Satellite glia are essential modulators of sympathetic neuron survival, activity, and autonomic function

Satellite glia are the major glial cells in sympathetic ganglia, enveloping neuronal cell bodies. Despite this intimate association, how satellite glia contribute to sympathetic functions remain unclear. Here, we show that satellite glia are critical for metabolism, survival, and activity of sympathetic neurons and modulate autonomic behaviors in mice. Adult ablation of satellite glia results in impaired mTOR signaling, soma atrophy, reduced noradrenergic enzymes, and loss of sympathetic neurons. However, persisting neurons have elevated activity, and satellite glia-ablated mice show increased pupil dilation and heart rate, indicative of enhanced sympathetic tone. Satellite glia-specific deletion of Kir4.1, an inward-rectifying potassium channel, largely recapitulates the cellular defects observed in glia-ablated mice, suggesting that satellite glia act in part via extracellular K+ buffering. These findings highlight neuron-satellite glia as functional units in regulating sympathetic output, with implications for disorders linked to sympathetic hyper-activity such as cardiovascular disease and hypertension.

Cytoarchitectonics of the Superior Parietal Cortex of an Outstanding Russian Scientist-Physiologist

The aim of the study is to identify possible cytoarchitectonic features of the structure of the cortex in the superior parietal region of an outstanding and talented scientist-physiologist.Material and methods. The cortex (area 7) of the superior parietal region of a scientist-physiologist and men of the senile age in the control group (8 hemispheres) was studied on the series of frontal brain slices, 20 μ thick, stained with cresyl purple according to Nissl method. The cortex area thickness, the thickness of the cytoarchitectonics layer III, the area of profile field of pyramidal neurons in layers III and V, the density of neurons surrounded by satellite glia and satellite glia density in layers III and V were measured in the cortex (area 7) of the superior parietal region in the left and right hemispheres of the brain.Results. We have identified several features of the cytoarchitectonics structure of the cortex (area 7) in the brain of the scientist-physiologist that may correlate with his outstanding scientific abilities. The cortex of a scientist-physiologist is characterized by a large thickness of the studied cortex and its cytoarchitectonic layers III and V, and a greater value of the area of the profile field of neurons if compared with the cortex in men of the senile age from the control group. A higher value of the neuron density and satellite glia in the cortex of the superior parietal region of the scientist-physiologist was revealed. There was also a lower severity of age-related changes in the cortex of the scientist-physiologist compared with the control group of men.Conclusion. The structure of the cortex (area 7) of the superior parietal region of the scientistphysiologist is characterized by a greater parameter of the cortical thickness and the thickness of the associative layer III, the size of neurons and the density of satellite glia if compared with those in men of the senile age of the control group. These features distinguish the structure of his cortex from the similar cortex of the control group of men and may be related to the features of the cognitive activity of the outstanding scientist-physiologist.

Diversity of satellite glia in sympathetic and sensory ganglia

Satellite glia are the major glial type found in ganglia of the peripheral nervous system and wrap around cell bodies of sympathetic and sensory neurons that are very diverse. Other than their close physical association with peripheral neurons, little is known about this glial population. Here, we performed single cell RNA sequencing analysis and identified five different populations of satellite glia from sympathetic and sensory ganglia. We identified three shared populations of satellite glia enriched in immune-response genes, immediate-early genes and ion channels/ECM-interactors, respectively. Sensory- and sympathetic-specific satellite glia are differentially enriched for modulators of lipid synthesis and metabolism. Sensory glia are also specifically enriched for genes involved in glutamate turnover. Further, satellite glia and Schwann cells can be distinguished by unique transcriptional signatures. This study reveals remarkable heterogeneity of satellite glia in the peripheral nervous system.

Etv5 is not required for Schwann cell development but is required to regulate the Schwann cell response to peripheral nerve injury

ABSTRACTSchwann cells are the principal glial cells of the peripheral nervous system, and their development into myelinating glia is critically dependent on MEK/ERK signaling. Ets-domain transcription factors (Etv1, Etv4, Etv5) are common downstream effectors of MEK/ERK signalling, but so far, only Etv1 has been ascribed a role in Schwann cell development, and only in non-myelinating cells. Here, we examined the role of Etv5, which is expressed in Schwann cell precursors, including neural crest cells and satellite glia, in Schwann cell lineage development. We analysed Etv5tm1Kmm mutants (designated Etv5−/−) at embryonic days (E) 12.5, E15.5 and E18.5, focusing on dorsal root ganglia. At these embryonic stages, satellite glia (glutamine synthetase) and Schwann cell markers, including transcriptional regulators (Sox10, Sox9, Tfap2a, Pou3f1) and non-transcription factors (Ngfr, BFABP, GFAP), were expressed in the DRG of wild-type and Etv5−/− embryos. Furthermore, by E18.5, quantification of Sox10+ Schwann cells and NeuN+ neurons revealed that these cells were present in normal numbers in the Etv5−/− dorsal root ganglia. We next performed peripheral nerve injuries at postnatal day 21, revealing that Etv5−/− mice had an enhanced injury response, generating more Sox10+ Schwann cells compared to wild-type animals at five days post-injury. Thus, while Etv5 is not required for Schwann cell development, possibly due to genetic redundancy with Etv1 and/or Etv4, Etv5 is an essential negative regulator of the peripheral nerve injury repair response.SIGNIFICANCE STATEMENTOur study sought to determine whether the ets domain transcription factor, Etv5, plays a role in regulating Schwann cell development and nerve repair. By using an embryonically and postnatally viable hypomorphic Etv5 mutant allele, we demonstrated that Etv5 is not required for the development of Schwann cells or other neural crest derivatives in the dorsal root ganglia, including satellite glia and neurons. Surprisingly, loss of Etv5 had a direct impact on the Schwann cell repair response post-injury, resulting in more Schwann cells populating the distal injured nerve site compared to wild-type animals. Thus, this work describes for the first time a role for Etv5 in regulating the Schwann cell repair response after peripheral nerve injury.