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  • 1
    Electronic Resource
    Electronic Resource
    Characterization of P2X3, P2Y1 and P2Y4 receptors in cultured HEK293-hP2X3 cells and their inhibition by ethanol and trichloroethanol (2003)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 85 (2003), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Membrane currents and changes in the intracellular Ca2+ concentration ([Ca2+]i) were measured in HEK293 cells transfected with the human P2X3 receptor (HEK293-hP2X3). RT-PCR and immunocytochemistry indicated the additional presence of endogenous P2Y1 and to some extent P2Y4 receptors. P2 receptor agonists induced inward currents in HEK293-hP2X3 cells with the rank order of potency α,β-meATP ≈ ATP 〉 ADP-β-S 〉 UTP. A comparable rise in [Ca2+]i was observed after the slow superfusion of ATP, ADP-β-S and UTP; α,β-meATP was ineffective. These data, in conjunction with results obtained by using the P2 receptor antagonists TNP-ATP, PPADS and MRS2179 indicate that the current response to α,β-meATP is due to P2X3 receptor activation, while the ATP-induced rise in [Ca2+]i is evoked by P2Y1 and P2Y4 receptor activation. TCE depressed the α,β-meATP current in a manner compatible with a non-competitive antagonism. The ATP-induced increase of [Ca2+]i was much less sensitive to the inhibitory effect of TCE than the current response to α,β-meATP. The present study indicates that in HEK293-hP2X3 cells, TCE, but not ethanol, potently inhibits ligand-gated P2X3 receptors and, in addition, moderately interferes with G protein-coupled P2Y1 and P2Y4 receptors. Such an effect may be relevant for the interruption of pain transmission in dorsal root ganglion neurons following ingestion of chloral hydrate or trichloroethylene.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2003.01716.x
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  • 2
    Electronic Resource
    Electronic Resource
    Muscarine Receptors Regulating Electrically Evoked Release of Acetylcholine in Hippocampus Are Linked to Pertussis Toxin-Sensitive G Proteins but Not to Adenylate Cyclase (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 61 (1993), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: [3H]Acetylcholine release elicited with 360 pulses/3 Hz from slices of rabbit hippocampus is facilitated in the presence of the muscarine (M) receptor antagonist atropine (indicating the existence of autoinhibition) and diminished by the M receptor agonists carbachol and oxotremorine. W-Ethylmaleimide (30 μM) and pertussis toxin (8 μg/ml) counteracted antagonist-induced facilitation and agonist-induced inhibition of release, suggesting that a pertussis toxin-sensitive GTP-binding protein is involved in the chain of events mediating activation of M receptors to inhibition of release. Neither 8-bromo-cyclic AMP (300 μM), a membrane analogue of cyclic AMP, nor rolipram (10 μM), a phosphodiesterase inhibitor, affected electrically evoked release of [3H]acetylcholine. They also did not influence the oxotremorine-induced inhibition of transmitter release. In conclusion, no evidence was found for the assumption that activation of M autoreceptors is linked to inhibition of adenylate cyclase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1993.tb03618.x
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  • 3
    Electronic Resource
    Electronic Resource
    Presynaptic K-Opioid Receptors on Noradrenergic Nerve Terminals Couple to G Proteins and Interact with the α2-Adrenoceptors (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Stimulation-induced noradrenaline (MA) release in rabbit hippocampus is inhibited by activation qf presynaptic α2-adrenoceptors and k-opioid receptors. The purpose of the present study was to investigate (a) an interference between the α2- and k-mechanisms, and (b) a coupling of the opioid receptors to pertussis toxin (PT)-sensitive guanine nucleotide-binding proteins (G proteins), as has been previously shown for the α2-receptors. [3H]NA release from hippocampal slices was evoked by electrical field stimulation (360 pulses/3 Hz). Inhibition of stimulation-evoked NA release by the preferential K-receptor agonist ethylketocyclazocine (EKC) was increased in the presence of the α2-adrenoceptor antagonist