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.
Researchers led by Emory University pathologist Andrew Gewirtz found that mice genetically deficient in an immune system receptor have altered gut bacteria, eat more
than normal mice do, and develop features of metabolic syndrome.
The NK1R - deficient mice consumed far less alcohol — especially later in the trial when alcohol concentration was higher —
than the normal mice did.
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.
The quest for better opioids got a much - needed jolt in 1999, when researchers at Duke University showed that mice lacking a protein called beta - arrestin 2 got more pain relief from morphine
than normal mice did.
Gordon and his team found several years ago that genetically obese mice (the animals lacked the ability to make leptin, a hormone that limits appetite) had 50 percent fewer Bacteroidetes bacteria and 50 percent more Firmicutes bacteria
than normal mice did.
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.
Normal mice saw benefits, too: Muscles and pancreas cells healed better in middle - aged
mice that got rejuvenation treatments
than in
mice that
did not.
«
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.
In general, the mutant
mice also had much thicker skin
than the
normal animals
did.
In subsequent tests, the
mice with the mutation
did a worse job
than normal mice at learning new motor skills.
Furthermore, more
than 75 % of
mice infected with virus bearing the
normal protein developed severe corneal autoimmune disease, whereas fewer
than 20 % of
mice infected with mutant virus
did, and their symptoms were barely detectable.
The
mice appear younger and more robust
than comparably - aged
normal mice, have better muscle tone, and
do not develop age - related tumors.
When they exposed these
mice to the cold, the animals developed far fewer beige fat cells
than did normal animals, suggesting that macrophages were key to browning of white fat.
At 14 months, however, the J20 / caspase -2 null
mice did significantly better in the water maze test
than the J20
mice and similarly to the
normal mice.
Normal mice produced more
than four times more melanocytes
than did the p53 «knockout»
mice.
He notes, however, that other attempts to stimulate bone growth in
mice by manipulating cell signaling proteins have produced denser
than normal bones — and he's surprised that Helms's team didn't see the same.
Although muscle cells
did not reduce in size or number in
mice lacking a protective antioxidant protein, they were weaker
than normal muscle cells, researchers from the Barshop Institute for Longevity and Aging Studies at The University of Texas Health Science Center San Antonio found.
Results showed the first two groups didn't develop PCOS, unlike the
mice in the control group, whereas the test subjects with ovary ARs still contracted the disease, albeit at a lower rate
than the
normal mice.
Over an eight - week period, a control group of
mice fed a high - fat diet predictably became obese, but the
mice whose Hedgehog pathway had been activated didn't gain any more weight
than another control group fed on a
normal diet.
Remarkably, outcomes following loss of the switch mirrored what the group had previously observed when they physically removed the gene itself: the lungs of mutant
mice contained many more melanoma cells
than did lungs of
normal mice.