Updated September 14th, 2021
Research Spotlight
The recovery of higher brain function after a loss of blood and oxygen supply, as during a stroke, depends on the interplay of excitatory and inhibitory neurons, which in the healthy brain synchronize each other to so-called brain oscillations. Grube et al. found that after a brief episode of hypoxia, inhibitory neurons – the conductors of synchronized brain oscillations – are less likely to recover. Still, brain oscillations re-emerge, but with distinct changes.
Hirschsprung disease (HSCR) is a congenital disorder characterized by the absence of enteric nervous system in the distal gut. Studies have suggested that inactivating mutations of the RET gene cause HSCR. Okamoto et al. now demonstrate that activating mutations of the RET gene can also cause the disease when the copy number of the RET gene is reduced.
In excitatory cortical neurons grown in culture, the calcium-dependent kinase CaMKIV coordinates different mechanisms that affect how strongly a neuron responds to its inputs. Trojanowski and Turrigiano tested if CaMKIV signaling plays a similar role in these neurons in the visual cortex of living mice. They found that CaMKIV activity was not necessary for maintaining baseline synaptic and intrinsic properties, which suggests that either CaMKIV does not play a role in this process in these neurons, or that loss of CaMKIV activity is robustly compensated.
3D Analysis of the Synaptic Organization in the Entorhinal Cortex in Alzheimer’s Disease
Cognition depends on correct communication between neurons at synapses in the brain. Using electron microscopy, Dominguez-Alvaro et al. have shown synaptic loss and changes in the morphology of the synapses in the entorhinal cortex of Alzheimer’s disease cases, which may contribute to the impairment of cognitive functions.
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