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  • 1
    Electronic Resource
    Electronic Resource
    The new neurokinin 1-sensitive receptor mediates the facilitation by endogenous tachykinins of the NMDA-evoked release of acetylcholine after suppression of dopaminergic transmission in the matrix of the rat striatum (2003)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 87 (2003), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Using an in vitro microsuperfusion procedure, the NMDA-evoked release of [3H]ACh was studied after suppression of dopamine (DA) transmission (α-methyl-p-tyrosine) in striatal compartments of the rat. The effects of tachykinin neurokinin 1 (NK1) receptor antagonists and the ability of appropriate agonists to counteract the antagonist responses were investigated to determine whether tachykinin NK1 classic, septide-sensitive and/or new NK1-sensitive receptors mediate these regulations. The NK1 antagonists, SR140333, SSR240600, GR205171 but not GR82334 and RP67580 (0.1 and 1 µm) markedly reduced the NMDA (1 mm + d-serine 10 µm)-evoked release of [3H]ACh only in the matrix. These responses unchanged by coapplication with NMDA of NK2 or NK3 agonists, [Lys5,MeLeu9,Nle10]NKA(4–10) or senktide, respectively, were completely counteracted by the selective NK1 agonist, [Pro9]substance P but also by neurokinin A and neuropeptide K (1 nm each). According to the rank order of potency of agonists for counteracting the antagonist responses ([Pro9]substance P, 0.013 nm 〉 neurokinin A, 0.15 nm ≫ substance P(6–11) 7.7 nm = septide 8.7 nm), the new NK1-sensitive receptors mediate the facilitation by endogenous tachykinins of the NMDA-evoked release of ACh in the matrix, after suppression of DA transmission. Solely the NK1 antagonists having a high affinity for these receptors could be used as indirect anti-cholinergic agents.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2003.02010.x
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  • 2
    Electronic Resource
    Electronic Resource
    Functional mu opioid receptors are expressed in cholinergic interneurons of the rat dorsal striatum: territorial specificity and diurnal variation (2005)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 21 (2005), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Striatal cholinergic interneurons play a crucial role in the control of movement as well as in motivational and learning aspects of behaviour. Neuropeptides regulate striatal cholinergic transmission and particularly activation of mu opioid receptor (MOR) inhibits acetylcholine (ACh) release in the dorsal striatum. In the present study we investigated whether this cholinergic transmission could be modulated by an enkephalin/MOR direct process. We show that mRNA and protein of MORs are expressed by cholinergic interneurons in the limbic/prefrontal territory but not by those in the sensorimotor territory of the dorsal striatum. These MORs are functional because potassium-evoked release of ACh from striatal synaptosomes was dose-dependently reduced by a selective MOR agonist, this effect being suppressed by a MOR antagonist. The MOR regulation of cholinergic interneurons presented a diurnal variation. (i) The percentage of cholinergic interneurons containing MORs that was 32% at the beginning of the light period (morning) increased to 80% in the afternoon. (ii) The MOR-mediated inhibition of synaptosomal ACh release was higher in the afternoon than in the morning. (iii) While preproenkephalin mRNA levels remained stable, enkephalin tissue content was the lowest (−32%) in the afternoon when the spontaneous (+35%) and the N-methyl-d-aspartate-evoked (+140%) releases of enkephalin (from microsuperfused slices) were the highest. Therefore, by acting on MORs present on cholinergic interneurons, endogenously released enkephalin reduces ACh release. This direct enkephalin/MOR regulation of cholinergic transmission that operates only in the limbic/prefrontal territory of the dorsal striatum might contribute to information processing in fronto-cortico-basal ganglia circuits.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.2005.04154.x