yohimbine (0.1 or 1.0 μM). When autoinhibitionn was completely removed, EKC (1 μM) almost abolished transmitter release. Pretreatment of hippocampal tissue wiih either PT (8 μg/ml; 18 h) or N-ethylmaleimide (NEM) (30 μM; 30 min), which has been shown to alkylate PT substrates, diminished the EKC-produced inhibition of NA release. The K-mecha-nism was still impaired by these compounds when the α2- receptors were blocked with yohimbine. An effect of NEM on the active site of the K-receptor seems to be unlikely, because NEM diminished the EKC-induced inhibition of release irrespective of whether or not the opioid receptor was occupied by EKC during exposure to NEM. The present results suggest an interference of both α2- and k-opioid receptor-coupled signal transduction possibly through competition for a common pool of G proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb08561.x
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  • 4
    Electronic Resource
    Electronic Resource
    UTP evokes noradrenaline release from rat sympathetic neurons by activation of protein kinase C (2001)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 77 (2001), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The pathway involved in UTP-evoked noradrenaline release was investigated in cultures of rat superior cervical ganglia. Northern blots revealed an age-related increase in levels of mRNA for P2Y6 receptors in cultures obtained at postnatal days 1 and 5, respectively, but no change in transcripts for P2Y1 and P2Y2. Likewise, UTP-evoked overflow of previously incorporated [3H]noradrenaline was six-fold higher in neurons obtained at postanatal day 5. Various protein kinase C inhibitors diminished UTP-, but not electrically, induced tritium overflow by 〉 70%, as did down-regulation of protein kinase C by 24 h exposure to phorbol ester. β-Phorbol-12,13-dibutyrate and dioctanoylglycerol caused concentration-dependent increases in [3H] outflow of up to 6% of total radioactivity, and the secretagogue actions of these agents were reduced in the presence of protein kinase C inhibitors and in neurons pretreated with phorbol ester. Overflow evoked by dioctanoylglycerol was attenuated in the absence of extracellular Ca2+ and in the presence of tetrodotoxin or Cd2+. In addition to triggering tritium overflow, UTP reduced currents through muscarinic K+ channels which, however, were not affected by phorbol esters. This action of UTP was not altered by protein kinase C inhibitors. These results indicate that P2Y6 receptors mediate UTP-evoked noradrenaline release from rat sympathetic neurons via activation of protein kinase C, but not inhibition of KM channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2001.00290.x
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  • 5
    Electronic Resource
    Electronic Resource
    Regulatory Proteins in Presynaptic Function (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 604 (1990), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1990.tb32001.x
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  • 6
    Electronic Resource
    Electronic Resource
    A role for protein kinase C in the electrically evoked release of [3H]γ-aminobutyric acid in rabbit caudate nucleus (1989)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 339 (1989), S. 302-305 
    Details
    ISSN: 1432-1912
    Keywords: GABA release ; Protein kinase C ; Phorbol esters ; Staurosporine ; Rabbit caudate nucleus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A possible participation of protein kinase C (PKC) in depolarization-induced release of γ-aminobutyric acid (GABA) in rabbit caudate nucleus was examined by means of phorbol esters and staurosporine. Slices of caudate nucleus were loaded with [3H]GABA, then superfused and stimulated electrically (3 ms, 5 Hz, 24 mA, 5 V/cm) for 2 min. Aminooxyacetic acid and the uptake inhibitor nipecotic acid were present throughout. The PKC activator 4β-phorbol 12,13-dibutyrate (4β-PDB) markedly enhanced the evoked [3H]GABA release. In contrast, its biologically inactive isomer, 4α-PDB, did not facilitate transmitter release. Staurosporine, an inhibitor of PKC, diminished [3H]GABA release and counteracted the effects caused by 4β-PDB. The above results suggest a participation of PKC in depolarization-induced GABA release in rabbit caudate nucleus. The mechanism underlying the modulation of GABA release by PKC seems to be independent of presynaptic GABA, dopamine and 5-hydroxytryptamine receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00173582
