 35 percent larger than normal, a new study found.
J147 increases the levels of BDNF in the hippocampus of normal rats, as well as in huAPP / PS1 transgenic mice [7], and its synthetic precursor, CNB - 001, increases BDNF levels in rat traumatic brain injury models [54].
«But the close link between neuronal stimulation and DSBs, and the finding that these DSBs were repaired after the mice returned to their home environment, suggest that DSBs are an integral part of normal brain activity.
When these mice were housed in chambers that contained normal air containing 21 percent oxygen, the equivalent of what a person would breathe at sea level, they developed brain lesions and had a median survival length of 58 days.
Mice lacking normal cilia in parts of their brain that were important for memory had trouble remembering a painful shock.
This early hint that age - related changes in EP2 action in microglia might be promoting some of the neuropathological features implicated in Alzheimer's was borne out in subsequent experiments for which Andreasson's team used mice genetically predisposed to get the mouse equivalent of Alzheimer's, as well as otherwise normal mice into whose brains the scientists injected either A-beta or a control solution.
In addition to the normal tools of the cell biologist's trade, Simona's lab uses intravital imaging to peer into the brains of mice.
The researchers looked at the dentate gyrus, a specific area of the brain that is critical to memory and particularly vulnerable in Alzheimer's disease, and compared the genes that were turned on and off in normal mice and a mouse model of Alzheimer's disease.
Compared to the brains of normal mice, those with microbe - free guts had more of some types of microRNAs and fewer of others.
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