Five Neuroscience Favorites

We’d like to take a moment to celebrate five of our favorite neuroscience publications from the past couple of years; exploring everything from gastrointestinal pain to volume control in mice to kidney oxygenation.


A therapeutic target for treating visceral pain associated with gastrointestinal disorders

Published in Neuron

Xie et al., investigate the role of Piezo2 channels in mediating visceral pain. In this article they demonstrate that Piezo2 channels in TRPV1-lineage neurons are crucial for sensing mechanical forces in the colon, particularly under conditions of inflammatory and functional gastrointestinal disorders like irritable bowel syndrome. By selectively ablating these Piezo2 channels in mice, the researchers found a significant reduction in pain responses caused by mechanical distension of the colon.

Read more: https://doi.org/10.1016/j.neuron.2022.11.015

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Activated astrocytes attenuate neocortical seizures in rodent models through driving sodium-potassium-ATPase

Published in Nature Communications

In this article, Zhao et al. explore the role of astrocytes in controlling seizures. The team used optogenetic techniques to activate astrocytes in rodent models of neocortical epilepsy. This activation significantly reduced seizure activity by inhibiting the firing of high-frequency pyramidal neurons. Importantly, this anti-seizure effect was not mediated through calcium signaling, as previously thought, but rather through astrocytic sodium-potassium-ATPase, which helps buffer extracellular potassium, a critical factor in controlling neuronal excitability during seizures. The findings suggest that targeting astrocytic sodium-potassium-ATPase could be a promising therapeutic strategy for treating intractable epilepsy.

Read more: https://doi.org/10.1038/s41467-022-34662-2

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A brainstem circuit for phonation and volume control in mice

Published in Nature Neuroscience

Veerakumar et al. have identified a key brainstem circuit involved in vocalization in mice. A specific group of neurons in the mouse brainstem's nucleus retroambiguus (RAm) express the neuropeptide precursor neurotensin. These neurotensin-expressing neurons are activated during both neonatal cries and adult social vocalizations, and their activity is crucial for producing sound and controlling its volume. By using optogenetics and neuronal mapping, the team demonstrated that these neurons control laryngeal and expiratory muscles, enabling sound production and volume modulation.

Read more: https://doi.org/10.1038/s41593-023-01478-2

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Neuronal NLRP3 Inflammasome Mediates Spreading Depolarization-evoked Trigeminovascular Activation

Published in Brain

Chen et al. explore the role of the NLRP3 inflammasome in mediating neuroinflammatory processes that are triggered by spreading depolarization, a mechanism linked to migraine aura. Using piezoresistive pressure transducers, the team found that NLRP3 inflammasome activation occurs specifically in neurons following spreading depolarization, contributing to cortical neuroinflammation and activation of the trigeminovascular system. These findings highlight the involvement of both neurons and microglia in these inflammatory cascades and suggest that inhibiting NLRP3 could mitigate migraine-related neuroinflammation.

Read more: https://doi.org/10.1093/brain/awad045

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Circadian Rhythm in Kidney Tissue Oxygenation in the Rat

Published in Frontiers in Physiology

Emans et al. have explored how oxygen levels in the kidneys of rats vary throughout a 24-hour period. The team hypothesized that kidney oxygenation, which depends on oxygen delivery and consumption, exhibits a circadian rhythm. Using Kaha Tissue Oxygen Telemetry, they continuously monitored oxygen levels in the renal cortex and medulla of rats over five days. The results showed that oxygen levels peaked during the active phase (lights-off) and decreased during the rest phase (lights-on), suggesting that oxygen delivery, determined by renal blood flow, follows a diurnal pattern.

Read more: https://doi.org/10.3389/fphys.2017.00205

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