We then hypothesized that deltaFosB might be regulating the production
of calbindin.»
«We found that seizures can increase the levels of deltaFosB in the hippocampus, which results in a decrease in the levels
of calbindin, a regulator of memory processes.
DeltaFosB has a relatively long half - life, therefore even when seizures are infrequent, deltaFosB remains in the hippocampus for weeks acting like a brake, reducing the production
of calbindin and other proteins, and disrupting the consequent brain activity involved in memory.
Not exact matches
The scientists found the same changes in deltaFosB and
calbindin levels in the hippocampus
of Alzheimer's disease patients and in the temporal lobe
of epilepsy patients.
«In fact, we found that when the levels
of deltaFosB increase, those
of other proteins, such as
calbindin, decrease.
And when researchers experimentally increased deltaFosB levels in normal mice,
calbindin expression was suppressed and the animals» memory deteriorated, demonstrating that deltaFosB and
calbindin are key regulators
of memory.
Calbindin also has been known for a long time to be involved in Alzheimer's disease and epilepsy, but its mechanism
of regulation was not known.
In layer 2, the density
of cartridges arising from a transcriptionally - unique subset
of chandelier cells containing
calbindin was nearly 3-fold higher in the schizophrenia group.
In contrast, there was no difference in the density
of chandelier cell cartridges lacking
calbindin in layer 2 or in either type
of cartridge across layers 3 - 6.
Aged mutant amyloid precursor protein mice with established disease showed a near complete restoration in levels
of synaptic and neuronal proteins after exposure to young blood in parabiosis (synaptophysin P =.02;
calbindin P =.02) or following intravenous plasma administration (synaptophysin P <.001;
calbindin P =.14).