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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].

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.

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

In recent years, research has begun to reveal that the lines of communication between the body’s organs are key regulators of aging. When these lines are open, the body’s organs and systems work well together. But with age, communication lines deteriorate, and organs don’t get the molecular and electrical messages they need to function properly.

A new study from Washington University School of Medicine in St. Louis identifies, in mice, a critical communication pathway connecting the brain and the body’s fat tissue in a feedback loop that appears central to energy production throughout the body. The research suggests that the gradual deterioration of this feedback loop contributes to the increasing health problems that are typical of natural aging.

The study—published in the journal Cell Metabolism—has implications for developing future interventions that could maintain the feedback loop longer and slow the effects of advancing age.