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  • 1
    Electronic Resource
    Electronic Resource
    UDP acting at P2Y 6 receptors is a mediator of microglial phagocytosis (2007)
    [s.l.] : Nature Publishing Group
    Nature 446 (2007), S. 1091-1095 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Microglia, brain immune cells, engage in the clearance of dead cells or dangerous debris, which is crucial to the maintenance of brain functions. When a neighbouring cell is injured, microglia move rapidly towards it or extend a process to engulf the injured cell. Because cells release or ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nature05704
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  • 2
    Electronic Resource
    Electronic Resource
    BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain (2005)
    [s.l.] : Nature Publishing Group
    Nature 438 (2005), S. 1017-1021 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Neuropathic pain that occurs after peripheral nerve injury depends on the hyperexcitability of neurons in the dorsal horn of the spinal cord. Spinal microglia stimulated by ATP contribute to tactile allodynia, a highly debilitating symptom of pain induced by nerve injury. Signalling between ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nature04223
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  • 3
    Electronic Resource
    Electronic Resource
    P2X 4 receptors induced in spinal microglia gate tactile allodynia after nerve injury (2003)
    [s.l.] : Macmillian Magazines Ltd.
    Nature 424 (2003), S. 778-783 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Pain after nerve damage is an expression of pathological operation of the nervous system, one hallmark of which is tactile allodynia—pain hypersensitivity evoked by innocuous stimuli. Effective therapy for this pain is lacking, and the underlying mechanisms are poorly understood. Here we ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nature01786
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  • 4
    Electronic Resource
    Electronic Resource
    Long-lasting change in brain dynamics induced by methamphetamine: enhancement of protein kinase C-dependent astrocytic response and behavioral sensitization (2005)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 93 (2005), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: It is well known that long-term exposure to psychostimulants induces neuronal plasticity. Recently, accumulating evidence suggests that astrocytes may actively participate in synaptic plasticity. In this study, we found that in vitro treatment of cortical neuron/glia co-cultures with either methamphetamine (METH) or morphine (MRP) caused the activation of astrocytes via protein kinase C (PKC). Purified astrocytes were markedly activated by METH, whereas MRP had no such effect. METH, but not MRP, caused a long-lasting astrocytic activation in cortical neuron/glia co-cultures. Furthermore, MRP-induced behavioral sensitization to hyper-locomotion was reversed by 2 months of withdrawal following intermitted MRP administration, whereas behavioral sensitization to METH-induced hyper-locomotion was maintained even after 2 months of withdrawal. Consistent with this cell culture study, in vivo treatment with METH, which was associated with behavioral sensitization, caused a PKC-dependent astrocytic activation in the cingulate cortex and nucleus accumbens of mice. These findings provide direct evidence that METH induces a long-lasting astrocytic activation and behavioral sensitization through the stimulation of PKC in the rodent brain. In contrast, MRP produced a reversible activation of astrocytes via neuronal PKC and a reversibility of behavioral sensitization. This information can break through the definition of drugs of abuse and the misleading of concept that morphine produces a long-lasting neurotoxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.2005.03097.x
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  • 5
    Electronic Resource
    Electronic Resource
    Mechanisms underlying extracellular ATP-evoked interleukin-6 release in mouse microglial cell line, MG-5 (2001)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 78 (2001), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Microglia play various important roles in the CNS via the synthesis of cytokines. The ATP-evoked production of interleukin-6 (IL-6) and its intracellular signals were examined using a mouse microglial cell line, MG-5. ATP, but not its metabolites, produced IL-6 in a concentration-dependent manner. Although ATP activated two mitogen-activated protein kinases, i.e. p38 and extracellular signal-regulated protein kinase, only p38 was involved in the IL-6 induction. However, the activation of p38 was not sufficient for the IL-6 induction because 2′- and 3′-O-(4-benzoylbenzoyl) ATP, an agonist to P2X7 receptors, failed to produce IL-6 despite the fact that it activated p38. Unlike in other cytokines in microglial cells, P2Y rather than P2X7 receptors seem to have a major role in the IL-6 production by the cells. The ATP-evoked IL-6 production was attenuated by Gö6976, an inhibitor of Ca2+-dependent protein kinase C (PKC). The P2Y receptor responsible for these responses was insensitive to pertussis toxin (PTX) and was linked to phospholipase C. Taken together, ATP acting on PTX-insensitive P2Y receptors activates p38 and Ca2+-dependent PKC, thereby resulting in the mRNA expression and release of IL-6 in MG-5. This is a novel pathway for the induction of cytokines in microglia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2001.00514.x
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  • 6
    Electronic Resource
    Electronic Resource
    Extracellular ATP Triggers Tumor Necrosis Factor-α Release from Rat Microglia (2000)
    Oxford UK : Blackwell Science Ltd.
