scholarly journals Satellite glial cells modulate cholinergic transmission between sympathetic neurons

2019 ◽  
Author(s):  
Joana Enes ◽  
Surbhi Sona ◽  
Nega Gerard ◽  
Alexander C. Mitchell ◽  
Marian Haburcak ◽  
...  
Keyword(s):  
Glial Cells ◽  
Neural Control ◽  
Synapse Formation ◽  
Close Contact ◽  
Sympathetic Neurons ◽  
Cell Types ◽  
Sympathetic Neuron ◽  
Sympathetic Ganglia ◽  
Satellite Glial Cells ◽  
Satellite Glia

AbstractPostganglionic sympathetic neurons and satellite glial cells are the two major cell types of the peripheral sympathetic ganglia. Sympathetic neurons project to and provide neural control of peripheral organs and have been implicated in human disorders ranging from cardiovascular disease to peripheral neuropathies. Here we show that satellite glia regulate postnatal development and activity of sympathetic neurons, providing evidence for local ganglionic control of sympathetic drive. We show changes in the cellular architecture of the rat sympathetic ganglia during the postnatal period, with satellite glia enwrapping sympathetic neuronal somata during a period of neuronal hypertrophy. In culture, satellite glia contribute to neuronal survival, promote synapse formation and play a modulatory role in neuron-to-neuron cholinergic neurotransmission, consistent with the close contact seen within the ganglia. Cultured satellite glia make and release neurotrophins, which can partially rescue the neurons from nerve growth factor deprivation. Electrophysiological recordings and immunocytochemical analysis on cultured sympathetic neurons show that satellite glial cells influence synapse number and total neuronal activity with little effect on neuronal intrinsic excitability. Thus, satellite glia play an early and ongoing role within the postnatal sympathetic ganglia, expanding our understanding of the contributions of local and target-derived factors in the regulation of sympathetic neuron function.

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

2021 ◽  
Author(s):  
Aurelia Mapps ◽  
Erica Boehm ◽  
Corinne Beier ◽  
William Thomas Keenan ◽  
Jennifer Langel ◽  
...  
Keyword(s):  
Sympathetic Neurons ◽  
Neuronal Cell ◽  
Sympathetic Neuron ◽  
Sympathetic Ganglia ◽  
Neuronal Cell Bodies ◽  
Intimate Association ◽  
Elevated Activity ◽  
Inward Rectifying Potassium Channel ◽  
Specific Deletion ◽  
Satellite Glia

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.

scholarly journals Migrating neural crest cells in the trunk of the avian embryo are multipotent

Development ◽  
1991 ◽  
Vol 112 (4) ◽  
pp. 913-920 ◽  
Author(s):  
S.E. Fraser ◽  
M. Bronner-Fraser
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Sympathetic Neurons ◽  
Morphological Characteristics ◽  
Neural Crest Cells ◽  
Cell Types ◽  
Sympathetic Ganglia ◽  
Avian Embryo ◽  
Developmental Potential ◽  
Trunk Neural Crest

Trunk neural crest cells migrate extensively and give rise to diverse cell types, including cells of the sensory and autonomic nervous systems. Previously, we demonstrated that many premigratory trunk neural crest cells give rise to descendants with distinct phenotypes in multiple neural crest derivatives. The results are consistent with the idea that neural crest cells are multipotent prior to their emigration from the neural tube and become restricted in phenotype after leaving the neural tube either during their migration or at their sites of localization. Here, we test the developmental potential of migrating trunk neural crest cells by microinjecting a vital dye, lysinated rhodamine dextran (LRD), into individual cells as they migrate through the somite. By two days after injection, the LRD-labelled clones contained from 2 to 67 cells, which were distributed unilaterally in all embryos. Most clones were confined to a single segment, though a few contributed to sympathetic ganglia over two segments. A majority of the clones gave rise to cells in multiple neural crest derivatives. Individual migrating neural crest cells gave rise to both sensory and sympathetic neurons (neurofilament-positive), as well as cells with the morphological characteristics of Schwann cells, and other non-neuronal cells (both neurofilament-negative). Even those clones contributing to only one neural crest derivative often contained both neurofilament-positive and neurofilament-negative cells. Our data demonstrate that migrating trunk neural crest cells can be multipotent, giving rise to cells in multiple neural crest derivatives, and contributing to both neuronal and non-neuronal elements within a given derivative.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Quantitative assessment of Fgfr1 expression in neurons and glia

