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Category: neuroscience – Page 374

2-Minute Neuroscience: Autism

Autism is characterized by impairments in social communication and interaction and restricted and repetitive behaviors. In this video, I discuss the neuroscience of autism along with potential factors and mechanisms involved in the development of autism.

TRANSCRIPT:

Autism, also known as autism spectrum disorder, is characterized by symptoms that include impairments in social communication and interaction and restricted and repetitive behaviors. Although the neuroscience of autism is still poorly understood, autism is considered to be a complex developmental disorder that involves atypical brain organization starting early in development.

Individuals with autism often experience a period of unusually rapid brain growth in infancy and early childhood. This accelerated brain growth is linked to an atypical pattern of connectivity between brain regions. A number of studies report that alterations in brain circuitry involved with social interaction and attention can be detected well before the symptoms of autism begin to appear. At this point, however, it’s unclear how brain overgrowth and atypical connectivity might be linked to the occurrence of autism symptoms.

Research suggests that the risk of autism is strongly influenced by genetics, yet studies consistently report that environmental factors also play a large role. Although a number of potential environmental factors have been identified, the risk factors for autism are far from definitive, and it remains unclear which factors are responsible for causing an increase in autism risk, and which are associated in a non-causal way. The risk factors that are most strongly linked to autism are associated with the prenatal or perinatal period. Thus, it’s possible they might be responsible for disruptions to typical neural development, leading to symptoms of autism months or years later. How these risk factors might interfere with neural development is still uncertain, but hypotheses have suggested potential mechanisms such as epigenetic effects, inflammation, oxidative stress, or damage caused by oxygen deficiency. More work needs to be done, however, to fully elucidate the genetic and environmental risk factors for autism, as well as the mechanisms for the development of autism symptoms.

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Neurovascular coupling: Motive unknown

It has been known for more than century that increases in neural activity in the brain drive changes in local blood flow, known as neurovascular coupling. The colloquial explanation for these increases in blood flow (referred to as functional hyperemia) in the brain is that they serve to supply the needs of metabolically active neurons. However, there is an large body of evidence that is inconsistent with this idea. In most cases, baseline blood flow is adequate to supply even elevated neural activity. Neurovascular coupling is irregular, absent, or inverted in many brain regions, behavioral states, and conditions. Increases in respiration can generate increases in brain oxygenation independently of flow changes. Simulations have shown that areas with low blood flow are inescapable and cannot be removed by functional hyperemia given the architecture of the cerebral vasculature. What physiological purpose might neurovascular coupling serve? Here, we discuss potential alternative functions of neurovascular coupling. It may serve supply oxygen for neuromodulator synthesis, to regulate cerebral temperature, signal to neurons, stabilize and optimize the cerebral vascular structure, deal with the non-Newtonian nature of blood, or drive the production and circulation of cerebrospinal fluid around and through the brain via arterial dilations. Understanding the ‘why’ of neurovascular coupling is an important goal that give insight into the pathologies caused by cerebrovascular disfunction.

Like all energy demanding organs, the brain is highly vascularized. When presented with a sensory stimulus or cognitive task, increases in neural activity in many brain regions are accompanied by local dilation of arterioles and other microvessels, increasing local blood flow, volume and oxygenation. The increase in blood flow in response to increased neural activity (known as functional hyperemia) is controlled by a multitude of different signaling pathways via neurovascular coupling (reviewed in [1,2]). These vascular changes can be monitored non-invasively in humans and other species, with techniques (like BOLD fMRI) that are cornerstones in modern neuroscience [3,4]. Chronic disruptions of neurovascular coupling have adverse health effects on the brain. Stress affects neurovascular coupling [5,6], and many neurodegenerative diseases are marked by vascular dysfunction [7].

How a Single Study Proved That Multiple Sclerosis Is Caused by a Virus

In 1,868, Jean-Martin Charcot, a neurologist at the Hôpital de Salpétrière in France, first coined the disease “la sclérose en plaques,” which means multiple sclerosis (MS) — to distinguish it from another type of movement disorder later known as Parkinson’s disease.

Though described in 1,868, the cause of MS puzzled scientists for more than a century. This is until a 2022 breakthrough study finally enlightens us that the cause is, oddly, the seemingly innocent Epstein-Barr virus (EBV), a common childhood virus that causes typical fever and sore throat.

Let’s see how one study single-handedly proves what we thought couldn’t be proved; how one study truly deserves to be called a breakthrough; and how thorough and near-perfect science is done.

TRNA ‘Wobble’ Helps Cells Boost Antibody Production

The various identities of cells, whether they are in the brain, heart, kidney, or any other tissue, are defined by the genes they expressed. In basic terms, the genes that are active in a cell are transcribed into RNA molecules that are then translated into proteins using tRNA molecules. In the genetic code, three base pair sequences of DNA, or codons, represent amino acids. These amino acids are moved into place by tRNA molecules, which have matching anticodons, to make proteins. There is redundancy in the genetic code as well, in which one amino acid can often be encoded by a few different codons.

Protein production varies considerably in different cells, and this is especially notable in cells that generate antibodies. These cells often have to spring into action and shift into high gear to generate many infection-fighting antibodies quickly. These antibody producers are B cells, and they often make significant metabolic adaptations when they’re needed.

Revealing the hidden precision of inhibitory circuits

A new study by Petr Znamenskiy, Tom Mrsic-Flogel, and colleagues present findings that overturn a decade-long idea that inhibitory neurons provide blanket normalising inhibition, showing that for PV+ inhibitory neurons this is not the case.

By April Cashin-Garbutt

Just like computers are characterised by their hardware, neural circuits in the brain are defined by their wiring. The synaptic organisation determines the function of neural circuits. While the connections of excitatory and inhibitory neurons were previously characterised, a new study has revealed the hidden precision of the synaptic strength of inhibitory circuits in the neocortex.

“People often think of excitatory neurons as doing the bulk of the interesting computations in the brain, whereas inhibitory neurons are thought to coordinate the activity of excitatory cells. We know from previous research that the connectivity of excitatory cells is very specific, whereas inhibitory neurons were thought to have very broad and non-specific connections,” explained Petr Znamenskiy, Group Leader at the Francis Crick Institute and former postdoctoral researcher in the Mrsic-Flogel Lab at the Sainsbury Wellcome Centre.

Research into the nature of memory reveals how cells that store information are stabilized over time

When neurons are activated in the hippocampus, not all are going to be firing at once.

Think of a time when you had two different but similar experiences in a short period. Maybe you attended two holiday parties in the same week or gave two presentations at work. Shortly afterward, you may find yourself confusing the two, but as time goes on that confusion recedes and you are better able to differentiate between these different experiences.

New research published in Nature Neuroscience reveals that this process occurs on a , findings that are critical to the understanding and treatment of memory disorders, such as Alzheimer’s disease.

Dynamic engrams store memories

The research focuses on engrams, which are in the brain that store memory information. “Engrams are the neurons that are reactivated to support ,” says Dheeraj S. Roy, Ph.D., one of the paper’s senior authors and an assistant professor in the Department of Physiology and Biophysics in the Jacobs School of Medicine and Biomedical Sciences at the University at Buffalo. “When engrams are disrupted, you get amnesia.”

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