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  • 3
    Electronic Resource
    Electronic Resource
    Developmental pattern of cyclic guanosine monophosphate production stimulated by atrial natriuretic peptide in glomeruli microdissected from kidneys of young rats (1990)
    Springer
    Pflügers Archiv 416 (1990), S. 519-525 
    Details
    ISSN: 1432-2013
    Keywords: Microdissection ; Glomeruli ; Cyclic guanosine monophosphate ; Atrial natriuretic peptide ; Carbamyl choline ; Sodium nitroprusside ; Ontogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cyclic guanosine monophosphate (GMP) productions by alpha rat atrial natriuretic peptide 1–28 (α-rANP), carbamylcholine or sodium nitroprusside were assessed in isolated glomeruli microdissected from collagenase-treated kidneys of 2- to 34-day-old and adult rats. In both young and adult animals, α-rANP-stimulated cyclic GMP generation was proportional to the number of glomeruli and was enhanced in a dose-dependent and saturable fashion with increasing α-rANP concentrations. The apparent activation constant values were 6.4 nM for 5-day-old and 9.7 nM for adult rats. Maximal doses of either α-rANP or rANP 5–28 elicited similar responses in young and adult animals. Clear differences appeared between the developmental patterns of cyclic GMP productions stimulated by either α-rANP, carbamylcholine or sodium nitroprusside. The response to α-rANP was very large in the youngest rats tested, declined sharply during the suckling period and represented about 1.6 times the adult control level in 34-day-old rats. In contrast, the response to carbamylcholine was low after birth and rose progressively with age up to the adult level at the end of the weaning period, and the response to nitroprusside seemed to be independent of the animal's age.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00382684
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of prostaglandin E2 on agonist-stimulated cAMP accumulation in the distal convoluted tubule isolated from the rabbit kidney (1993)
    Springer
    Pflügers Archiv 422 (1993), S. 577-584 
    Details
    ISSN: 1432-2013
    Keywords: Rabbit kidney ; Microdissected distal convoluted tubule ; cAMP accumulation ; Prostaglandin E2 ; Calcitonin ; Vasoactive intestinal peptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of calcitonin, vasoactive intestinal peptide (VIP), parathyroid hormone (PTH) and isoprenaline on intracellular cAMP accumulation were determined in the distal tubule (DCT) microdissected from collagenase-treated rabbit kidney. In DCTb (the initial “bright” portion) calcitonin (10 ng/ml) elicited a highly reproducible response 203.7±19.1 fmol cAMP mm−1 4 min−1 (SE, N=13) whereas VIP-induced cAMP accumulation was less and more variable from one experiment to another (1 μM, 97.2±17.8 fmol mm−1 4 min−1, SE, N=12). When used in combination, these two agonists were non-additive, indicating stimulation of a single pool of cAMP in DCTb. In DCTg, (“granular”) which consists of at least two cell types, PTH (100 nM) elicited a marked, reproducible accumulation of cAMP (154.3±27.0 fmol mm−1 4 min−1; SE, N=5). Isoprenaline (1 μM) and VIP (1 μM) induced much smaller increases in cAMP levels 20.9±2.7 and 29.4±4.1 fmol mm−1 4 min−1 (SE, N=5) respectively, and, when used in combination, were non-additive, demonstrating that VIP and isoprenaline are active on the same cell type. In DCTb, prostaglandin E2 (PGE2) inhibited both calcitoninand VIP-stimulated cAMP accumulation (calcitonin 57.8±2.7% inhibition, SE, N=16; VIP, 80.6±2.1% inhibition, SE, N=5). The EC50 values for calcitonin were 1.21±0.33 ng/ml and 1.83±0.25 ng/ ml (SD, N=3) in the absence and presence of PGE2 (300 nM) respectively with