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  • 1
    ISSN: 1365-2230
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1365-2230
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-8221
    Keywords: μ-, δ-,and κ-opioids ; enkephalinase inhibitor ; analgesia ; motor activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Analgesic and suppressive effects of selective μ- (DAGO), δ- (DME), and κ- (DAKLI) opioid agonists are compared with those of aminopeptidase N and neutral endopeptidase RB101 in rats of WAG/G and Fischer-344 rats. Fischer-344 rats were more susceptible to suppressive effects of DAGO and analgesic effect of DME. It is concluded that in these rats peculiarities of the μ- and δ-opioid systems determine susceptibility to locomotor depression and analgesia, respectively. There is no correlation between effects of DAGO and RB101 in these strains. This implies that depressive effect of RB101 is not mediated though μ-opioid systems. In contrast, the effects of DMA on pain sensitivity in WAG/G and F-344 rats are opposite to those of RB101. This suggests that specific features in the activity of cerebral δ-OS can determine the sensitivity of RB101-induced analgesia.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-2072
    Keywords: RB 101 ; CCKB antagonist ; Conditioned place preference ; Reward ; Endogenous enkephalins ; PD-134,308
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The interaction between cholecystokinin and endogenous opioid systems on rewarding responses was examined. Motivational effects induced by peripheral administration of a complete inhibitor of enkephalin catabolism, RB 101 or the CCKB antagonist PD-134,308, and by both compounds in combination were evaluated in the conditioned place preference test in rats. RB 101 (5, 10, 20, 40 and 80 mg/kg, IP, and 20 mg/kg, IV) given alone produced a bell-shaped dose-effect function. A significant increase of the preference for the drug-associated compartment was only observed at doses of 10 and 20 mg/kg (IP). The effect observed with morphine was stronger, and all the doses used of this compound (1.25, 2.5 and 5 mg/kg, SC) were found to be active. These results suggest that the inhibitor of enkephalin catabolism has weak rewarding properties. Pretreatment with the CCKB antagonist PD-134,308 (0.1, 0.3, 1 and 3 mg/kg, IP) alone failed to produce a reliable aversion or preference on the paradigm studied. When PD-134,308 (0.3 mg/kg, IP) was coadministered with a subthreshold dose of morphine (0.6 mg/kg, SC) or RB 101 (5 mg/kg, IP), a conditioned place preference was observed, indicating that the CCKB antagonist facilitated the motivational responses induced by endogenous enkephalins as compared to morphine. This suggests that endogenous cholecystokinin, acting through CCKB receptors, modulates the rewarding effects of endogenous enkephalins.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-2072
    Keywords: Key words Conditioned place preference ; Chronic unpredictable mild stress ; Reward ; CCKB receptor antagonist ; Depression ; Stress ; Morphine ; Imipramine ; PD-134 ; 308
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Chronic exposure to mild unpredictable stress has been found to abolish the acquisition of preference for a distinctive environment paired with morphine, whereas morphine induced conditioning place preference in non-stressed rats. Chronic treatment for 21 days with the tricyclic antidepressant imipramine reversed the motivational effects produced by chronic mild stress, and animals showed a place preference for the morphine-paired compartment. When the CCKB receptor antagonist PD-134,308 was co-administered with morphine in stressed animals during the conditioning period, the preference for the morphine-paired compartment was also re-established. The CCKB receptor antagonist given alone did not induce rewarding effects in this paradigm. These findings indicate that the administration of a CCKB receptor antagonist reversed the effects of chronic mild stress on opiate rewarding properties.
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  • 6
    ISSN: 1432-2072
    Keywords: Conditioned suppression of motility ; Antidepressant-like effects ; Enkephalin-degrading enzymes ; RB 101 ; L-365,260 ; BC 264 ; L-364,718 ; δ-Opioid receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Systemic administration of RB 101, a complete inhibitor of the enkephalin degrading enzymes, has been reported to induce naltrindole-reversed anti-depressant-like effects in the conditioned suppression of motility (CSM) test in mice. The selective CCKB antagonist L-365,260 also elicits the same naltrindole-blocked responses on CSM. The aim of this study was therefore to investigate the possible modulation of RB 101 induced behavioral responses by activation or blockade of CCK receptors. Thus, the effects induced by RB 101 administered alone or associated with an ineffective dose of a selective CCKB agonist (BC 264), a CCKB antagonist (L-365,260) or a CCKA antagonist (L-364,718), were evaluated on the CSM in mice. RB 101 alone decreased the stress-induced loss of motility, as previously reported. The antidepressant-like effect of RB 101 was potentiated by L-365,260, and suppressed by BC 264 and to a lesser extent by L-364,718. The facilitatory effect induced by L-365,260 on RB 101 responses was blocked by the delta selective antagonist naltrindole. All these effects occurred only in shocked animals. The present results suggest that the activation of CCKA and CCKB receptors by endogenous CCK, could play an opposite role in the control of behavioral responses induced by endogenous enkephalins. Delta opioid receptors seem to be selectively involved in this interaction.