    Journal of neurochemistry 75 (2000), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Brain microglia are a major source of inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), which have been implicated in the progression of neurodegenerative diseases. Recently, microglia were revealed to be highly responsive to ATP, which is released from nerve terminals, activated immune cells, or damaged cells. It is not clear, however, whether released ATP can regulate TNF-α secretion from microglia. Here we demonstrate that ATP potently stimulates TNF-α release, resulting from TNF-α mRNA expression in rat cultured brain microglia. The TNF-α release was maximally elicited by 1 mM ATP and also induced by a P2X7 receptor-selective agonist, 2′- and 3′-O-(4-benzoylbenzoyl)adenosine 5′-triphosphate, suggesting the involvement of P2X7 receptor. ATP-induced TNF-α release was Ca2+-dependent, and a sustained Ca2+ influx correlated with the TNF-α release in ATP-stimulated microglia. ATP-induced TNF-α release was inhibited by PD 098059, an inhibitor of extracellular signal-regulated protein kinase (ERK) kinase 1 (MEK1), which activates ERK, and also by SB 203580, an inhibitor of p38 mitogen-activated protein kinase. ATP rapidly activated both ERK and p38 even in the absence of extracellular Ca2+. These results indicate that extracellular ATP triggers TNF-α release in rat microglia via a P2 receptor, likely to be the P2X7 subtype, by a mechanism that is dependent on both the sustained Ca2+ influx and ERK/p38 cascade, regulated independently of Ca2+ influx.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2000.0750965.x
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  • 7
    Electronic Resource
    Electronic Resource
    Downregulation of P2X3 receptor-dependent sensory functions in A/J inbred mouse strain (2002)
    Oxford, UK : Blackwell Science, Ltd
    European journal of neuroscience 15 (2002), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: There is large variability in the various pain responses including those to tissue injury among inbred mouse strains. However, the determinant factors for the strain-specific differences remain unknown. The P2X3 sensory-specific ATP-gated channel has been implicated as a damage-sensing molecule that evokes a pain sensation by receiving endogenous ATP from injured tissue. In this study, to clarify the contribution of the sensory P2X3 signalling to strain-specific differences in tissue injury pain, we examined whether the P2X3-mediated in vivo and in vitro responses in dorsal root ganglion (DRG) neurons are changed in the A/J inbred mouse strain, which is known to be resistant to tissue injury pain caused by formalin. Here we found that A/J mice exhibited a low magnitude of nocifensive behaviour induced by the P2X agonist α,β-methylene ATP (αβmeATP) into the hindpaw compared with C57BL/6 J mice. This behaviour was blocked by P2X3 antisense oligodeoxynucleotides. The low magnitude of the in vivo pain sensation could be observed similarly in the in vitro response; the increase in the intracellular Ca2+ increase by αβmeATP in capsaicin-sensitive DRG neurons from A/J mice was significantly lower than that from C57BL/6 J mice. In A/J DRG neurons the P2X3 protein level was significantly lower compared with C57BL/6 J DRG neurons. The change in P2X3 protein was selective because P2X2 protein was expressed equally in both strains. The present study suggests that the downregulation of sensory P2X3 could be one of the molecular predispositions to low sensitivity to tissue injury pain in the A/J inbred mouse strain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.2002.01982.x
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  • 8
    Electronic Resource
    Electronic Resource
    Mechanisms underlying facilitation by dopamine of ATP-activated currents in rat pheochromocytoma cells (1993)
    Springer
    Pflügers Archiv 422 (1993), S. 458-464 
    Details
    ISSN: 1432-2013
    Keywords: ATP ; Ligand-gated channel ; Dopamine ; Whole-cell recording ; PC12 cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Mechanisms underlying facilitation by dopamine of extracellular adenosine 5′-triphosphate (ATP)-activated current were investigated in rat pheochromocytoma PC12 cells using the whole-cell voltage-clamp techniques. Dopamine (10 and 100 μM) augmented the peak amplitude of an inward current elicited by ATP (3–100 μM). The activation time course of the ATP-evoked current was accelerated by dopamine; the presence of 10 μM dopamine shifted the dependence of activation rate constants on the concentration of ATP toward a lower concentration range two fold. Dopamine also accelerated the inactivation and the deactivation, which was determined from the current decay upon washout of ATP. Intracellular mediators responsible for the dopamine-induced facilitation was estimated by loading various compounds in patch pipettes. Facilitation was not observed when K-252a (1 μM), a protein kinase inhibitor, was included in the intracellular solution. In addition, facilitation was also attenuated by intracellular adenosine 5′-O-(thiotriphosphate)tetralithium salt (ATPγS (1 mM) or α-β-methylene ATP (1 mM). Inclusion of adenosine 3′, 5′-cyclic monophosphate sodium salt (cAMP, 100 μM), guanosine 3′,5′-cyclic monophosphate sodium salt (cGMP, 100 μM), 12-O-tetradecanoylphorbol-13-acetate (TPA, 1 μM) or phorbol-12,13-dibutylate (1 μM) in the intracellular solution did not affect the facilitation. Guanonsine 5′-O-(thiotriphosphate)tetralithium salt (GTPγS, 500 μM) or guanosine 5′-O(2-thiodiphosphate)-trilithium salt (GDPβS, 500 μM) did not modify the facilitation either. The results suggest that dopamine augments the ATP-activated inward current by facilitating association of ATP to its binding site, and that the augmentation may be mediated through some protein kinase which is different from cyclic-nucleotide-dependent protein kinases or protein kinase C.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00375072
