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  • 1
    Electronic Resource
    Electronic Resource
    Pretreatment of Mouse Striatal Neurons in Primary Culture with 17β-Estradiol Enhances the Pertussis Toxin-Catalyzed ADP-Ribosylation of Gαo,i Protein Subunits (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 55 (1990), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Pretreatment of striatal neurons from mouse embryos in primary culture with 17β-estradiol (10−9M, 24 h) enhanced the ADP-ribosylation of Gαo,i proteins catalyzed by pertussis toxin (PTX). As estimated by quantitative ADP-ribosylation of Gαs with cholera toxin and immunoblot experiments using anti-Gαo and anti-Gβ sera, 17β-estradiol pretreatment did not modify the levels of the major GTP-binding protein (G protein) constituent subunits Gαs, Gαo, and Gβ. Thus, 17β-estradiol should induce a qualitative modification of these G proteins, perhaps by stabilizing the association of the heterotrimers Gαo,iβγ, which are the targets of PTX. Such a hypothesis is in agreement with observations indicating that 17β-estradiol both suppressed the D2 dopamine- and opiate receptor-induced inhibitions of adenylate cyclase activity and enhanced the positive coupling between biogenic amine receptors (D1 dopamine, β-adrenergic, and A2 adenosine) and adenylate cyclase. In addition, PTX pretreatment, which is known to uncouple receptors associated with Go,i proteins and thus to impair the dissociation of the heterotrimers Gαo,iβγ, mimicks the effects of the steroid on the responses of adenylate cyclase to inhibitory and stimulatory agonists. Finally, the chemical specificity of the steroids was the same in the ADP-ribosylation as in the adenylate cyclase experiments: Testosterone (10−9M) mimicked the effects of 17β-estradiol, whereas 17α-estradiol, progesterone, and dexamethasone did not. Because 17β-estradiol enhanced uniformly the PTX-catalyzed ADP-ribosylation of Gαo and Gαi proteins, it can be expected that transducing systems other than adenylate cyclase involving these G proteins, such as ionic channels or phospholipases, are also affected by the steroid pretreatment of striatal neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1990.tb03131.x
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  • 2
    Electronic Resource
    Electronic Resource
    A Nitric Oxide Synthase Activity Selectively Stimulated by NMDA Receptors Depends on Protein Kinase C Activation in Mouse Striatal Neurons (1992)
    Oxford, UK : Blackwell Publishing Ltd
    European journal of neuroscience 4 (1992), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In mouse striatal neurons in primary culture, the maximal increase in intracellular cyclic guanosine monophosphate level evoked by N-methyl-d -aspartic acid (NMDA) receptor activation was twice that induced by kainate, KCI and ionomycin. Quisqualate was almost inactive. All responses were mediated by nitric oxide (NO) production since they were blocked by haemoglobin (a NO scavenger) and by L-NG-monomethylarginine and L-NG nitroarginine, the effects of both arginine analogues being reversed by an excess of L-arginine. Several results indicate that NMDA receptors stimulate a specific NO synthase activity. This specifically NMDA-activated NO synthase was blocked by nanomolar concentrations of L-NG nitroarginine, whereas the responses evoked by other agents, including kainate, KCI and ionomycin, were only blocked by micromolar concentrations of this NO synthase inhibitor. The NMDA response could not be totally reproduced by an increase in cytosolic calcium (Ca2+) alone. In contrast, in the presence of staurosporine, an inhibitor of protein kinases C (PKC), as well as after desensitization of PKC induced by long-term treatment with the phorbol ester, phorbol-12, 13-dibutyrate, NMDA-stimulated NO production was selectively reduced, reaching the level evoked by kainate or Ca2+ increase. In conclusion, our results suggest that in striatal neurons, NMDA selectively stimulates a NO synthase activity which is inhibited by low concentrations of L-NG nitroarginine, through a mechanism involving PKC.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.1992.tb00892.x
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  • 3
    Electronic Resource
    Electronic Resource
    Activation of a Large-conductance Ca2+-Dependent K+ Channel by Stimulation of Glutamate Phosphoinositide-coupled Receptors in Cultured Cerebellar Granule Cells (1991)
    Oxford, UK : Blackwell Publishing Ltd
