Congratulations, Hari, from the entire Frist Center Family. We are excited to see the results of your research!
FCAI Neurodiversity Inspired Science and Engineering Fellow Hari Srinivasan has been awarded the 2024 Autistic and Neurodivergent Scholars Working for Equity in Research (ANSWER) Scholars Program Award for his project “Navigating the Near: Virtual Reality Investigations of Peripersonal Space in Autism.” Srinivasan will receive a $10,000 award next academic year to work toward this research.
Hari’s continued outstanding achievements never fail to impress us! Congratulations, Hari, from the entire Frist Center Family. We are excited to see the results of your research!
Backyard Visitors
A deer family (mom and 2 baby deer) frequenting our backyard this summer. The young deer frolicking, chasing each other and running around is a delight to watch.
Here is a children's short story I wrote sometime ago.
Poster at CAN 2024
Yeah, I have another Poster Acceptance for the College Autism Network Summit 2024 in Oct.
================From: College Autism Network
Sent: Tuesday, July 16, 2024 2:41 PM
To: Srinivasan, Hari
Subject: College Autism Summit Submission Accepted - Poster
Dear Poster Participant:
We are pleased to inform you that your College Autism Summit submission titled 'Navigating the Near: Virtual Reality Investigations of Peripersonal Space in Autism' has been accepted.
………..
Best,
Amy Radochonski and Cherie Fishbaugh, Program Co-Chairs
Exploring Short-Term Synaptic Plasticity and Its Implications in Autism
Short-term synaptic plasticity, a temporary change in synaptic strength lasting from seconds to minutes, is a crucial mechanism for neural communication and information processing. Two key types of short-term plasticity are paired pulse facilitation (PPF) and paired pulse depression (PPD). Understanding these mechanisms can provide insight into the molecular & genetic underpinnings of autism.
Paired Pulse Facilitation (PPF) occurs when two signals (pulses) arrive in quick succession at a synapse, with the second pulse producing a stronger response than the first. This is due to residual calcium (Ca2+) remaining in the presynaptic terminal after the first pulse, which enhances neurotransmitter release upon the arrival of the second pulse. This phenomenon is particularly significant at synapses with low initial release probability, ensuring that enough neurotransmitters are available for subsequent release.
Paired Pulse Depression (PPD), on the other hand, is characterized by a diminished response to the second pulse. This occurs at synapses with high initial release probability, where the first pulse depletes the readily releasable pool of neurotransmitters, leaving insufficient resources for the second pulse. The timing between the pulses is critical; if the interval is too long, Ca2+ dissipates, and vesicles are replenished, mitigating these effects.
In the context of autism, alterations in short-term plasticity have been linked to the disorder's characteristic neural and behavioral features. Research has shown that mutations in synaptic genes such as SYN1 and SYN2, which regulate synaptic vesicle dynamics, can disrupt short-term plasticity. These mutations result in increased PPF at excitatory synapses and enhanced synaptic depression at inhibitory synapses, leading to an excitatory/inhibitory (E/I) imbalance that contributes to network hyperexcitability and altered neuronal communication (Frontiers, 2015) (Frontiers).
Furthermore, neuroligin-3 mutations, associated with autism, have been found to differentially alter synaptic function in the hippocampus and cortex. These mutations can increase inhibitory synaptic transmission and disrupt endocannabinoid signaling, further impacting short-term plasticity and neural circuitry (Molecular Psychiatry, 2015) (Nature). These findings underscore the significant role of short-term plasticity in maintaining neural circuit function and how its disruption can contribute to pathogenesis.
2 versions of this post
For the Academic/Scientific Audience
PlainSpeak in plain language for the lay reader
Transcription Bloopers
Actual Audio: You want to go into superior colliculus a bit more?
Transcription Software: You want to go into the spiritual leaders a bit more.
Audio: So the input is converging.
Software: So the imprint is converging
Disability and Poverty is a tough cycle
In PlainSpeak for Lay Audience
Disability and Poverty: A Tough Cycle
Disability and poverty are closely connected. This makes life harder for disabled people. Here’s why.
Education: Many disabled people don’t get a good education. This makes it hard for them to learn skills needed for good jobs.
Jobs: Disabled people often face problems finding jobs. There aren’t enough job opportunities, and some employers discriminate against them. Without good jobs, it’s hard to earn enough money.
Healthcare: Poor people often can’t afford good healthcare. This can lead to untreated health problems that cause or worsen disabilities.
Support Services: Disabled people need special support, like assistive devices or home modifications, but these can be expensive. Without money, they can’t get the help they need.
The National Council on Disability says that these problems make more disabled people live in poverty. The World Health Organization also says that we need to solve both poverty and disability issues together.
To break this cycle, we need to:
- Provide better education for disabled people.
- Create more job opportunities and stop workplace discrimination.
- Offer better social support services.
- Make healthcare and housing affordable and accessible for everyone.
When we invest in these areas, we help disabled people live better lives. This also helps reduce poverty and builds a stronger, fairer society for everyone.
2 versions of this post
UCLA-AIRP Answer Scholars Award
Congratulations! On behalf of the Autistic and Neurodivergent Scholars Working for Equity in Research (ANSWER) of the AIR-P, we are pleased to inform you that your project... has been selected for the 2024 ANSWER Scholars Program for the project period September 1st, 2024 – August 31, 2025. Your application, achievements, and qualifications truly impressed our review committee.
The False Moral Authority of Titles
The False Moral Authority of Titles
In today's world, holding an advanced degree or prestigious title leads those individuals to think that they are entitled to the role of moral and legal gatekeeper. Such a perspective is not only outdated but dangerously arrogant.
