«If you inhibit [endocytosis in the nerve terminal], then the vesicle recycling becomes slower and the supply of the vesicles is inhibited,» OIST Professor Tomoyuki Takahashi from the Cellular and
Molecular Synaptic Function Unit explains.
Not exact matches
In summary, we believe that this is a groundbreaking study that opens new lines of inquiry which will increase understanding of the
molecular details of
synaptic function in health and disease.»
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.
Homeostatic control of
synaptic function has been demonstrated in diverse organisms, including flies, rodents, and humans, yet the genes and
molecular mechanisms governing these processes remain unclear.
Published on April 20 in the journal
Molecular Psychiatry, this work reveals that the loss of
function of this gene involved in intellectual disability and autism, leads to
synaptic dysfunction.