2016 ◽  
Author(s):  
Lisha Choubey ◽  
Jantzen C Collette ◽  
Karen Muller Smith
Keyword(s):  
Glial Cells ◽  
Synapse Formation ◽  
Fluorescent Protein ◽  
Neuropsychiatric Disorders ◽  
Cell Types ◽  
Lipid Binding ◽  
Bergmann Glia ◽  
Radial Glial Cells ◽  
Postnatal Maturation ◽  
Green Fluorescent

Fibroblast growth factors (FGFs) and their receptors (FGFRs) have numerous functions in the developing and adult CNS. For example, the FGFR1 receptor is important for proliferation of radial glial cells in the cortex and hippocampus, oligodendrocyte proliferation and regeneration, midline glia morphology and soma translocation, Bergmann glia morphology, and cerebellar morphogenesis. In addition, FGFR1 signaling in astrocytes is required for postnatal maturation of interneurons expressing parvalbumin (PV). FGFR1 is implicated in synapse formation in the hippocampus, and alterations in the expression of Fgfr1 and its ligand, Fgf2 accompany major depression. Understanding which cell types express Fgfr1 during development may elucidate its roles in normal development of the brain as well as illuminate possible causes of certain neuropsychiatric disorders. Here, we used a BAC transgenic reporter line to trace Fgfr1 expression in the developing murine CNS. The specific transgenic line employed was created by the GENSAT project, tgFGFR1-EGFPGP338Gsat, and includes a gene encoding enhanced green fluorescent protein (EGFP) under the regulation of the Fgfr1 promoter, to trace Fgfr1 expression in the developing CNS. This model reveals that Fgfr1 is primarily expressed in glial cells, in both astrocytes and oligodendrocytes, along with some neurons. Dual labeling experiments indicate that the proportion of GFP+ (Fgfr1+) cells that are also GFAP+ increases from postnatal day 7 (P7) to 1 month, illuminating dynamic changes in Fgfr1 expression during postnatal development of the cortex. In postnatal neurogenic areas, GFP expression was also observed in SOX2, doublecortin (DCX), and brain lipid-binding protein (BLBP) expressing cells. Fgfr1 is also highly expressed in DCX positive cells of the dentate gyrus, but not in the rostral migratory stream. Fgfr1 driven GFP was also observed in tanycytes and GFAP+ cells of the hypothalamus, as well as in Bergmann glia and astrocytes of the cerebellum. Understanding which cell types express Fgfr1 may elucidate its role in neuropsychiatric disorders and brain development.

scholarly journals Cell Surfaces and Fibre Relationships in Sympathetic Ganglion Cultures: A Scanning Electron-Microscopic Study

1974 ◽  
Vol 14 (3) ◽  
pp. 657-669
Author(s):  
CARYL E. HILL ◽  
JULIE H. CHAMLEY ◽  
G. BURNSTOCK
Keyword(s):  
Connective Tissue ◽  
Glial Cells ◽  
Cell Types ◽  
Sympathetic Ganglia ◽  
Nerve Fibres ◽  
Electron Microscopic ◽  
3 Dimensional ◽  
Wide Range ◽  
Tissue Cells ◽  
Scanning Electron

Sympathetic ganglia from newborn rats and guinea-pigs were grown in modified Rose chambers and examined with scanning electron microscopy after 5-7 days. The cell types seen were macrophages, neurons, glial cells and connective tissue cells. They presented a wide range of surface morphologies and 3-dimensional configurations, from spheroid with an irregular surface to flattened with a smooth surface. The arrangement of the nerve fibres and cells in the outgrowth was essentially 2-layered with connective tissue cells nearest the substrate and nerve fibres, glial cells and macrophages lying over them. The relationships of sympathetic nerve fibres to the different cell types were also investigated. In all cases nerve fibres closely followed the cellular surface contours although the nature of the relationships varied. Fine finger-like cytoplasmic projections were sometimes seen from connective tissue cells and macrophages. The possible role of these structures in adhesion and motility is discussed.

scholarly journals Quantitative assessment of Fgfr1 expression in neurons and glia

2016 ◽  
Author(s):  
Lisha Choubey ◽  
Jantzen C Collette ◽  
Karen Muller Smith
Keyword(s):  
Glial Cells ◽  
Synapse Formation ◽  
Fluorescent Protein ◽  
Neuropsychiatric Disorders ◽  
Cell Types ◽  
Lipid Binding ◽  
Bergmann Glia ◽  
Radial Glial Cells ◽  
Postnatal Maturation ◽  
Green Fluorescent