(This echoes the colonial mindset where the "educated colonizers" claimed ipso facto moral and legal authority over those they deemed "uneducated primitives").
One quick path to fame and relevance today is the spread of negative news, fueled by algorithms that amplify these messages. As as Sri Sri Ravi Shankar noted, humans already have a tendency to doubt the positive but not the negative. For instance, when someone says "I love you," it's often met with skepticism ("Really?"), while "I hate you" is silently accepted.
Negative news triggers larger outward reactions, whereas positive news generates internal feel-good responses that don't spread as widely. As a result, negative spins and conspiracy theories have become a quick road to staying relevant and profits in the form of online followers, book deals, speaking engagements.... which in turn helps justify the perception of them as an "expert" and the "moral authority."
This phenomenon has many parallels in the field of autism. Select groups have positioned themselves as the sole experts of autism, their way the only way, and the lone voice of morality. They effectively shut down alternative lines of research in autism or approaches by being the loudest or most powerful voice. This is accompanied by vicious attacks, harassment, and doxxing of those they consider "others." This helps maintain their positions of power, fame and profit - (Perhaps they also get a rush out of this bullying).
The irony is that existing evidence-based practices are often weaponized or misrepresented to justify their stance. Just because something isn't fully explainable or understood yet doesn't mean it should be dismissed as pseudoscience. Rather, it represents science-in-progress. Complex phenomena like autism often defy simple cause-and-effect explanations, waiting for the right methods, technologies, or even an evolution in our scientific thinking to fit neatly into an explainable model.
A 'certification degree' or Ph.D. does not make one all-knowing about a highly heterogeneous condition like autism. We are all still trying to figure autism out. If we had all the explanations and solutions, the quality of life for all autistic individuals would be infinitely better. It’s crucial to remember that science is a process, not a destination. It thrives on curiosity, openness, and the willingness to challenge existing paradigms. True progress in understanding autism, and indeed any complex phenomenon, requires humility, collaboration, and an openness to diverse perspectives.
Let's resist the allure of false authority and the spread of negativity. Instead, let's foster a culture of inquiry and respect, where every voice is heard, and every avenue of research is explored. Only then can we hope to make meaningful progress in understanding and improving the lives of those within the autism community and beyond.
The Role of Parvalbumin Neurons in Autism
A PlainSpeak version for the Lay Reader
The Role of Parvalbumin Neurons in Autism
Background
Scientists believe that a special type of brain cell called Parvalbumin (PV) interneurons (INs) may play a key role in autism. Even though autism can be caused by many different genetic and environmental factors, people with autism often show similar behaviors. This suggests that there might be a common issue in the brain across different individuals with autism (1).
Understanding the role of PV+ interneurons in autism helps us see why many symptoms of autism occur, like sensory sensitivity and seizures.
The Balance of Brain Signals
Our brains need a balance between "go" signals (excitation) and "stop" signals (inhibition) to work properly. In autism, it was first thought that there is too much excitation and not enough inhibition, leading to an imbalance. This imbalance could explain why some people with autism have seizures (4,5). However, this idea is too simple because many types of brain cells are involved in maintaining this balance.
What We Know About PV+ Cells in Autism
Researchers have found that PV+ cells in the brains of autistics are often not working as they should:
- Fewer PV+ cells: There are fewer of these cells in the brain, and they produce less of a protein called parvalbumin.
- Changes in brain waves: These cells help control brain waves called gamma oscillations. In autism, the power of these gamma waves is higher than normal.
- Reduced activity: PV+ cells show less activity in response to visual signals.
PV+ cells are the most common type of inhibitory ("stop/slow down") neuron in the brain, but other types of neurons may also be involved in autism.
Brain Excitability and Sensory Sensitivity
When PV+ cells don't function properly, the brain becomes overly excitable and synchronized, making seizures more likely. This can also cause exaggerated responses to sensory inputs, like touch or sound. For example, in a mouse model of autism, the response to whisker movement is weaker in certain brain cells.
Sensory Overload
Autistics often experience sensory overload because their brains can't tune out irrelevant information. This may be due to a failure of brain cells to adapt to continuous stimulation (2).
Visual Processing
PV+ neurons are important for fine-tuning the way we see things, helping us to distinguish between different visual inputs.
Brain Waves and Communication
Increased gamma wave activity, which is linked to sensory and communication issues, is common in autism. PV+ cells help generate these waves, and their dysfunction leads to irregular brain activity patterns (3).
2 Versions of this Post
For the Science/Academic Reader
References
- 1.Contractor, A., Klyachko, V. A., & Portera-Cailliau, C. (2021). Reduced density and activity of parvalbumin interneurons in autism. Journal of Neurodevelopmental Disorders, 13(1), 1-15.
- 2.Green, S. A., & Gu, Y. (2015). Sensory hypersensitivity in autism spectrum disorders. Current Biology, 25(18), R876-R879.
- 3.Guyon, N., & Nahmani, M. (2021). Role of parvalbumin interneurons in gamma oscillations and sensory processing in autism. Frontiers in Neuroscience, 15, 692872.
- 4. Hussman, J. P. (2001). Suppressed GABAergic inhibition as a common factor in suspected etiologies of autism. Journal of Autism and Developmental Disorders, 31(2), 247-248.
- 5. Rubenstein, J. L., & Merzenich, M. M. (2003). Model of autism: Increased ratio of excitation/inhibition in key neural systems. Genes, Brain and Behavior, 2(5), 255-267.
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