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  • 7
    Electronic Resource
    Electronic Resource
    Activation of dopamine D1 receptors does not affect D2 receptor-mediated inhibition of acetylcholine release in rabbit striatum (1992)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 345 (1992), S. 16-20 
    Details
    ISSN: 1432-1912
    Keywords: Evoked acetylcholine release ; Single pulse stimulation ; Dopamine D1 receptors ; Presynaptic dopamine D2 receptors ; Rabbit caudate nucleus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possible involvement of dopamine D1 receptors in the regulation of acetylcholine release in the rabbit caudate nucleus was investigated. Caudate slices, preincubated with [3H]choline, were superfused continuously and subjected to electrical field stimulation with only a single pulse. In agreement with the view that the release of acetylcholine evoked by a single electrical pulse is not influenced by endogenous transmitters, atropine and domperidone failed to icnrease the evoked release of [3H]acetylcholine, whereas oxotremorine and quinpirole caused a concentration-dependent inhibition of transmitter release. Neither the dopamine D1 receptor antagonist SCH 23390 nor the Dt agonist SKF 38393 in a concentration range of 0.01–1 μmol/l changed the evoked [3H]acetylcholine release. The inhibitory effect of the dopamine D2 receptor agonist quinpirole was virtually abolished in the presence of 0.1 μmol/l domperidone and diminished in the presence of 1 μmol/l SCH 23390. It remained unchanged in the presence of 1 μmol/l SKF 38393. It is concluded that the inhibition of acetylcholine release by dopamine is mediated exclusively via presynaptic dopamine D2 receptors and that the antagonistic effect of SCH 23390 on the inhibition of acetylcholine release by quinpirole is due to its interaction with dopamine D2 rather than D1 receptors located on cholinergic nerve terminals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00175463
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  • 8
    Electronic Resource
    Electronic Resource
    N-ethylmaleimide (NEM) diminishes α2-adrenoceptor mediated effects on noradrenaline release (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 333 (1986), S. 104-109 
    Details
    ISSN: 1432-1912
    Keywords: N-ethylmaleimide ; α2-Adrenoceptor ; Noradrenaline release ; Rabbit hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of N-ethylmaleimide (NEM), which has been shown to abolish rather selectively inhibition of adenylate cyclase, on the α2-adrenoceptor modulation of noradrenaline release was studied. Slices of the rabbit hippocampus were loaded with 3H-noradrenaline, superfused continuously and stimulated twice electrically. NEM (30 μmol/l) applied for 30 min enhanced both basal and stimulation-evoked tritium overflow significantly. Occupation of the receptor by the α2-adrenoceptor agonist clonidine prior to and during NEM treatment did not protect the α2-adrenoceptor-mediated autoinhibitory feedback system from being affected by NEM. Preincubation of the hippocampal slices with NEM was without any influence on 3H-noradrenaline uptake. The inhibitory effect of clonidine on 3H-noradrenaline release was attenuated in a non-competitive manner. In addition, the facilitatory effect of the α2-adrenoceptor antagonist yohimbine on the stimulusevoked tritium overflow was reduced. The facilitation of the evoked noradrenaline release by yohimbine or yohimbine and NEM converged with increasing concentrations of yohimbine, suggesting that yohimbine and NEM were acting at the same signal-transduction system. These results are compatible with the idea that NEM, by alkylating the Ni-unit of a presynaptically located adenylate cyclase, prevents the α2-adrenoceptor-mediated modulation of noradrenaline release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00506511
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  • 9
    Electronic Resource
    Electronic Resource
