In ARHGAP33 KO mice, TrkB is not sufficiently transported to synaptic sites due to the lack of ARHGAP33, which eventually leads to
impaired synaptic functions and behaviors.
Then, the research group examined the molecular mechanism behind
the impaired synaptic functions and behaviors in ARHGAP33 KO mice and found that ARHGAP33 is localized to the Golgi apparatus to regulate intracellular protein trafficking of the Tropomyosin receptor kinase B (TrkB) receptor, a neurotrophin receptor, to synaptic sites.
Not exact matches
In October researchers at Columbia University reported that young mice predisposed to acquiring Alzheimer's accumulate protein clusters in
synaptic mitochondria and that these clusters directly
impair synapse
function.
The research group showed that a molecule, ARHGAP33 regulates
synaptic functions and behaviors via intracellular protein trafficking and that the lack of ARHGAP33 causes neuropsychiatric disorder - related
impaired higher brain
functions.
Maternal alcohol consumption prior to and during pregnancy significantly affects cognitive
functions in offspring, which may be related to changes in cyclin - dependent kinase 5 because it is associated with modulation of
synaptic plasticity and
impaired learning and memory.
One final example is the prefrontal cortex, which is thought to play an important role in regulating behavior by suppressing impulses and emotions arising from the amygdala and other parts of the limbic system.50 — 52 In animal studies, exposure to chronic stress or glucocorticoids alters the
synaptic connectivity within the prefrontal cortex, 52,53 and this may limit the ability of the prefrontal cortex to (1) suppress the impulsivity and aggression of the limbic system, and (2) execute adaptive responses (rather than maladaptive responses) to stress.54 — 56 Stress - induced changes in brain structure parallel the well - described impact of significant childhood adversity on a variety of brain
functions, including the modulation of physiologic responses (hyper - responsive or chronically active stress response), learning (
impaired memory), and the regulation of behavior (the ability to execute adaptive vs maladaptive responses to stress).3, 39,57