Recently, a group of researchers from the Nara Institute of Science and Technology, in Japan, have made an important discovery in reference to memory and learning in the human being. It is a study with international significance.
Specifically, these researchers have found the missing link behind memory and learning by discovering that the structural plasticity of dendritic spines requires of the coupling of cell adhesion molecules and polymerizing actin by shootin1a.
This discovery suggests that alterations in this coupling may be a causative factor in numerous neurological disorders, such as Alzheimer's disease or autism spectrum disorders.
In addition, these findings also constitute a new way to identify novel pharmacological targets for this type of disorders that affect memory and cognitive function.
Key finding about learning and memory
The researchers, authors of this study, explain that in neurons, changes in the size of dendritic spines are a key mechanism in learning and memory . However, at present the specific way in which these types of structural changes originate is still unknown.
Thus, in this study, whose results have been published in the second half of the year 2021, the Researchers reveal that the union of cell adhesion molecules with actin is essential in this process of structural plasticity.
In this regard, the author Naoyuki Inagaki, explains that “current models of structural plasticity in dendritic spines do not take mechanical force into account. We had already identified the role of shootin1a, a protein involved in neuronal development, in the growth of axons, so we wanted to investigate whether this protein could also play a role in the structural plasticity of dendritic spines ».
Thus, to analyze this aspect, the researchers used neurons from control rodents and from rodents with shootin1a knockout in order to observe if this was also involved in the formation dendritic spines that affect memory and learning.
Regarding this analysis, Professor Inagaki points out that «we discovered that shootin1a mechanically linked the polymerizing actin with the cell adhesion molecules in the dendritic spines, and we revealed that the synaptic activity enhanced this coupling, thus allowing the actin will push against the membranes and enlarge the spines. ”
The interesting thing about this story is that the results of this research work are the first to relate mechanical force with the elasticity of dendritic spines dependent on synaptic activity. Therefore, it provides new knowledge regarding the mechanisms of structural plasticity in these spines.
Ultimately, these findings suggest that alteration of shootin1a can lead to the development of neurological disorders. Thus, it is expected that new studies focused on the mechanism of structural plasticity in dendritic spines may offer new therapeutic targets for disorders that affect learning and memory.