In the nervous system, there is an internal mechanism that maintains its normal function, which scientists call homeostatic plasticity
However, how the steady-state plasticity of the nervous system is activated is still a mystery
On August 17, the team of Zhou Zikai, a researcher at the Shanghai Institute of Materia Medica , Chinese Academy of Sciences, and Zhengping Jia, a professor at the University of Toronto/Toronto Children’s Hospital in Canada , reported on Cell Reports on the neurotrophic factor NGPF2 and its related molecular mechanisms that drive neurohomeostasis plasticity.
Cell Reports, Chinese Academy of Sciences Chinese Academy of Sciences Closely related to diseases such as autism
Closely related to diseases such as autism Plasticity refers to the transformation of the nervous system into another structural or functional state due to the influence of internal or external factors
Taking a short eye-opening period in the growth process of animals as an example, Zhou Zikai introduced to the China Science Daily that during this period the eyes suddenly receive a large amount of light stimulation, and the synaptic transmission of the main neurons in the visual cortex will adapt accordingly.
However, homeostatic plasticity can sometimes be abnormal, causing abnormalities in mental, memory, or cognition
"A variety of genetic or environmental factors that cause neuropsychiatric diseases can cause them to be abnormal
In addition, studies have also found that neurohomeostasis plasticity may be an important pharmacological mechanism of psychotropic drugs
Zoom out
Start exploring mechanisms of synaptic scaling paradigm around to explore the mechanism starts around synaptic scaling paradigm explore the mechanism starts around synaptic scaling paradigm The role of neurohomeostasis plasticity is very significant, but the research on the molecular mechanism that promotes the active initiation of neurons has not yet made important progress
In the study of steady-state plasticity, synaptic scaling is the most commonly used experimental model
In the study, the researchers first used tetrodotoxin to block the action potential of the primary cortical neurons cultured in vitro, depriving the nerve activity; then, through technical improvements, they purified a very small amount of protein in the neuron culture medium, which contained neurons.
"Through neuroelectrophysiological recording, glutamatergic AMPA receptor membrane positioning and dendritic spine morphological analysis, it is found that both endogenous and recombinantly expressed NGPF2 protein can significantly promote synaptic transmission, dendritic spine maturation and other synaptic amplification Effect
At the downstream molecular mechanism level, further studies have found that under the above-mentioned neural inactivation conditions, NGPF2 is rapidly synthesized by the protein translation mechanism regulated by FMRP1 and secreted in large quantities to the periphery, thereby activating the receptor tyrosine kinase ALK (gradual lymphoma) Kinase), causing downstream LIMK-cofilin-mediated cytoskeleton reorganization to support the enhancement of synaptic transmission and maturation of dendritic spine, and finally manifested as the compensatory synaptic function enhancement caused by the deprivation of nerve activity, that is, synaptic amplification
It is worth mentioning that the expression and synthesis of other neurotrophic factors that have been reported are all positively correlated with the level of nerve activity
"In the follow-up, we will focus on neurological diseases with persistent nerve inactivation as the main pathological process, and study the use of recombinant NGPF2 protein as a biotechnology drug for the treatment of such diseases
.
" Zhou Zikai said
.
(Source: Qin Zhiwei, China Science News)
Related paper information: https://doi.
org/10.
1016/j.
celrep.
2021.
109515
https://doi.
org/10.
1016/j.
celrep.
2021.
109515
This article is an English version of an article which is originally in the Chinese language on echemi.com and is provided for information purposes only.
This website makes no representation or warranty of any kind, either expressed or implied, as to the accuracy, completeness ownership or reliability of
the article or any translations thereof. If you have any concerns or complaints relating to the article, please send an email, providing a detailed
description of the concern or complaint, to
service@echemi.com. A staff member will contact you within 5 working days. Once verified, infringing content
will be removed immediately.