Astrocytic Calcium Dynamics Along the Pain Pathway

Cho, Jeiwon; Huh, Yeowool

doi:10.3389/fncel.2020.594216

Cited by 11 publications

(8 citation statements)

References 116 publications

(148 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This participation may take the form of modulating presynaptic transmitter release, or shaping the postsynaptic excitatory signal through tonic or acute release of GABA or other transmitters (Chaudhari, 2021). Indeed, the participation of astrocytes in shaping sensory signals is an area of much recent investigation (Kozlov et al, 2006;Cirillo et al, 2012;Leonard et al, 2018;Cho and Huh, 2020;Ung et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

“Tripartite Synapses” in Taste Buds: A Role for Type I Glial-like Taste Cells

et al. 2021

View full text Add to dashboard Cite

In mammalian taste buds, Type I cells comprise half of all cells. These are termed “glial-like” based on morphologic and molecular features, but there are limited studies describing their function. We tested whether Type I cells sense chemosensory activation of adjacent chemosensory (i.e., Types II and III) taste bud cells, similar to synaptic glia. UsingGad2;;GCaMP3 mice of both sexes, we confirmed by immunostaining that, within taste buds, GCaMP expression is predominantly in Type I cells (with no Type II and ≈28% Type III cells expressing weakly). In dissociated taste buds, GCaMP+ Type I cells responded to bath-applied ATP (10-100 μm) but not to 5-HT (transmitters released by Type II or III cells, respectively). Type I cells also did not respond to taste stimuli (5 μmcycloheximide, 1 mmdenatonium). In lingual slice preparations also, Type I cells responded to bath-applied ATP (10-100 μm). However, when taste buds in the slice were stimulated with bitter tastants (cycloheximide, denatonium, quinine), Type I cells responded robustly. Taste-evoked responses of Type I cells in the slice preparation were significantly reduced by desensitizing purinoceptors or by purinoceptor antagonists (suramin, PPADS), and were essentially eliminated by blocking synaptic ATP release (carbenoxolone) or degrading extracellular ATP (apyrase). Thus, taste-evoked release of afferent ATP from type II chemosensory cells, in addition to exciting gustatory afferent fibers, also activates glial-like Type I taste cells. We speculate that Type I cells sense chemosensory activation and that they participate in synaptic signaling, similarly to glial cells at CNS tripartite synapses.SIGNIFICANCE STATEMENTMost studies of taste buds view the chemosensitive excitable cells that express taste receptors as the sole mediators of taste detection and transmission to the CNS. Type I “glial-like” cells, with their ensheathing morphology, are mostly viewed as responsible for clearing neurotransmitters and as the “glue” holding the taste bud together. In the present study, we demonstrate that, when intact taste buds respond to their natural stimuli, Type I cells sense the activation of the chemosensory cells by detecting the afferent transmitter. Because Type I cells synthesize GABA, a known gliotransmitter, and cognate receptors are present on both presynaptic and postsynaptic elements, Type I cells may participate in GABAergic synaptic transmission in the manner of astrocytes at tripartite synapses.

show abstract

Section: Discussionmentioning

confidence: 99%

“Tripartite Synapses” in Taste Buds: A Role for Type I Glial-like Taste Cells

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Generally, Ca 2+ entry into astrocytes includes active transport by different types of voltage gated calcium channels (VGCCs) distributed in the membrane and passive leakage [ 152 ]. Upregulation of L-type VGCCs expression in astrocytes has been shown in pathological conditions, such as those related to AD [ 153 ]. Anekonda et al [ 154 ] have demonstrated that L-type Ca 2+ current blockers can protect cells from the inductive effect of Aβ.…”

Section: The Role Of Ca 2+ Homeostasis Dysfunction...mentioning

confidence: 99%

Role of Microglia and Astrocytes in Alzheimer’s Disease: From Neuroinflammation to Ca2+ Homeostasis Dysregulation

Benedetto

Burgaletto

Bellanca

et al. 2022

Cells

View full text Add to dashboard Cite

Alzheimer’s disease (AD) is the most common form of dementia worldwide, with a complex, poorly understood pathogenesis. Cerebral atrophy, amyloid-β (Aβ) plaques, and neurofibrillary tangles represent the main pathological hallmarks of the AD brain. Recently, neuroinflammation has been recognized as a prominent feature of the AD brain and substantial evidence suggests that the inflammatory response modulates disease progression. Additionally, dysregulation of calcium (Ca2+) homeostasis represents another early factor involved in the AD pathogenesis, as intracellular Ca2+ concentration is essential to ensure proper cellular and neuronal functions. Although growing evidence supports the involvement of Ca2+ in the mechanisms of neurodegeneration-related inflammatory processes, scant data are available on its contribution in microglia and astrocytes functioning, both in health and throughout the AD continuum. Nevertheless, AD-related aberrant Ca2+ signalling in astrocytes and microglia is crucially involved in the mechanisms underpinning neuroinflammatory processes that, in turn, impact neuronal Ca2+ homeostasis and brain function. In this light, we attempted to provide an overview of the current understanding of the interactions between the glia cells-mediated inflammatory responses and the molecular mechanisms involved in Ca2+ homeostasis dysregulation in AD.

show abstract

“…Astrocytes fill the space between neurons in the nervous system, play the role of supporting and separating nerve cells, and actively provide nutrients for the brain and spinal cord, maintain homeostasis, and regulate synaptic transmission. − Astrocytes can produce chemokines and cytokines, which have a bearing on neuronal receptors to promote the interaction between neurons and glial cells. − IL-1β can activate astrocytes to produce an inflammatory cascade that further enhances and prolongs neuroinflammation-induced chronic pain, , so blocking IL-1R with an IL-1R antagonist may be a potential treatment for the early or late development of pain sensitivity . Various signaling molecules, protein kinases, and cell surface receptors in activated astrocytes increase, and they interact and transmit signals to each other in response to pain.…”

Section: Glial Cells In the Central Nervous System And Inflammatory Painmentioning

confidence: 99%

A Novel Progress: Glial Cells and Inflammatory Pain

Wang

2022

ACS Chem. Neurosci.

View full text Add to dashboard Cite

Inflammatory pain is the perception of noxious stimuli that occurs during inflammation or an immune response. Glial cells are widespread in the central and peripheral nervous systems, supporting and guiding the migration of neurons, participating in the immune response, forming the myelin sheath and blood–brain barrier, and maintaining the concentration of potassium ions outside nerve cells. Recent studies have shown that glial cells have a significant connection with the production and development of inflammatory pain. This article reviews the relationship, mechanisms, therapeutic targets between five types of glial cells and inflammatory pain, and the medicine composition that can effectively inhibit inflammatory pain. It expands the study on the mechanism of glial cells regulating pain and provides new ideas for the therapy of inflammatory pain.

show abstract

Astrocytic Calcium Dynamics Along the Pain Pathway

Cited by 11 publications

References 116 publications

“Tripartite Synapses” in Taste Buds: A Role for Type I Glial-like Taste Cells

“Tripartite Synapses” in Taste Buds: A Role for Type I Glial-like Taste Cells

Role of Microglia and Astrocytes in Alzheimer’s Disease: From Neuroinflammation to Ca2+ Homeostasis Dysregulation

A Novel Progress: Glial Cells and Inflammatory Pain

Contact Info

Product

Resources

About