Modulation of Microglial Process Convergence Toward Neuronal Dendrites by Extracellular Calcium

Eyo, Ukpong B.; Gu, Nan; De, Srijisnu; Dong, Hailong; Richardson, Jason R.; Wu, Long Jun

doi:10.1523/jneurosci.3279-14.2015

Cited by 111 publications

(102 citation statements)

References 39 publications

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“…This process involves the activation of neuronal NMDA receptors, calcium influx, subsequent ATP release, and the activation of P2Y 12 receptors (Eyo et al, 2014). A similar phenomenon, described recently and termed microglial process convergence (MPC) involves the convergence of microglial processes on neuronal dendrites in response to a reduction of extracellular Ca 2þ (Eyo et al, 2015). The induction of microglial migration, morphological transformation and process extension towards various pathological signals by P2Y 12 receptors probably represents a protective mechanism which could be beneficial during early stages of injury.…”

Section: The Role Of P2y Receptors In Neuroinflammationmentioning

confidence: 89%

Purinergic mechanisms in neuroinflammation: An update from molecules to behavior

et al. 2016

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a b s t r a c tThe principle functions of neuroinflammation are to limit tissue damage and promote tissue repair in response to pathogens or injury. While neuroinflammation has utility, pathophysiological inflammatory responses, to some extent, underlie almost all neuropathology. Understanding the mechanisms that control the three stages of inflammation (initiation, propagation and resolution) is therefore of critical importance for developing treatments for diseases of the central nervous system. The purinergic signaling system, involving adenosine, ATP and other purines, plus a host of P1 and P2 receptor subtypes, controls inflammatory responses in complex ways. Activation of the inflammasome, leading to release of pro-inflammatory cytokines, activation and migration of microglia and altered astroglial function are key regulators of the neuroinflammatory response. Here, we review the role of P1 and P2 receptors in mediating these processes and examine their contribution to disorders of the nervous system. Firstly, we give an overview of the concept of neuroinflammation. We then discuss the contribution of P2X, P2Y and P1 receptors to the underlying processes, including a discussion of cross-talk between these different pathways. Finally, we give an overview of the current understanding of purinergic contributions to neuroinflammation in the context of specific disorders of the central nervous system, with special emphasis on neuropsychiatric disorders, characterized by chronic low grade inflammation or maternal inflammation. An understanding of the important purinergic contribution to neuroinflammation underlying neuropathology is likely to be a necessary step towards the development of effective interventions.

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Section: The Role Of P2y Receptors In Neuroinflammationmentioning

confidence: 89%

Purinergic mechanisms in neuroinflammation: An update from molecules to behavior

et al. 2016

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“…Visual deprivation reduced microglial process motility, which was reversed after light-reexposure. Evo et al [22*] observed that microglial processes converge at dendritic spines in mouse brain slices in response to reduced extracellular calcium. They describe this phenomenon as “microglial process convergence”, which is apparently mediated by purinergic signaling.…”

Section: Introductionmentioning

confidence: 99%

“…Microglia-neuronal contact alters with changes in neuronal input. In P2Y12 receptor (P2Y12R) knock-out mice, microglial process convergence towards neuronal dendrites was eliminated [22*]. Tatsumi et al [30] recently show that microglial P2Y12R signaling following nerve injury involves downstream Rho-associated protein kinase (ROCK) that acts at actin.…”

Section: Introductionmentioning

confidence: 99%

“…], neurotrophic factors (nerve growth factor, brain-derived neurotrophic factor), and chemokines [chemokine (C-C motif) ligand 2 (CCL2), CX3CL1 etc. ], even direct nerve stimulation, had no effect [22*,39]. To induce release of CatS in microglia, ATP alone was insufficient.…”

Section: Introductionmentioning

confidence: 99%

“…Although there is no direct evidence at the spinal level, this concept is supported by functional anatomy data from brain that demonstrate mutual contacts between the four components in the brain and their dynamic sensitivity to sensory input and signaling molecules [20-22*] (Fig. 1).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Activity-triggered tetrapartite neuron–glial interactions following peripheral injury

Ren

Dubner

2016

Current Opinion in Pharmacology

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Recent studies continue to support the proposition that non-neuronal components of the nervous system, mainly glial cells and associated chemical mediators, contribute to the development of neuronal hyperexcitability that underlies persistent pain conditions. In the event of peripheral injury, enhanced or abnormal nerve input is likely the most efficient way to activate simultaneously central neurons and glia. Injury induces phenotypic changes in glia and triggers signaling cascades that engage reciprocal interactions between presynaptic terminals, postsynaptic neurons, microglia and astrocytes. While some responses to peripheral injury may help the nervous system to adapt positively to counter the disastrous effect of injury, the net effect often leads to long-lasting sensitization of pain transmission pathways and chronic pain.

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Structural analysis of the microglia–interneuron interactions in the CA1 hippocampal area of the APP/PS1 mouse model of Alzheimer's disease

Gervais

Iloun

Martianova

et al. 2021

J of Comparative Neurology

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Microglia can interact with glutamatergic neurons and, through control of synaptic elements, regulate their physiological function. Much less is known about the partnership between microglia and GABAergic inhibitory interneurons. Here, we compared the interactions between microglia and parvalbumin (PV+) and somatostatin (SOM+) expressing interneurons in the CA1 hippocampal area of APP/PS1 transgenic mice that mimic certain aspects of the Alzheimer's disease (AD). We first uncovered a high level of interactions between microglia and two types of interneurons, with 98% of SOM+ and 90% of PV+ cells receiving different types of putative microglial contacts. The latter included the microglia soma to the interneuron soma (SomaMG‐to‐SomaIN), the microglia process to the interneuron soma (ProcessMG‐to‐SomaIN) and the microglia process to the interneuron dendrite (ProcessMG‐to‐DendIN) interactions. Moreover, we found significantly larger areas of interaction for the SomaMG‐to‐SomaIN and the ProcessMG‐to‐DendIN type of contacts between microglia and SOM+ cells. In contrast, PV+ cells exhibited larger areas for the ProcessMG‐to‐SomaIN interactions. Second, in APP/PS1 mice, although the overall microglia interactions with interneurons remained preserved, the fraction of interneurons receiving putative microglia contacts on their dendrites was reduced, and larger areas of interactions were observed for somatic contacts, suggesting a stronger modulation of the interneuron output by microglia in AD. In summary, these results reveal microglia as important partners of hippocampal PV+ and SOM+ GABAergic cells, with interneuron type‐specific pattern of interactions. Thus, microglia may play an essential role in the operation of interneurons under normal conditions and their dysfunction in disease.

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Modulation of Microglial Process Convergence Toward Neuronal Dendrites by Extracellular Calcium

Cited by 111 publications

References 39 publications

Purinergic mechanisms in neuroinflammation: An update from molecules to behavior

Purinergic mechanisms in neuroinflammation: An update from molecules to behavior

Activity-triggered tetrapartite neuron–glial interactions following peripheral injury

Structural analysis of the microglia–interneuron interactions in the CA1 hippocampal area of the APP/PS1 mouse model of Alzheimer's disease

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