    European journal of neuroscience 3 (1991), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Trans-1-amino-cyclopentyl-1,3-dicarboxylic acid (trans-ACPD), a specific agonist of the glutamate phosphoinositide-coupled receptor (Qp receptor), increased the amplitude of the outward K+ current recorded in the whole-cell configuration of the patch-clamp technique in mouse cultured cerebellar granule cells. This effect was abolished by buffering internal Ca2+ with BAPTA [1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid]. Activation of a large-conductance K+ channel was observed when trans-ACPD or quisqualic acid (QA), another Qp receptor agonist, was applied outside the cell-attached patch pipettes. No activation was observed with alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), a specific agonist of ionotropic non-N-methyl-d-aspartate (non-NMDA) receptors. The effects of trans-ACPD or QA were potentiated in the presence of external Ca2+. The channel was also directly activated by both micromolar concentrations of internal Ca2+ and membrane depolarization. Its unitary conductance was 100–115 pS under asymmetrical K+ and 195–235 pS under high symmetrical K+ conditions. In the absence of agonist, the channel was blocked by 1 mM external tetraethylammonium. This is the first description of a large conductance Ca2+-activated K+ channel in cultured cerebellar granule cells. It possesses properties similar to those of the so-called ‘big K+ channel’ described in other preparations. Our cell-attached experiments demonstrated an indirect coupling between Qp receptors and this channel. The most likely hypothesis is that the second messenger system inositol 1,4,5-triphosphate (IP3)-Ca2+ was involved in the coupling process. This hypothesis was further strengthened by our whole-cell experiments. On the basis of the voltage- and Ca2+-sensitivities of the studied channel, we estimated an increase of 350 to 570 nM in internal Ca2+ concentration when Qp receptors were stimulated by 100 μM trans-ACPD. Under physiological conditions, stimulation of Qp receptors by the endogenous neurotransmitter should lead to similar K+ channel activation and therefore would tend to reduce the efficacy of ionotropic glutamate synaptic receptor stimulation responsible for cell excitation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.1991.tb01674.x
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  • 4
    Electronic Resource
    Electronic Resource
    Insulin releasing effects of mastoparan and amphiphilic substance P receptor antagonists on RINm5F insulinoma cells (1992)
    Springer
    Molecular and cellular biochemistry 109 (1992), S. 133-138 
    Details
    ISSN: 1573-4919
    Keywords: insulin secretion ; mastoparan ; G-proteins ; amphiphilic drugs ; RINm5F cells ; substance P
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract It has been proposed that mastoparan (INLKALAALAKKIL) and other mast cell secretagogues such as substance P (SP) or compound 48/80 act by direct activation of the pertussis toxin (PTX)-sensitive G-proteins in intact cells. Here we have investigated whether or not the antagonists of SP, [D-Trp7, 9, 10] SP1-11 and [D-Trp7, 9, 10, N-leu11] SP1-11, can similarly induce exocytosis from RINm5F cells. In intact cells mastoparan and the SP antagonists stimulated insulin release in a dose-dependent manner at concentrations ranging from 10 to 100 µM. The maximal effect on insulin release, of both mastoparan and the SP antagonists was comparable to that obtained with 100 µM forskolin. Pretreatment of the intact cells, for 18 h with PTX or 6 h with cholera toxin, did not change the responses induced by both mastoparan and the SP antagonists. This absence of PTX effect, despite the fact that the three PTX substrates at 41, 40 and 39 kDa were ADP ribosylated after pretreatment suggests intrinsic differences between mast and RINm5F cells. Thus the SP antagonists behave similarly to mastoparan in its ability to induce insulin release in RINm5F cells. However, the higher concentrations required with RINm5F cells compared to that needed for mast cells suggest differences either in G-proteins composition or in the phospholipid composition of the membranes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00229767
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  • 5
    Electronic Resource
    Electronic Resource
    Azabicycloalkyl benzimidazolone derivatives as a novel class of potent agonists at the 5-HT4 receptor positively coupled to adenylate cyclase in braina (1991)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 343 (1991), S. 245-251 
    Details
    ISSN: 1432-1912
    Keywords: 5-HT4 receptor ; Azabicycloalkyl benzimidazolone ; cAMP stimulation ; Colliculi neurons