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  • 9
    Electronic Resource
    Electronic Resource
    Effects of ATP antagonists on purinoceptor-operated inward currents in rat phaeochromocytoma cells (1991)
    Springer
    Pflügers Archiv 418 (1991), S. 214-219 
    Details
    ISSN: 1432-2013
    Keywords: Adenosine triphosphate ; Purinoceptor ; Antagonist ; Non-specific cation channel ; Phaeochromocytoma cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of suramin, reactive blue 2 (RB2) and d-tubocurarine (d-TC) were investigated electrophysiologically to elucidate the mechanisms underlying their antagonism of P2 purinoceptor-mediated responses. All three compounds inhibited an adenosine triphosphate (ATP)-activated inward current in rat phaeochromocytoma PC12 cells in a concentration-dependent manner. The order of potency was RB2 〉 suramin 〉 d-TC. The inhibition induced by suramin or RB2 was reversible, whereas that induced by d-TC was not reversed after a 5-min rinse. The inactivation of the ATP-activated current was accelerated by d-TC but not by suramin or RB2. RB2 administered simultaneously with ATP exerted much weaker inhibition compared to that induced by prior administration, suggesting that RB2 is a slowly acting antagonist. This was not observed for suramin or d-TC. Suramin and RB2 caused a parallel shift in the concentration/response curve for the ATP-activated current. With d-TC the maximal response of ATP was decreased but the concentration producing half-maximal response was unchanged. The voltage dependency of the ATP-activated current showed less inward rectification in the presence of d-TC. Suramin or RB2 did not affect the voltage dependency. These results suggest that suramin and RB2 reversibly block binding of ATP to receptors, whereas d-TC blocks ion permeability through the ATP-activated channel.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00370517
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  • 10
    Electronic Resource
    Electronic Resource
    Facilitation by 5-hydroxytryptamine of ATP-activated current in rat pheochromocytoma cells (1994)
    Springer
    Pflügers Archiv 427 (1994), S. 492-499 
    Details
    ISSN: 1432-2013
    Keywords: ATP-activated channels ; 5-Hydroxytryptamine ; Dopamine ; PC12 cells ; Voltage-clamp
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of 5-hydroxytryptamine (5-HT) on an inward current activated by extracellular ATP were investigated in rat pheochromocytoma PC12 cells. Under whole-cell voltage-clamp conditions 5-HT (10 μM) reversibly enhanced the amplitude of the current activated by 30 μM ATP. The enhancement may not be due to an increase in the number of functional channels because the current activated by 300 μM ATP was not remarkably augmented compared with the current activated by 30 μM ATP. The current enhancement by 100 μM 5-HT was less obvious than that by 10 μM 5-HT. When the current kinetics were compared, activation of the ATP-evoked current was accelerated to the same extent by either 10 or 100 μM 5-HT, whereas deactivation was largely more accelerated by 100 μM 5-HT. Propranolol (10 μM), a 5-HT1 receptor antagonist, or LY53857 (10 μM), a 5-HT2 receptor antagonist, exerted an agonistic effect: the ATP-activated current was facilitated by these compounds. Metoclopramide (10 μM), a 5-HT3 receptor antagonist, neither facilitated the ATP-activated current, nor blocked the current facilitation by 5-HT. Guanosine 5′-O-(2-thiodiphosphate) (GDP[βS]) (2 mM), the non-hydrolysable analog of guanosine 5′-triphosphate (GTP), or K-252a (2 μM), a protein kinase inhibitor, did not affect the facilitation by 5-HT of the ATP-activated current when they were included in the intracellular solution. The ATP-activated current pre-facilitated by 10 μM dopamine was not enhanced by 10 μM 5-HT. Similarly, the pre-facilitation by 5-HT attenuated the current enhancement by dopamine. The results suggest that 5-HT facilitates the ATP-activated channels through receptors that are not readily classified into conventional subclasses of 5-HT receptors. The reciprocal masking between the current facilitation by 5-HT and that by dopamine, combined with their sensitivities to the compounds involved in the intracellular solution, indicates that the facilitation by 5-HT may share not all, but some, common cellular mechanism with that by dopamine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374266
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