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 s
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 s
mice,» 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.