Effects of ATP and derivatives on neuropile glial cells of the leech central nervous system

Müller, Michael; Henrich, A.; Klockenhoff, Johannes; Dierkes, Paul Wilhelm; Schlue, Wolf-Rüdiger

doi:10.1002/(sici)1098-1136(20000201)29:3<191::aid-glia1>3.0.co;2-r

Cited by 15 publications

(12 citation statements)

References 49 publications

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“…The similar effects of ATP and AMP prompted us to examine what kind of purinergic receptor might be mediating these actions. It has been reported previously that the nonselective P2‐receptor antagonist PPADS (pyridoxal‐phosphate‐6‐azophenyl‐2′, 4′‐disulphonic acid; 0.2 mM) completely abolishes ATP‐induced (2 mM) glial cell depolarization in the leech ganglion (Müller, Henrich, Klockenhoff, Dierkes, & Schlue, ). However, when PPADS was included in the saline along with the ATP, there was no significant antagonistic effect ( n = 5; p = 0.8) on dye passage as compared to the ATP alone preparations.…”

Section: Resultsmentioning

confidence: 95%

Purinergic modulation of neuronal gap junction circuits in the CNS of the leech

Segura

Abdulnoor

Hua

et al. 2020

J of Neuroscience Research

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Gap junctions (GJs) are widely distributed in brains across the animal kingdom. To visualize the GJ-coupled networks of two major mechanosensory neurons in the ganglia of medicinal leeches, we injected these cells with the GJ-permeable tracer Neurobiotin. When diffusion time was limited to only 30 min, tracer coupling was highly variable for both cells, suggesting a possible modulation of GJ permeability. In invertebrates the innexins (homologs of vertebrate pannexins) form the GJs.Because extracellular adenosine triphosphate (ATP) modulates pannexin and leech innexin hemichannel permeability and is released by leech glial cells following injury, we tested the effects of bath application of ATP after the injection of Neurobiotin and observed a significant increase in the number of neurons tracer coupled to the sensory neurons. This effect required the elevation of intracellular Ca 2+ and could be produced by bath application of caffeine. Conversely, scavenging endogenous extracellular ATP with the ATPase apyrase decreased the number of coupled cells.ATP also increased electrical conductance and tracer permeability between the bilateral Retzius neurons. This modulatory effect of ATP on GJ coupling was blocked by siRNA knockdown of a P1-like adenosine receptor. Finally, exposure of leech ganglia to extracellular ATP induced a characteristic low frequency (<0.3 Hz) rhythmic bursting activity that was roughly synchronous among multiple neurons, a behavior that was significantly attenuated by the GJ blocker octanol. These findings highlight the mediation by ATP of a robust physiological mechanism for modifying neuronal circuits by rapidly recruiting neurons into active networks and entraining synchronized bursting activity.

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Section: Resultsmentioning

confidence: 95%

Purinergic modulation of neuronal gap junction circuits in the CNS of the leech

Segura

Abdulnoor

Hua

et al. 2020

J of Neuroscience Research

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“…1998a). Functional evidence from the leech central nervous system suggests that the leech glial cells in situ co‐express metabotropic P2Y and P1 purinoceptors (Muller et al . 2000).…”

Section: Discussionmentioning

confidence: 99%

Developmental expression of metabotropic P2Y₁ and P2Y₂ receptors in freshly isolated astrocytes from rat hippocampus

