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Category: neuroscience – Page 20

Role of brain’s immune system in social withdrawal during sickness

“I just can’t make it tonight. You have fun without me.” Across much of the animal kingdom, when infection strikes, social contact shuts down. A new study details how the immune and central nervous systems implement this sickness behavior.

It makes perfect sense that when we’re battling an infection, we lose our desire to be around others. That protects them from getting sick and lets us get much needed rest. What hasn’t been as clear is how this behavior change happens.

In the research published in Cell, scientists used multiple methods to demonstrate causally that when the immune system cytokine interleukin-1 beta (IL-1β) reaches the IL-1 receptor 1 (IL-1R1) on neurons in a brain region called the dorsal raphe nucleus, that activates connections with the intermediate lateral septum to shut down social behavior.

“Our findings show that social isolation following immune challenge is self-imposed and driven by an active neural process, rather than a secondary consequence of physiological symptoms of sickness, such as lethargy,” said study co-senior author.

Neurons use physical signals, not electricity, to stabilize communication

Every movement you make and every memory you form depends on precise communication between neurons. When that communication is disrupted, the brain must rapidly rebalance its internal signaling to keep circuits functioning properly. New research from the USC Dornsife College of Letters, Arts and Sciences shows that neurons can stabilize their signaling using a fast, physical mechanism—not the electrical activity scientists long assumed was required.

The discovery, published recently in Proceedings of the National Academy of Sciences, reveals a system that doesn’t depend on the flow of charged particles to maintain signaling when part of a synapse—the junction between neurons—suddenly stops working.

Maintaining this balance between neurons is essential for muscle control, learning and overall brain health. Failure to maintain this “homeostasis” has been linked to neurological conditions such as epilepsy and autism.

Fertility gene helps glioblastoma tumors survive chemotherapy and return after treatment, researchers discover

Research by University of Sydney scientists has uncovered a mechanism that may explain why glioblastoma returns after treatment, offering new clues for future therapies which they will now investigate as part of an Australian industry collaboration.

Glioblastoma is one of the deadliest brain cancers, with a median survival rate of just 15 months. Despite surgery and chemotherapy, more than 1,250 clinical trials over the past 20 years have struggled to improve survival rates.

Published in Nature Communications, the study shows that a small population of drug-tolerant cells known as “persister cells” rewires its metabolism to survive chemotherapy, using an unexpected ally as an invisibility cloak: a fertility gene called PRDM9.

Abstract: From synaptogenic to synaptotoxic

This issue’s cover features work by Alberto Siddu & team on the promotion of synapse formation in human neurons by free amyloid-beta peptides, in contrast to aggregated forms that are synaptotoxic:

The image shows a human induced neuron exposed to a nontoxic concentration of amyloid-beta42 peptide, revealing enhanced synaptogenesis, visible as synaptic puncta along the dendritic arbor.

Address correspondence to: Alberto Siddu, Lorry Lokey Stem Cell Building, 265 Campus Dr., Room G1015, Stanford, California 94,305, USA. Phone: 650.721.1418; Email: [email protected]. Or to: Thomas C. Südhof, Lorry Lokey Stem Cell Building, 265 Campus Dr., Room G1021, Stanford, California 94,305, USA. Phone: 650.721.1418; Email: [email protected].

‘Mob breaker’ TRIM37 prevents abnormal cell division by eliminating extra spindle poles

In 2000, researchers discovered that mutations that inactivate a gene known as TRIM37 cause a developmental disease called Mulibrey nanism. The extremely rare inherited disorder leads to growth delays and abnormalities in several organs, causing afflictions of the heart, muscles, liver, brain and eyes. In addition, Mulibrey nanism patients exhibit high rates of cancer and are infertile.

In 2016, UC San Diego School of Biological Sciences researchers in the labs of Professors Karen Oegema and Arshad Desai began understanding how TRIM37, when operating normally, plays a key role in preventing conditions that lead to Mulibrey nanism. They linked TRIM37 to spindles, which separate chromosomes during , and centrosomes, the spherical organizing structures at each end of spindles.

The image above shows a normal mitotic cell (left) compared to a cell lacking TRIM37 (right), with spindle microtubules (green), centrosomal protein centrobin (magenta) and DNA (white). Normal cells have two spindle poles that ensure proper cell division. Cells lacking TRIM37 frequently have extra spindle poles, containing a cluster of centrobin molecules that disrupt proper cell division. Patients with Mulibrey nanism lack TRIM37 and their cells show similar extra spindle poles.

Too Little and Too Much: Balanced Hippocampal, But Not Medial Prefrontal, Neural Activity Is Required for Intact Novel Object Recognition in Rats

Impaired GABAergic inhibition, so-called neural disinhibition, in the prefrontal cortex and hippocampus has been linked to cognitive deficits. The novel object recognition (NOR) task has been used widely to study cognitive deficits in rodents. However, the contribution of prefrontal cortical and hippocampal GABAergic inhibition to NOR task performance has not been established. Here, we investigated NOR task performance in male Lister hooded rats following regional neural disinhibition or functional inhibition, using intracerebral microinfusion of the GABAA receptor antagonist picrotoxin or agonist muscimol, respectively. Our infusion targets were the medial prefrontal cortex (mPFC), dorsal hippocampus (DH), and ventral hippocampus (VH).

Is bioluminescence the key to safe, effective brain imaging?

A decade ago, a group of scientists had the literally brilliant idea to use bioluminescent light to visualize brain activity.

“We started thinking: ‘What if we could light up the brain from the inside?’” said Christopher Moore, a professor of brain science at Brown University. “Shining light on the brain is used to measure activity — usually through a process called fluorescence — or to drive activity in cells to test what role they play. But shooting lasers at the brain has down sides when it comes to experiments, often requiring fancy hardware and a lower rate of success. We figured we could use bioluminescence instead.”

With a major grant from the National Science Foundation, the Bioluminescence Hub at Brown’s Carney Institute for Brain Science launched in 2017 based on collaborations between Moore (associate director of the Carney Institute), Diane Lipscombe (the institute’s director), Ute Hochgeschwender (at Central Michigan University) and Nathan Shaner (at the University of California San Diego).

The scientists’ goal was to develop and disseminate neuroscience tools based on giving nervous system cells the ability to make and respond to light.

In a study published in Nature Methods, the team described a bioluminescence tool it recently developed. Called the Ca2+ BioLuminescence Activity Monitor — or “CaBLAM,” for short — the tool captures single-cell and subcellular activity at high speeds and works well in mice and zebrafish, allowing multi-hour recordings and removing the need for external light.

More said that Shaner, an associate professor in neuroscience and in pharmacology at U.C. San Diego, led the development of the molecular device that became CaBLAM: “CaBLAM is a really amazing molecule that Nathan created,” Moore said. “It lives up to its name.”

Measuring ongoing activity of living brain cells is essential to understanding the functions of biological organisms, Moore said. The most common current approach uses imaging with fluorescence-based genetically encoded calcium-ion indicators.

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