The researchers measured 40 % more of the enzyme PDE4A5 in the brains of sleep - deprived mice than
in normal mouse brains.
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.
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.
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.
«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.
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.
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.
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 brai
In mice with A-T, the cerebellum appears
normal and they do not exhibit the obvious degeneration seen
in the human brai
in the human
brain.
The
brains of the
mice were smaller than
normal and had fewer neurons
in areas that controlled the affected behaviors.
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.
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.
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].
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.
In their experiments the researchers measured acidity in the endosomes of brain cells of normal mice and in mice with mutations in the NHE6 gen
In their experiments the researchers measured acidity
in the endosomes of brain cells of normal mice and in mice with mutations in the NHE6 gen
in the endosomes of
brain cells of
normal mice and
in mice with mutations in the NHE6 gen
in mice with mutations
in the NHE6 gen
in the NHE6 gene.
Because the SD of
brain progranulin
in wild - type
mice was about 10 % of the mean level, progranulin levels
in Grn + / −
mice would need to increase from 50 % of
normal to 80 % of
normal, i.e. by 30 % of the
normal value, to reach the lower limit of
normal.
The
brain cells of
normal mice seemed unaffected, suggesting the protein had stayed
in the blood.
But when they looked at the activity
in the bad NMDA channels, they found more
in HD
mouse brains than
normal mouse brains.
Glucose is the sole metabolic fuel used for nearly all
brain functions under
normal physiological conditions, but the
brain will metabolize ketone bodies for energy when access to glucose is limited, as would occur during water - only therapeutic fasting
in humans or during calorie restriction
in mice.
Following disruption of the
normal flora balance,
mice became less cautious, and changes
in the animals»
brain - derived neurotrophic factor — a protein associated with mood disorders — increased significantly.
The researchers also showed that regular feeding with the Lactobacillus strain caused changes
in the expression of receptors for the neurotransmitter GABA
in the
mouse brain, which is the first time that it has been demonstrated that potential probiotics have a direct effect on
brain chemistry
in normal situations.