Introduction/Background

In an article published in the Journal of Neuroscience in 2017, Caitlin R. Siu and associates primarily focused on the development of glutamatergic proteins within the human visual cortex across a lifespan. The study looked at how five specific glutamate proteins (PSD-95, GluN1, GluN2A, GluN2B, and GluA2) influenced visual plasticity and processing, and how they regulate receptive field properties, amongst other things (Siu et al, 2017). 

The human visual cortex, also called the striate cortex or V1, is the area of the brain that is responsible for processing visual information and relaying it to the extrastriate cortex. The visual cortex (V1) is part of the cerebral cortex and lies in the occipital lobe on both hemispheres. It extends into calcarine sulcus, and as a result of this only a small portion can be visualized from the surface of the cerebral cortex (Dingman, 2016; Huff, Mahabadi, & Tadi, 2020). The visual cortex has six distinct layers, the first being the outermost or surface layer, which were introduced by Brodmann (Schmolesky, 2007). The first layer is comprised of mainly inhibitory neurons, about 80%, but only around 20% of each of the remaining 5 layers is made up of inhibitory neurons. The remainder of the cells are excitatory neurons, such as spiny pyramidal and spiny stellate cells (Schmolesky, 2007).

Because the main focus on the development of five specific proteins within this specific area of the brain, the study was conducted using tissue samples from the human visual cortex of thirty individuals between 20 days after birth and 80 years of age. The tissues were postmortem and obtained from the Brain and Tissue Bank for Developmental Disorders in the University of Baltimore in Baltimore, Maryland (Siu et al, 2017). All of the tissues samples were from individuals with no family history of neurological or brain disorders and had little very trauma as a result of the cause of death. The samples consisted of the superior and inferior portions if the calcarine fissure and were taken from the left hemisphere (Siu et al, 2017).

Methods and Results 

To determine which of the proteins were abundant during which period in life, a series of different techniques and methods were used to quantify the target proteins. These techniques and methods included synaptosome preparation to enrich synaptic proteins, Western blot analysis, BCA assay, immunoblotting, band analysis and manipulation of the band image. Once that was completed, curve-fitting and statistical analyses were used to visual the results with scatter plots (for changes in expression across the lifespan), and model-fitting approach using the best curve-fit (for determining the trajectory of those changes) (Siu et al, 2017). Because the proteins in question were being looked at across a lifespan, the sample were separated based on the age of the individual.

-Age groups: Neonates (<0.3 years), Infants (0.3-1 years), Young Children (1-4 years), Older Children (5-11 years), Teens (12-20 years), Young Adults (21-55 years), and Older Adults (>55 years).

The Western blotting technique used on the samples was to quantify the proteins so they could be tracked throughout the lifetime as the V1 matured (Siu et al, 2017). The development of the proteins occurred in five stages. The first stage, stage 1 (neonates and infants), had high expression of GluN1 until the 1-year mark. The GluN2B protein also had a relatively high expression, showing that this stage was responsible for the establishment of excitatory synapses and plasticity within the V1 (Siu et al, 2017). The second stage (young children), there were increases in GluA2, PSD-95, and GluN2A but the data couldn’t be used to distinguish between if the proteins increasing in waves reflect interindividual variability or intraindividual variability in children (Siu et al, 2017). Stage three (older children) was the closure of the critical period with peaks in GluN2B, PSD-95, and GluA2. The end of the critical period signal could the start of ocular dominance plasticity (Huang et al, 2015), and this stage also marks the end of children being susceptible to developing amblyopia (Siu et al, 2017; Lewis & Maurer, 2005). In the fourth stage (teens and young adults), there was a peak expression of GluN2A around 40 years of age. The peak is thought to occur late so the synaptic modification threshold could be adjusted, reflecting synaptic stability. The final stage, stage five (older adults), showed a decrease in all of the proteins and degeneration of the V1 (Siu et al, 2017).

Conclusion

The study showed that while the physical/anatomical structure of the primary visual cortex developed and mature early on in life (Burkhalter, 1993), vision matured much slowly with changes throughout childhood, adolescence, and straight through to adulthood (Owsley, 2011). The maturation of vision was aided by the expression of glutamatergic proteins in different stages. The proteins had been determined to individually peak at different stages to coincide with changes to visual perception, aid in the visual development and processing, and in the plasticity of the primary visual cortex (Siu et al, 2017) before falling off due to age-related degeneration. 

[+] References

[+] Other Work By Abigail Bondurant