Can Light Treat Mental Disorders?
The history of mental health in our society is shaking: from mental asylums and marginalizing the mentally ill to the de-stigmatization of mental disorders, we have socially come a long way. In the medical world of mental disorders, we have made progress with treatment spanning from different forms of therapy to psychiatric drugs such as Lorazapem or Adderall. As brain pathology becomes more researched, more and more medical advancements occur in the scope of mental health treatment. The basis of all treatments, though, target an area of the brain - clinically or therapeutically - in an effort to lessen or diminish the symptoms experienced by the mentally ill. In recent studies, the technique of optogenetics has been used with the same intent.
Optogenetics research is a fairly new process a little over a decade old. The process involves introducing genes with light-sensitive proteins into a specific neuronal target of interest in an organism's brain and manipulating their activation using light that is usually blue. Without a doubt, introducing this new technique in neuroscience significantly changed the way research was performed. In a neuroscience seminar at Loyola University of Chicago, Dr. Stephan Steidl, a professor and researcher, presented about his use of optogenetics in studying appetitively motivated behavior and the dopaminergic reward pathway in rats. He hopes to "contribute to defining critical cell groups that communicate with other parts of reward circuitry" using the method of optogenetics (Steidl, 2017). Dr. Steidl's research provides significant information for the mental disorder of substance addiction and dependence. In addition, Steidl stated that before the method of optogenetics, neuroscience researchers would approach a study in this scope with lesions or electrical stimulation, which would risk excitation of outputs of not only the target area, but other areas too.
Using the same technique, Dr. Karl Deisseroth, a professor of bioengineering and psychiatry at Stanford University in California, attempted to manipulate the social behavior in a mouse model of autism. Autism's prevalence in the United States is striking, with "approximately 1 in 68 children" being identified with an Autism Spectrum Disorder ("How Common"). With this in mind, any sort of research in the scope of autism is progressive. In 2011, Dr. Deisseroth's team targeting a set of excitatory neurons in the prefrontal cortex, a region involved in social behavior. By activating these neurons, the findings showed that mice "lost interest in interacting with other mice" (Zeliadt). In the newest study that was conducted, Dr. Deisseroth's team used mice which lacked both copies of the CNTNAP2 gene that is linked in autism. These mice show typical characteristics of autism - hyperactivity and lack of interest in social interaction.
So how exactly did they use optogenetics to control autism symptoms?
The team's goal was to investigate whether acutely reducing excitation to inhibition balance could "correct" the loss of social interaction experienced by many of the autism phenotype. Researchers inserted an opsin into interneurons, flashed blue light, and placed another mouse, unfamiliar to the subject, in the same cage. Based on the observations, the team found that instead of intentionally avoiding social interaction with the new mouse, they willingly approached it and displayed the same social behavior as a control mouse without autism did. The tangible results of the study conclude that "acute and reversible reduction in cellular excitation to inhibition balance in the mPFC region of adult mouse brain, either by increasing PV neuron excitability or reducing PYR neuron excitability, rescued social behavior deficits in the CNTNAP2 knockout autism-like mouse model" (Selimbeyoglu).
Although the use of optogenetics in humans is far fetched, published research has been exposing ways that the technique benefits mental disorders that are traditionally treated clinically or therapeutically.
The concept of light seems rudimentary and we often take for granted how the discovery of light has shaped our day to day lives. However, light, in all its complexity, has become the foundation of an expansive and useful neuroscience technique -- optogenetics.
Using the same technique, Dr. Karl Deisseroth, a professor of bioengineering and psychiatry at Stanford University in California, attempted to manipulate the social behavior in a mouse model of autism. Autism's prevalence in the United States is striking, with "approximately 1 in 68 children" being identified with an Autism Spectrum Disorder ("How Common"). With this in mind, any sort of research in the scope of autism is progressive. In 2011, Dr. Deisseroth's team targeting a set of excitatory neurons in the prefrontal cortex, a region involved in social behavior. By activating these neurons, the findings showed that mice "lost interest in interacting with other mice" (Zeliadt). In the newest study that was conducted, Dr. Deisseroth's team used mice which lacked both copies of the CNTNAP2 gene that is linked in autism. These mice show typical characteristics of autism - hyperactivity and lack of interest in social interaction.
So how exactly did they use optogenetics to control autism symptoms?
The team's goal was to investigate whether acutely reducing excitation to inhibition balance could "correct" the loss of social interaction experienced by many of the autism phenotype. Researchers inserted an opsin into interneurons, flashed blue light, and placed another mouse, unfamiliar to the subject, in the same cage. Based on the observations, the team found that instead of intentionally avoiding social interaction with the new mouse, they willingly approached it and displayed the same social behavior as a control mouse without autism did. The tangible results of the study conclude that "acute and reversible reduction in cellular excitation to inhibition balance in the mPFC region of adult mouse brain, either by increasing PV neuron excitability or reducing PYR neuron excitability, rescued social behavior deficits in the CNTNAP2 knockout autism-like mouse model" (Selimbeyoglu).
Although the use of optogenetics in humans is far fetched, published research has been exposing ways that the technique benefits mental disorders that are traditionally treated clinically or therapeutically.
The concept of light seems rudimentary and we often take for granted how the discovery of light has shaped our day to day lives. However, light, in all its complexity, has become the foundation of an expansive and useful neuroscience technique -- optogenetics.
“How Common is Autism?” Autism Science Foundation, Autism Science Foundation, autismsciencefoundation.org/what-is-autism/how-common-is-autism/.
(image). http://optogenetics.weebly.com/uploads/6/6/7/1/6671814/109682706.jpg?602
Selimbeyoglu, Aslihan, et al. Modulation of prefrontal cortex excitation/inhibition balance rescues social behavior in CNTNAP2-deficient mice “Http://Ljournal.ru/Wp-Content/Uploads/2016/08/d-2016-154.Pdf.” Science Translational Medicine, vol. 9, no. 401, 2 Aug. 2017, doi:10.18411/d-2016-154.
Steidl, Stephen. Neuroscience Seminar, Loyola University of Chicago. 2017
No comments:
Post a Comment