an IC50 for PGE2 of 26.3±6.3 nM (SE, N=4). In contrast, no effects of PGE2 were seen in DCTg vis à vis PTH, isoprenaline or VIP. The percentage inhibition of calcitonin-stimulated cAMP accumulation by PGE2 was of the same order in the presence of isobutylmethylxanthine (an inhibitor of all types of phosphodiesterase), Ro 20-1724 (inhibitor of low-K m cAMP-specific phosphodiesterase) or in the absence of inhibitor. Preincubation of DCTb with pertussis toxin for up to 8 h in different experimental conditions did not relieve the inhibition by PGE2. Protein kinase C activation by phorbol ester did not attenuate calcitonin responses. These data demonstrate that the inhibition by PGE2 of cAMP production is restricted to the initial portion (DCTb) of the distal convoluted tubule and is effective on both calcitonin and VIP responses. When tested in the presence of Ro 20-1724, ionomycin, A1-adenosine, α2-adrenergic and muscarinic agonists were without effect on calcitoninand PTH-stimulated cAMP accumulation in DCTb and DCTg respectively.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374005
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  • 5
    Electronic Resource
    Electronic Resource
    PGE2-induced inhibition of AVP-dependent cAMP accumulation in the OMCD of the rat kidney is cumulative with respect to the effects of α2-adrenergic and A1-adenosine agonists, insensitive to pertussis toxin and dependent on extracellular calcium (1993)
    Springer
    Pflügers Archiv 423 (1993), S. 397-405 
    Details
    ISSN: 1432-2013
    Keywords: Rat medullary collecting tubule ; cAMP accumulation ; Arginine vasopressin ; PGE2 ; Cumulative inhibition ; Pertussis toxin ; Intracellular calcium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The accumulation of cyclic adenosine 3′,5′-phosphate (cAMP) elicited by antidiuretic hormone (arginine vasopressin, AVP) in the medullary collecting tubule (OMCD) microdissected from the rat kidney is inhibited by different factors: the A1 agonist of adenosine (-)-N 6-(R-phenylisopropyl) adenosine (PIA), an α 2-adrenergic agonist clonidine (CLO), and prostaglandin E2 (PGE2). The negative regulation elicited by PGE2 was further characterized by measuring summation of inhibition with other inhibitors, by testing the effect of pertussis toxin and by studying the part played by extracellular calcium. Inhibitors were used at concentrations inducing maximum effects. The simultaneous addition of 0.3 μM PGE2 with either 0.1 μM PIA or 1 μM CLO led to an inhibition of the response to AVP (80.0±3.5%, SEM, N=7 and 92.6±0.8%, N=5, respectively) greater than those elicited by each agent alone. In contrast, PIA and CLO added together induced an inhibition similar to that due to CLO alone. The action of PGE2 in combination with either PIA or CLO corresponded to a partial summation fitting with the values calculated by assuming a cumulative inhibition. Preincubation of OMCD samples with pertussis toxin (100 ng/ml or 1 μg/ml) relieved the inhibitory effects of CLO and PIA but did not affect the action of PGE2. PGE2-induced inhibition was prevented in a calcium-free medium [0 Ca2++0.1 mM [ethylene-bis (oxyethylenenitrilo)] tetraacetate (EGTA)]: values were 67.0 ±2.1% and 5.8±8.7% (± SEM) in 2 mM Ca2+ and 0 Ca2+ medium, respectively, N=7. When applied to Fura-2-loaded OMCD, 0.3 μM PGE2 increased intracellular calcium concentration ([Ca2+]i) with a peak phase (in 2 mM or 0 Ca2+ medium) followed by a plateau phase (observed only in 2 mM Ca2+ medium). It is concluded that: (1) in the rat OMCD, PGE2, PIA and CLO act on the same AVP-sensitive cell, (2) PGE2 induces a cumulative inhibition on the cAMP level when combined with other inhibitors by a mechanism insensitive to pertussis toxin, (3) the presence of extracellular calcium is a prerequisite condition to observe PGE2-induced inhibition, and (4) the inhibition by PGE2 might be linked to its capacity of increasing [Ca2+]i.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374933