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  • 7
    ISSN: 1432-2072
    Keywords: Key words Antidepressant-like effects ; Enkephalin degrading enzymes ; RB 101 ; PD-134 ; 308 ; CCK-B receptors ; Anterior nucleus accumbens ; Central amygdala ; Caudate nucleus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Systemic administration of RB 101, a complete inhibitor of enkephalin catabolism, has been reported to induce antidepressant-like responses in mice which were potentiated by an ineffective dose of a CCK-B antagonist. The aim of this study was to investigate the neuroanatomical substrate involved in the facilitatory effects induced by CCK-B antagonists on RB 101 behavioural responses. Thus, the CCK-B antagonist PD-134,308 was locally administered into different brain structures (anterior nucleus accumbens, central amygdala and caudate nucleus) and its effects on the antidepressant-like response induced by systemic administration of RB 101 were evaluated in the conditioned suppression of motility (CSM) test in rats. RB 101 administered alone by the IV route decreased the CSM in rats, as previously obtained in mice. Systemic administration of a non effective dose of PD-134,308 facilitated the antidepressant-like effect induced by RB 101. Local injection of PD-134,308 into the anterior nucleus accumbens, the central amygdala or the caudate nucleus did not modify CSM. The antidepressant-like effects elicited by RB 101 in this test were potentiated by PD-134,308 after microinjection in the anterior nucleus accumbens and central amygdala, but not in the caudate nucleus. All these effects were observed only in shocked animals. The present results suggest that the mesolimbic system, particularly the anterior nucleus accumbens and the central amygdala, seems to play an important role in the interaction occurring between the endogenous CCK and opioid system in the control of behavioural responses.
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  • 8
    ISSN: 1573-4919
    Keywords: cAMP ; prostaglandins ; glomerular basement membrane ; perlecan ; glomerular epithelial cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Perlecan, the basement membrane heparan sulfate proteoglycan (HSPG), has been fully cloned from mouse and human tissues. When a cRNA probe of murine perlecan cDNA was employed in RNase protection assay to test whether rat glomerular epithelial cells (GEC) constitutively express perlecan, several bands of hybridization were seen, suggesting that sequences between rat and murine perlecan may not be identical. Using primers based on published cDNA sequences of murine and human perlecan and polyA+ RNA of rat GEC, we synthesized a 497 by product (RPD-1) by RT PCR. The deduced aminoacid sequence showed an 85% and 88% homology with domain I of murine and human perlecan, respectively. The three putative sites containing the consensus sequence SGD for attachment of heparan sulfate chains were fully conserved in the rat perlecan as was a site (NFT) for attachment of N-linked oligosaccharide. RPD-I detected a 〉 9.5 kb transcript of perlecan in RNA of GEC, similar in size to that present in rat glomeruli. Employing a riboprobe synthesized from RPD-I in RNase protection assay we examined whether dbcAMP regulated perlecan expression in the GEC. At 1, 6, 24 and 48 h of incubation, l mM dbcAMP caused 43%, 32%, 47% and 40% reduction in mRNA abundance of perlecan, respectively. Immunoprecipitation showed a corresponding reduction of 61%, 70% and 65% in the synthesis of 35SO4 labeled basement membrane HSPG by the GEC following 12, 24 and 48 h of incubation with dbcAMP Following incubation for 1 and 24 h prostaglandins, PGE1 and PGE2 (1 uM), known activators of glomerular adenylate cyclase, reduced perlecan mRNA abundance to a similar extent as dbcAMP on northern analysis. Our results show that glomerular basement membrane HSPG synthesized by the GEC belongs to the perlecan family. Decrease of GEC perlecan gene expression and synthesis by cAMP and prostaglandins may be of relevance to proteinuric states characterized by activation of these mediators.
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  • 9
    ISSN: 1432-1912
    Keywords: Key words Protein kinases ; Tyrosine kinase inhibitor ; Serine/threonine kinase inhibitor ; Locus coeruleus ; Periaqueductal gray matter ; Morphine withdrawal ; Naloxone.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The aim of this study was to evaluate the role played in the behavioral expression of morphine withdrawal syndrome by protein kinases in the locus coeruleus and the periaqueductal gray matter. Two different families of specific protein kinases have been investigated: serine/threonine and tyrosine kinases. Rats were implanted with cannulas into both the lateral ventricle and the locus coeruleus or the periaqueductal gray matter. Physical dependence was induced by chronic peripheral administration of morphine (from 7 to 30 mg/kg) and withdrawal syndrome was precipitated by injection of naloxone (2 μg) into the lateral ventricle. The administration of the serine/threonine kinase inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine, H7 (1, 3, 10, and 30 nmol per side) into the locus coeruleus induced a strong attenuation of morphine withdrawal behavior. Signs related to the motor component of abstinence, such as jumping, rearing, and hyperactivity, were the most severely reduced. However, this effect was not dose-dependent, and the response was almost the same with all the doses used. A similar attenuation was observed after the injection of H7 (1, 3, and 10 nmol per side) into the periaqueductal gray matter, but in this case motor signs were less strongly reduced and a larger number of signs were modified, mainly when using the highest dose. The administration of the tyrosine kinase inhibitor 2-hydroxy-5-[N-[(2,5-dihydroxyphenyl)methyl] amino]-benzoic acid 3-phenylpropyl ester, KB23 (0.3, 1, and 3 nmol per side) into the locus coeruleus or the periaqueductal gray matter had no effect on the withdrawal syndrome behavior, except on teeth chattering. These results suggest that, in the locus coeruleus and in the periaqueductal gray matter, serine/threonine kinases are implicated in the behavioral expression of morphine abstinence. In these brain structures, tyrosine kinases appear not to be involved.
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