SynapShot, developed by an international research team, marks a major advancement in neuroscience by enabling real-time, live observation of synaptic changes in the brain.
The human brain contains approximately 86 billion neurons and 600 trillion synapses that exchange signals between the neurons to help us control the various functions of the brain including cognition, emotion, and memory. Interestingly, the number of synapses decrease with age or as a result of diseases like Alzheimer’s, and research on synapses thus attracts a lot of attention. However, limitations have existed in observing the dynamics of synapse structures in real-time.
We’re reading more than ever before – but much of it is on screens rather than physical books. Is it changing the way our brains work? Reading books has so many physical, emotional and economic benefits — here’s why how we read might be more important than what or how much we read.
Video by Daniel Nils Roberts.
Made in partnership with the Open University.
If you liked this video then why not watch this one about the power of stories to shape our minds 👉 • How stories shape our minds | The sci…
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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.
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].
The potential applications of Neuralink are vast and could potentially change humanity in many ways. While there are potential drawbacks, the potential benefits make the development of this technology an exciting prospect.
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.
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.
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.