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  • 6
    Electronic Resource
    Electronic Resource
    The activation of protein kinase C prevents PGE2-induced inhibition of AVP-dependent cAMP accumulation in the rat outer medullary collecting tubule (1993)
    Springer
    Pflügers Archiv 425 (1993), S. 417-425 
    Details
    ISSN: 1432-2013
    Keywords: Rat kidney ; Outer medullary collecting tubule ; Protein kinase C activation ; cAMP accumulation ; Arginine vasopressin ; PGE2 ; α 2-Adrenergic agonist ; Intracellular calcium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previous studies have demonstrated that prostaglandin E2 (PGE2) inhibits arginine vasopressin-(AVP)dependent adenosine 3′,5′-cyclic monophosphate (cAMP) accumulation in microdissected rat outer medullary collecting tubules (OMCD), by a mechanism unrelated to the inhibition of cAMP synthesis. The potential role of the activation of protein kinase C (PKC) to explain the negative regulation elicited by PGE2 was investigated in this study. Single OMCD samples were pre-incubated (10 min, 30°C) in the presence or absence of either activators of PKC, phorbol 12-myristate 13-acetate (PMA), 1-oleoyl-2-acetyl-glycerol (OAG), dioctanoylglycerol (DOG) or an inhibitor of PKC, staurosporine (SSP). These compounds were present also with the agonists tested during the incubation period (4 min, 35°C). In contrast to PGE2, activators of PKC did not decrease AVP-dependent cAMP accumulation (mean ±SEM): 1nM AVP=47.1±6.8 fmol · mm−1· 4 min−1; AVP + 0.3 μM PGE2=20.1±2.7, P〈0.01 versus AVP; AVP + 10 nM PMA=42.0±4.7, NS versus AVP; AVP + 50 μg/ml OAG=44.1±4.8. NS versus AVP, N= 5 experiments. However, 10 nM PMA prevented PGE2-induced inhibition: AVP + PGE2= 44.2±3.5% of the response to AVP and 90.3±3.2% without and with PMA respectively, N= 16. Similar results were obtained with either 50 μg/ml OAG or 25 μg/ ml DOG (AVP + PGE2 + OAG=92.9±6.6% of the response to AVP, N= 8; AVP + PGE2 + DOG=94.1 ±5.3%, N= 7). OAG, DOG, PMA or PMA + PGE2 had no intrinsic agonist activity in the rat OMCD and the addition of an inactive phorbol ester did not prevent PGE2-induced inhibition. SSP, 50 nM or 0.1 μM, did not affect the inhibition due to PGE2 but abolished the reversion by PMA of PGE2-induced inhibition. A similar regulation was observed on forskolin-(FK)dependent cAMP accumulation: 5 μM FK + 0.3 μM PGE2= 37.7±6.2% of the response to FK; FK + PGE2 + 10 nM PMA=89.5±6.7%; FK + PGE2 + PMA + 0.1 μM SSP=43.1±7.9%, N= 4. The inhibition induced by an α 2-adrenergic agonist, clonidine 1 μM, was not blocked by the activation of PKC. In fura-2-loaded OMCD samples, 10nM PMA decreased by 63.3±5.0% and by 57.2±7.1% the peak and plateau phases, respectively, of the increase in intracellular calcium concentration ([Ca2+]i) obtained with PGE2 when compared to control responses in the same tubules (n=12) and did not affect the increase in [Ca2+]i induced by 0.1 mM carbachol. It is concluded that: (1) in the rat OMCD the activation of PKC by PMA or analogues of diacylglycerol did not reproduce PGE2-induced inhibition of AVP- or FK-dependent cAMP accumulation, but prevented specifically this inhibitory action; and (2) this reversion might be the consequence of the effect of PKC activation which impaired the rises in [Ca2+]i induced by PGE2.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374867
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  • 7
    Electronic Resource
    Electronic Resource
    Arachidonic acid inhibits hormone-stimulated cAMP accumulation in the medullary thick ascending limb of the rat kidney by a mechanism sensitive to pertussis toxin (1995)
    Springer
    Pflügers Archiv 429 (1995), S. 636-646 
    Details
    ISSN: 1432-2013