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recent experimental evidence indicates that central 5-HT4 receptors which are positively coupled to adenylate cyclase, are stimulated by a family of 2-methoxy-4-amino-5-chloro substituted benzamide derivatives. These compounds are also potent stimulants of the gastro-intestinal motility. In this study the ability of three azabicycloalkyl benzimidazolone derivatives, BIMU 1, BIMU 8, and DAU 6215 (structural formulas are given in the text), to stimulate cAMP formation in colliculi neurons in primary culture have been tested. Two of the compounds, BIMU 1 and BIMU 8, which show prokinetic activity in various animal models, were also good agonists at the 5-HT4 receptors, whereas DAU 6215, a drug devoid of prokinetic activity, was only a weak, partial agonist at 5-HT4 receptors. The rank order of their potencies as compared with those of 5-HT and cisapride was as follows: BIMU 8 = cisapride 〉 5-HT 〉 BIMU 1 〉 DAU 6215. The efficacies of BIMU 8 and cisapride were comparable (133 ± 9% and 124 ± 8% of the maximal 5-HT efficacy, respectively), whereas BIMU 1 and DAU 6215 elicited, respectively, only 72 ± 11 % and 16 ± 4% of the maximal 5-HT effect. The activities of the azabicycloalkyl benzimidazolone derivatives and 5-HT on cAMP formation were not additive and ICS 205–930 antagonized the stimulatory effect of these compounds with low potency (pKi = 6.1–6.4), further strengthening the notion of interaction with 5-HT4 receptors. In addition, cross desensitization between the effects of 5-HT and the azabicycloalkyl benzimidazolones on adenylate cyclase was noted, another argument in favor of an interaction of these drugs on 5-HT4 receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00251122
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  • 6
    Electronic Resource
    Electronic Resource
    Characterization of a novel 5-HT4 receptor antagonist of the azabicycloalkyl benzimidazolone class: DAU 6285 (1992)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 345 (1992), S. 264-269 
    Details
    ISSN: 1432-1912
    Keywords: 5-HT4 receptor antagonist ; 5-HT3 receptor antagonist ; Azabicycloalkyl benzimidazolone derivatives
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Three chemical classes of serotonin 5-HT4 receptor agonists have been identified so far: 5-substituted indoles (e.g. 5-HT), benzamides (e.g. renzapride) and benzimidazolones (e.g. BIMU 8). In a search for 5-HT4 receptor antagonists, we have discovered that the benzimidazolone derivative DAU 6285 (for structure see text), is 3–5 times more potent than tropisetron in blocking 5-HT, renzapride and BIMU 8 induced stimulation of adenylate cyclase activity in mouse embryo colliculi neurons. Schild plot analysis yielded Ki values of 220, 181 and 255 nmol/l, respectively. In addition, DAU 6285 showed poor activity as a 5-HT3 receptor ligand with respect to tropisetron, as demonstrated by in vitro binding studies (Ki, 322 vs 2.8 nmol/l) and by its antagonistic activity in the Bezold-Jarisch reflex test (ID50, 231 vs 0.5 μg/kg, i.v.). No significant binding (Ki〉10 μmol/l) of DAU 6285 to serotonergic 5-HT1A, 5-HT1B, 5-HT1C, 5-HT1D, and 5-HT2 receptors as well as to adrenergic α1, α2, dopaminergic D1, D2 or muscarinic M1–M3 receptor subtypes was found. The data indicate that DAU 6285 has a somewhat higher affinity than tropisetron for 5-HT4 receptors, a property confirmed in functional tests, and much lower affinity than tropisetron for 5-HT3 receptors. The compound represents a new interesting tool for investigating the pharmacological and physiological properties of 5-HT4 receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168685
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  • 7
    Electronic Resource
    Electronic Resource
    Inhibitory effects of dihydropyridines on macroscopic K+ currents and on the large-conductance Ca2+-activated K+ channel in cultured cerebellar granule cells (1994)
    Springer
    Pflügers Archiv 429 (1994), S. 176-182 
    Details
    ISSN: 1432-2013
    Keywords: Cerebellum ; Potassium channels ; Dihydropyridines ; Mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In cultured cerebellar granule cells, we examined the effects of dihydropyridines (DHPs) on K+ currents, using the whole-cell recording configuration of the patch-clamp technique and on Ca2+-activated K+ channels (“maxi K+ channels”) using outside-out patches. We found that micromolar concentrations of nicardipine, nifedipine, (+) and (−) BAY K 8644, nitrendipine, nisoldipine and (−) nimodipine block 10–60% of macroscopic K+ currents. The most potent of these DHPs was nicardipine and the least potent, (−) BAY K 8644. (+) Nimodipine had no effect on this current. The inhibitory effects of nifedipine and nicardipine were not additive with those of 1 mM tetraethylammonium (TEA). Outside-out recordings of “maxi K+ channels” showed a main conductance of 200 pS (in 77% of the patches) and two subconductance states (in 23% of the patches). Neither nifedipine nor nicardipine affected the main conductance, but decreased the values of the subconductance levels. In 10% of these patches, nicardipine induced a flickering activity of the channel. These findings show that both Ca2+ and K+ channels have DHP-sensitive sites, suggesting similarity in electrostatic binding properties of these channels. Furthermore, cerebellar granule cells may express different subtypes of “maxi K+ channels” having different sensitivities to DHPs. These drugs may provide new tools for the molecular study of K+ channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374310
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