Fibroblast growth factors (FGFs) and their receptors (FGFRs) have numerous functions in the developing and adult CNS. For example, the FGFR1 receptor is important for proliferation of radial glial cells in the cortex and hippocampus, oligodendrocyte proliferation and regeneration, midline glia morphology and soma translocation, Bergmann glia morphology, and cerebellar morphogenesis. In addition, FGFR1 signaling in astrocytes is required for postnatal maturation of interneurons expressing parvalbumin (PV). FGFR1 is implicated in synapse formation in the hippocampus, and alterations in the expression of Fgfr1 and its ligand, Fgf2 accompany major depression. Understanding which cell types express Fgfr1 during development may elucidate its roles in normal development of the brain as well as illuminate possible causes of certain neuropsychiatric disorders. Here, we used a BAC transgenic reporter line to trace Fgfr1 expression in the developing murine CNS. The specific transgenic line employed was created by the GENSAT project, tgFGFR1-EGFPGP338Gsat, and includes a gene encoding enhanced green fluorescent protein (EGFP) under the regulation of the Fgfr1 promoter, to trace Fgfr1 expression in the developing CNS. This model reveals that Fgfr1 is primarily expressed in glial cells, in both astrocytes and oligodendrocytes, along with some neurons. Dual labeling experiments indicate that the proportion of GFP+ (Fgfr1+) cells that are also GFAP+ increases from postnatal day 7 (P7) to 1 month, illuminating dynamic changes in Fgfr1 expression during postnatal development of the cortex. In postnatal neurogenic areas, GFP expression was also observed in SOX2, doublecortin (DCX), and brain lipid-binding protein (BLBP) expressing cells. Fgfr1 is also highly expressed in DCX positive cells of the dentate gyrus, but not in the rostral migratory stream. Fgfr1 driven GFP was also observed in tanycytes and GFAP+ cells of the hypothalamus, as well as in Bergmann glia and astrocytes of the cerebellum. Understanding which cell types express Fgfr1 may elucidate its role in neuropsychiatric disorders and brain development.

scholarly journals Satellite glial cells modulate cholinergic transmission between sympathetic neurons

PLoS ONE ◽  
2020 ◽  
Vol 15 (2) ◽  
pp. e0218643 ◽  
Author(s):  
Joana Enes ◽  
Marián Haburčák ◽  
Surbhi Sona ◽  
Nega Gerard ◽  
Alexander C. Mitchell ◽  
...  
Keyword(s):  
Glial Cells ◽  
Sympathetic Neurons ◽  
Cholinergic Transmission ◽  
Satellite Glial Cells

scholarly journals Differential expression of connexins in trigeminal ganglion neurons and satellite glial cells in response to chronic or acute joint inflammation

2008 ◽  
Vol 4 (4) ◽  
pp. 295-306 ◽  
Author(s):  
Filip G. Garrett ◽  
Paul L. Durham
Keyword(s):  
Glial Cells ◽  
Trigeminal Ganglion ◽  
Joint Inflammation ◽  
Plaque Formation ◽  
Cx43 Expression ◽  
Satellite Glial Cells ◽  
Inflammatory Stimuli ◽  
Trigeminal Ganglion Neurons ◽  
Ganglion Neurons ◽  
Satellite Glia

Trigeminal nerve activation in response to inflammatory stimuli has been shown to increase neuron–glia communication via gap junctions in trigeminal ganglion. The goal of this study was to identify changes in the expression of gap junction proteins, connexins (Cxs), in trigeminal ganglia in response to acute or chronic joint inflammation. Although mRNA for Cxs 26, 36, 40 and 43 was detected under basal conditions, protein expression of only Cxs 26, 36 and 40 increased following capsaicin or complete Freund's adjuvant (CFA) injection into the temporomandibular joint (TMJ). While Cx26 plaque formation between neurons and satellite glia was transiently increased following capsaicin injections, Cx26 plaque formation between neurons and satellite glia was sustained in response to CFA. Interestingly, levels of Cx36 and Cx40 were only elevated in neurons following capsaicin or CFA injections, but the temporal response was similar to that observed for Cx26. In contrast, Cx43 expression was not increased in neurons or satellite glial cells in response to CFA or capsaicin. Thus, trigeminal ganglion neurons and satellite glia can differentially regulate Cx expression in response to the type and duration of inflammatory stimuli, which likely facilitates increased neuron–glia communication during acute and chronic inflammation and pain in the TMJ.

scholarly journals Quantitative assessment of fibroblast growth factor receptor 1 expression in neurons and glia

PeerJ ◽  
2017 ◽  
Vol 5 ◽  
pp. e3173 ◽  
Author(s):  
Lisha Choubey ◽  
Jantzen C. Collette ◽  
Karen Müller Smith
Keyword(s):  
Glial Cells ◽  
Synapse Formation ◽  
Fluorescent Protein ◽  
Growth Factor Receptor ◽  
Neuropsychiatric Disorders ◽  
Cell Types ◽  
Lipid Binding ◽  
Bergmann Glia ◽  
Fibroblast Growth ◽  
Postnatal Maturation