    Keywords: Microdissected rat medullary thick ascending limb ; cAMP accumulation Intracellular calcium ; Arachidonic acid ; Pertussis toxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The possible regulation of adenosine 3′,5′-cyclic monophosphate (cAMP) accumulation by arachidonic acid (AA) was studied in segments, microdissected from the rat kidney, which are sensitive to arginine vasopressin (AVP). In the presence of 5 μM indomethacin, the addition of 5 μM AA did not impair AVP-dependent cAMP accumulation (measured during 4 min at 35° C) in the cortical or outer medullary collecting tubule, but decreased this response in the thick ascending limb with an inhibition much more pronounced in the medullary portion (MTAL) than in the cortical portion. In MTAL, the response to 10 nM AVP was inhibited by 34.4±9.6% (SEM) and 65.8±5.4% with 1 μM and 5 μM AA, respectively, N=5 experiments. AVP-, glucagon- and calcitonin-sensitive cAMP levels in MTAL were inhibited by 5 μM AA to a similar extent. AA-induced inhibition was unaffected by the presence of inhibitors of AA metabolism: (1) either 10 μM indomethacin or 50 μM ibuprofen added to all media; (2) a 10-min pre-incubation and a 4-min incubation of MTAL samples with 10 μM eicosa-5,8,11,14-tetrayonic acid, (3) a 1-h preincubation with either 30 μM SKF-525A, 20 μM ketoconazole, or 20 μM nordihydroguariaretic acid. In contrast to AA, 11 other saturated or unsaturated fatty acids had no inhibitory effect on the AVP-dependent cAMP level. In fura-2-loaded MTAL samples, AA induced a slow increase of the intracellular calcium concentration ([Ca2+]i) which reached 21.0±3.8 nM and 92.9 ±21.4 nM over basal values (n=11) at 2 min and 4 min, respectively, after the beginning of the superfusion of 5 μM AA. AA-induced inhibition of AVP-dependent cAMP accumulation was due neither to the increase in [Ca2+]i elicited by AA, nor to an activation of protein kinase C because this inhibition: (1) was not blocked when MTAL samples were incubated either in zero Ca2+ medium, or in the presence of 1,2-bis(2-aminophenoxy)ethane-N, N, N′ N′-tetraacetic acid (BAPTA) to chelate [Ca2+ i, and (2) it was not reproduced by a pre-treatment of MTAL segments with a phorbol ester. Pre-incubation of MTAL (6 h at 35° C) with 500 ng/ml pertussis toxin (PTX) prevented AA-induced inhibition: in the presence of PTX inhibition was 24.7±6.6% vs 10 nM AVP, as compared to 81.6 ± 4.0% in control groups, i.e in the absence of PTX, N=6. AA had no effect on the cAMP level induced by 5μM forskolin. It is concluded that AA inhibits AVP-dependent cAMP accumulation in the rat MTAL by a mechanism which implicates a GTP-dependent protein sensitive to PTX.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00373984
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  • 8
    Electronic Resource
    Electronic Resource
    NMR approach to properties of polymeric membranes. Kinetics of membrane formation (1993)
    Bognor Regis [u.a.] : Wiley-Blackwell
    Journal of Polymer Science Part B: Polymer Physics 31 (1993), S. 1567-1576 
    Details
    ISSN: 0887-6266
    Keywords: membrane ; polyetherimide ; nuclear magnetic resonance ; kinetics of formation ; Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology , Physics
    Notes: Nuclear magnetic resonance (NMR) is used to characterize properties of polyetherimide membranes obtained from a phase inversion process. At the end of the phase inversion and prior to the subsequent thermal treatments, the membrane is made of a porous structure filled of solvent and nonsolvent molecules embedded in a concentrated polymer-solvent matrix in the glassy state. The confinement of the small solvent and non solvent molecules in the porous system leads to a restriction of their mobility. The kinetics of membrane formation is observed from NMR. It is found that the penetration of non-solvent and the propagation of the glassy phase into the system obey simple diffusion laws. © 1993 John Wiley & Sons, Inc.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/polb.1993.090311113
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