    Cultured chick sympathetic neurons: ATP-induced noradrenaline release and its blockade by nicotinic receptor antagonists (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 25-30 
    Details
    ISSN: 1432-1912
    Keywords: Noradrenaline release ; P2-purinoceptors ; Adenine nucleotides ; Suramin ; Reactive blue 2 ; Nicotinic receptors ; Nicotinic receptor antagonists ; Cultured sympathetic neurons
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The ATP-induced increase in tritium outflow from cultured chick sympathetic neurons prelabelled with [3H]-noradrenaline was investigated. Seven days-old dissociated cell cultures of embryonic paravertebral ganglia, loaded with [3H]-noradrenaline (0.05 μM), were superfused in the presence of (+)-oxaprotiline and exposed to ATP, ATP-analogues, or 1,1-dimethyl-4-piperazinium (DMPP) for 2 min. ATP (3 μLM-3 mM), 2-methylthio-ATP (3–100 μM), as well as DMPP (10 and 100 μM) induced a significant overflow of tritium. The EC50-value of ATP was 20 μM. Both the ATP-induced and the DMPP-induced tritium overflow was Ca2+-dependent and sensitive to tetrodotoxin (0.3 μM) and ω-conotoxin (0.1 μM); in addition, it was inhibited by the α2-adrenoceptor agonist 5-bromo-6-(2-imidazoline-2-ylamino)-quinoxaline (UK-14,304; 1 μM). The effects of ATP and DMPP were not additive. The ATP-induced as well as the DMPP-induced overflow of tritium was diminished by the P2-purinoceptor antagonists suramin (300 μM) and reactive blue 2 (3 μM); in all 4 cases, the inhibition amouted to approximately 40%. The tritium overflow induced by ATP or DMPP was almost abolished by the nicotinic receptor antagonist mecamylamine (10 μM) and markedly inhibited by hexamethonium (100 μM). Neither ATP nor electrical stimulation caused an overflow of tritium from cultures loaded with [3H]-choline. The results suggest that ATP at μmolar concentrations induces noradrenaline release from cultured chick sympathetic neurons via an action on a subclass of the nicotinic cholinoceptor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169186
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  • 10
    Electronic Resource
    Electronic Resource
    Cultured chick sympathetic neurons: modulation of electrically evoked noradrenaline release by P2-purinoceptors (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 17-24 
    Details
    ISSN: 1432-1912
    Keywords: Noradrenaline release ; Cultured sympathetic neurons ; Regulatory P2-purinoceptors ; Adenine nucleotides ; 2-Methylthio-ATP ; Suramin ; Reactive blue 2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study investigates the pharmacological profile of P2-purinoceptors modulating noradrenaline release from cultured chick sympathetic neurons. ATP (30 μM-3 mM) and 2-methylthio-ATP (3–100 μM), but not α,β-methylene-ATP (up to 100 μM), caused a significant facilitation of electrically evoked [3H]-noradrenaline release when added 2 min before depolarization. The facilitation declined with time of exposure suggesting receptor desensitization. The facilitatory effect was markedly diminished by the P2-purinoceptor antagonists reactive blue 2 (3 μM) and suramin (300 μM), but not changed by mecamylamine (10 μM), a nicotinic receptor antagonist. At 1 mM and higher concentrations, ATP added for 12 min, inhibited noradrenaline release; release was virtually abolished by 6 mM ATP. The inhibitory effect of ATP was slightly diminished by suramin but not affected by reactive blue 2. Electrically evoked [3H]-noradrenaline release remained unaffected in the presence of the adenosine (P1)-receptor agonists R(−)N6-(2-phenylisopropyl)adenosine (R-PIA), 2-[p-(2-carboxyethyl)phenylethylamino]5′-N-ethylcarboxamidoadenosine (CGS-21680), 5′-N-ethylcarboxamidoadenosine (NECA), and N6-2-(4-aminophenyl)ethyladenosine (APNEA), used up to 1 μM. The present results confirm the existence of two P2-purinoceptors affecting noradrenaline release: 1) a facilitatory receptor which is activated by 2-methyl thio-ATP as well as ATP, and blocked by suramin as well as reactive blue 2, and 2) an inhibitory receptor which is activated by ATP, only slightly affected by suramin but not at all by reactive blue 2 and does not belong to the established P2-purinoceptor subtypes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169185
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