Zhu

Kimelberg

2001

Journal of Neurochemistry

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There are at least three subtypes of cloned metabotropic P2 receptors linked to intracellular Ca 21 rises in rat brain cells, namely, P2Y 1 , P2Y 2 and P2Y 4 . In this study we explore the subtypes of the metabotropic P2 receptors seen in freshly isolated astrocytes (FIAs) from P8-P25 rats. We found by single cell RT-PCR that in process-bearing FIAs from hippocampi of P8-P12 rats, 31% of the glial ®brillary acidic protein (GFAP) mRNA (1) cells expressed P2Y 1 mRNA while only 5% of the cells tested expressed P2Y 2 mRNA. The expression of P2Y 1 receptor mRNA was not changed in FIAs from the hippocampi of P18-P25 rats, but 38% of the GFAP mRNA (1) cells in the P18-P25 age group then showed P2Y 2 mRNA. We also studied whether the mRNA was expressing functional receptor protein by measuring Ca 21 responses to speci®c agonists for P2Y 1 and P2Y 2 . We found that similar proportions of GFAP mRNA (1) FIAs responded to ATP or UTP as showed mRNAs for P2Y 1 and P2Y 2, respectively. Total tissue RNA from P9 and P24 rat hippocampus showed a 2.8-fold increase in P2Y 2 mRNA levels from P9 to P24 with a decrease in P2Y 1 mRNA. Thus, this study shows a marked up-regulation of mRNA for P2Y 2 from 9 to 24 days in rat hippocampus, and some of this increase is likely due to the protoplasmic astrocytes which is being translated into functional receptor protein in these cells.

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“…Although genomic studies have not yet identified P2Y receptors in invertebrates (Brody et al, 2000), there is substantial pharmacological evidence for them, including in the leech (Müller et al, 2000). Moreover, it has been shown that 50 μM RB2 significantly reduces microglial migration to lesions for at least 24 h (Ngu et al, 2007).…”

Section: Methodsmentioning

confidence: 99%

ATP and NO dually control migration of microglia to nerve lesions

Duan

Sahley

Muller

2008

Developmental Neurobiology

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Microglia migrate rapidly to lesions in the central nervous system (CNS), presumably in response to chemoattractants including ATP released directly or indirectly by the injury. Previous work on the leech has shown that nitric oxide (NO), generated at the lesion, is both a stop signal for microglia at the lesion and crucial for their directed migration from hundreds of micrometers away within the nerve cord, perhaps mediated by a soluble guanylate cyclase (sGC). In this study, application of 100 lM ATP caused maximal movement of microglia in leech nerve cords. The nucleotides ADP, UTP, and the nonhydrolyzable ATP analog AMP-PNP (adenyl-59-yl imidodiphosphate) also caused movement, whereas AMP, cAMP, and adenosine were without effect. Both movement in ATP and migration after injury were slowed by 50 lM reactive blue 2 (RB2), an antagonist of purinergic receptors, without influencing the direction of movement. This contrasted with the effect of the NO scavenger cPTIO (2-(4-carboxyphenyl)-4,4,5,5-teramethylimidazoline-oxyl-3-oxide), which misdirected movement when applied at 1 mM. The cPTIO reduced cGMP immunoreactivity without changing the immunoreactivity of eNOS (endothelial nitric oxide synthase), which accompanies increased NOS activity after nerve cord injury, consistent with involvement of sGC. Moreover, the sGC-specific inhibitor LY83583 applied at 50 lM had a similar effect, in agreement with previous results with methylene blue. Taken together, the experiments support the hypothesis that ATP released directly or indirectly by injury activates microglia to move, whereas NO that activates sGC directs migration of microglia to CNS lesions. ' 2008 Wiley Periodicals, Inc. Develop Neurobiol 69: 60-72, 2009

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Effects of ATP and derivatives on neuropile glial cells of the leech central nervous system

Cited by 15 publications

References 49 publications

Purinergic modulation of neuronal gap junction circuits in the CNS of the leech

Purinergic modulation of neuronal gap junction circuits in the CNS of the leech

Developmental expression of metabotropic P2Y₁ and P2Y₂ receptors in freshly isolated astrocytes from rat hippocampus

ATP and NO dually control migration of microglia to nerve lesions

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Effects of ATP and derivatives on neuropile glial cells of the leech central nervous system

Cited by 15 publications

References 49 publications

Purinergic modulation of neuronal gap junction circuits in the CNS of the leech

Purinergic modulation of neuronal gap junction circuits in the CNS of the leech

Developmental expression of metabotropic P2Y1 and P2Y2 receptors in freshly isolated astrocytes from rat hippocampus

ATP and NO dually control migration of microglia to nerve lesions

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Developmental expression of metabotropic P2Y₁ and P2Y₂ receptors in freshly isolated astrocytes from rat hippocampus