BackgroundFibroblast growth factors (FGFs) and their receptors (FGFRs) have numerous functions in the developing and adult central nervous system (CNS). For example, the FGFR1 receptor is important for proliferation and fate specification of radial glial cells in the cortex and hippocampus, oligodendrocyte proliferation and regeneration, midline glia morphology and soma translocation, Bergmann glia morphology, and cerebellar morphogenesis. In addition, FGFR1 signaling in astrocytes is required for postnatal maturation of interneurons expressing parvalbumin (PV). FGFR1 is implicated in synapse formation in the hippocampus, and alterations in the expression ofFgfr1and its ligand,Fgf2accompany major depression. Understanding which cell types expressFgfr1during development may elucidate its roles in normal development of the brain as well as illuminate possible causes of certain neuropsychiatric disorders.MethodsHere, we used a BAC transgenic reporter line to traceFgfr1expression in the developing postnatal murine CNS. The specific transgenic line employed was created by the GENSAT project,tgFGFR1-EGFPGP338Gsat, and includes a gene encoding enhanced green fluorescent protein (EGFP) under the regulation of theFgfr1promoter, to traceFgfr1expression in the developing CNS. Unbiased stereological counts were performed for several cell types in the cortex and hippocampus.ResultsThis model reveals thatFgfr1is primarily expressed in glial cells, in both astrocytes and oligodendrocytes, along with some neurons. Dual labeling experiments indicate that the proportion of GFP+ (Fgfr1+) cells that are also GFAP+ increases from postnatal day 7 (P7) to 1 month, illuminating dynamic changes inFgfr1expression during postnatal development of the cortex. In postnatal neurogenic areas, GFP expression was also observed in SOX2, doublecortin (DCX), and brain lipid-binding protein (BLBP) expressing cells.Fgfr1is also highly expressed in DCX positive cells of the dentate gyrus (DG), but not in the rostral migratory stream.Fgfr1driven GFP was also observed in tanycytes and GFAP+ cells of the hypothalamus, as well as in Bergmann glia and astrocytes of the cerebellum.ConclusionsThetgFGFR1-EGFPGP338Gsatmouse model expresses GFP that is congruent with known functions of FGFR1, including hippocampal development, glial cell development, and stem cell proliferation. Understanding which cell types expressFgfr1may elucidate its role in neuropsychiatric disorders and brain development.

Estimating Use-Dependent Synaptic Gain in Autonomic Ganglia by Computational Simulation and Dynamic-Clamp Analysis

2004 ◽  
Vol 92 (5) ◽  
pp. 2659-2671 ◽  
Author(s):  
Diek W. Wheeler ◽  
Paul H. M. Kullmann ◽  
John P. Horn
Keyword(s):  
Sympathetic Neurons ◽  
Computational Simulation ◽  
Sympathetic Neuron ◽  
Sympathetic Ganglia ◽  
Spike Timing ◽  
Calcium Currents ◽  
Dynamic Clamp ◽  
Autonomic Ganglia ◽  
Postsynaptic Spike ◽  
Synaptic Gain

Biological gain mechanisms regulate the sensitivity and dynamics of signaling pathways at the systemic, cellular, and molecular levels. In the sympathetic nervous system, gain in sensory-motor feedback loops is essential for homeostatic regulation of blood pressure and body temperature. This study shows how synaptic convergence and plasticity can interact to generate synaptic gain in autonomic ganglia and thereby enhance homeostatic control. Using a conductance-based computational model of an idealized sympathetic neuron, we simulated the postganglionic response to noisy patterns of presynaptic activity and found that a threefold amplification in postsynaptic spike output can arise in ganglia, depending on the number and strength of nicotinic synapses, the presynaptic firing rate, the extent of presynaptic facilitation, and the expression of muscarinic and peptidergic excitation. The simulations also showed that postsynaptic refractory periods serve to limit synaptic gain and alter postsynaptic spike timing. Synaptic gain was measured by stimulating dissociated bullfrog sympathetic neurons with 1–10 virtual synapses using a dynamic clamp. As in simulations, the threshold synaptic conductance for nicotinic excitation of firing was typically 10–15 nS, and synaptic gain increased with higher levels of nicotinic convergence. Unlike the model, gain in neurons sometimes declined during stimulation. This postsynaptic effect was partially blocked by 10 μM Cd2+, which inhibits voltage-dependent calcium currents. These results support a general model in which the circuit variations observed in parasympathetic and sympathetic ganglia, as well as other neural relays, can enable functional subsets of neurons to behave either as 1:1 relays, variable amplifiers, or switches.

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