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  • 1
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1074, No. 1 ( 2006-08), p. 97-103
    Abstract: Abstract:  Repeated amphetamine administration results in behavioral sensitization. Behavioral sensitization related to abuse and/or relapse may be associated with stable changes in gene expression. To explore the participating genes, we examined the changes in gene expression levels 24 h or 21 days (long‐term withdrawal period) after chronic methamphetamine (METH) treatment for 2 weeks. The expression of several genes related to glutamatergic neural transmission was altered, although changes in the corresponding protein expression were not always consistent with the results for mRNA expression. Of interest, in the frontal cortex of mice treated with METH for 2 weeks, protein expression levels of KIF17 and the N‐methyl‐D‐asparate (NMDA) receptor channel ɛ2 subunit (NRɛ2) were concomitantly increased. The alteration in expression of these proteins, KIF17 and NRɛ2, might be a part of the molecular basis of the behavioral sensitization to METH.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2006
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  • 2
    Online Resource
    Online Resource
    Wiley ; 2004
    In:  Annals of the New York Academy of Sciences Vol. 1025, No. 1 ( 2004-10), p. 370-375
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1025, No. 1 ( 2004-10), p. 370-375
    Abstract: A bstract : Individual differences in responses to opioids limit effective pain treatment with these drugs. Identifying the mechanism could help to improve the analgesic effects of them. Since the molecular cloning of the mu opioid receptor (muOR) gene, substantial advances in opioid research have been made, including the discoveries that muOR plays a mandatory role in the analgesic effects of opioids and that the sequence of the muOR gene varies from one individual to another. It is conceivable that the differences in the muOR gene cause individual differences in opioid actions. The present review summarizes the recent advances made in research on human and mouse muOR genes and proposes that the variances in the 3′ untranslated region (39‐UTR) of the muOR gene might participate in the variability of the opioid response.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2004
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
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  • 3
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 101, No. 16 ( 2004-04-20), p. 6110-6115
    Abstract: M cells located in the follicle-associated epithelium of Peyer's patches (PP) are shown to be the principal sites for the sampling of gut luminal antigens. Thus, PP have long been considered the gatekeepers of the mucosal immune system. Here, we report a distinct gateway for the uptake of gut bacteria: clusters of non-follicle-associated epithelium-associated Ulex europaeus agglutinin (UEA)-1 + cells, which we have designated intestinal villous M cells. Interestingly, villous M cells are developed in various PP [or gut-associated lymphoid tissue (GALT)]-null mice, such as in utero lymphotoxin β receptor (LTβR)-Ig-treated, lymphotoxin α (LTα) -/- , tumor necrosis factor/LTα -/- , and inhibition of differentiation 2 (Id2) -/- mice. Intestinal villous M cells have been observed to take up GFP-expressing Salmonella, Yersinia , and Escherichia coli -expressing invasin, as well as gut bacterial antigen for subsequent induction of antigen-specific immune responses. Thus, the identified villous M cells could be an alternative and PP-independent gateway for the induction of antigen-specific immune responses by means of the mucosal compartment.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    RVK:
    RVK:
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2004
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
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  • 4
    Online Resource
    Online Resource
    Wiley ; 2006
    In:  Annals of the New York Academy of Sciences Vol. 1074, No. 1 ( 2006-08), p. 295-302
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1074, No. 1 ( 2006-08), p. 295-302
    Abstract: Abstract:  The monoamine transporters are the main targets of psychostimulant drugs, including methamphetamine (METH) and cocaine. Interestingly, the rewarding effects of cocaine are retained in dopamine transporter (DAT) knockout (KO) mice, while serotonin transporter (SERT) and DAT double KO mice do not exhibit conditioned place preference (CPP) to cocaine. These data suggest that SERT inhibition decreases the rewarding effects of psychostimulants. To further test this hypothesis, in the present study, we investigated the effects of intraperitoneal (i.p.) injections of 20 mg/kg fluoxetine, a selective serotonin reuptake inhibitor (SSRI), on 2 mg/kg METH (i.p.) CPP and locomotor sensitization to 1 mg/kg METH (i.p.) in C57BL/6J mice. Fluoxetine treatment before both the conditioning and preference tests abolished METH CPP. A two‐way analysis of variance (ANOVA) revealed that METH CPP tended to be lower in mice pretreated with fluoxetine before the preference test than in control mice pretreated with saline before the preference test. Furthermore, pretreatment with fluoxetine had inhibitory effects on METH‐induced locomotor sensitization. These results suggest that fluoxetine, a widely used medication for depression, may be also a useful tool for treating METH dependence.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2006
    detail.hit.zdb_id: 2834079-6
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    SSG: 11
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  • 5
    Online Resource
    Online Resource
    Wiley ; 2006
    In:  Annals of the New York Academy of Sciences Vol. 1074, No. 1 ( 2006-08), p. 418-426
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1074, No. 1 ( 2006-08), p. 418-426
    Abstract: Abstract:  Donepezil, a choline esterase inhibitor, has been widely used as a medicine for Alzheimer's disease. Recently, a study showed that donepezil inhibited addictive behaviors induced by cocaine, including cocaine‐conditioned place preference (CPP) and locomotor sensitization to cocaine. In the present study, we investigated the effects of donepezil on methamphetamine (METH)‐induced behavioral changes in mice. In counterbalanced CPP tests, the intraperitoneal (i.p.) administration of 3 mg/kg donepezil prior to 2 mg/kg METH i.p. failed to inhibit METH CPP, whereas pretreatment with 3 mg/kg donepezil abolished the CPP for cocaine (10 mg/kg, i.p.). Similarly, in locomotor sensitization experiments, i.p. administration of 1 mg/kg donepezil prior to 2 mg/kg METH i.p. failed to inhibit locomotor sensitivity to METH, whereas pretreatment with 1 mg/kg donepezil significantly inhibited locomotor sensitivity to cocaine (10 mg/kg, i.p.). These results suggest that donepezil may be a useful tool for treating cocaine dependence but not for treating METH dependence. The differences in the donepezil effects on addictive behaviors induced by METH and cocaine might be due to differences in the involvement of acetylcholine in the mechanisms of METH and cocaine dependencies.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2006
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
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  • 6
    Online Resource
    Online Resource
    Proceedings of the National Academy of Sciences ; 2021
    In:  Proceedings of the National Academy of Sciences Vol. 118, No. 4 ( 2021-01-26)
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 118, No. 4 ( 2021-01-26)
    Abstract: Basal ganglia contribute to object-value learning, which is critical for survival. The underlying neuronal mechanism is the association of each object with its rewarding outcome. However, object values may change in different environments and we then need to choose different objects accordingly. The mechanism of this environment-based value learning is unknown. To address this question, we created an environment-based value task in which the value of each object was reversed depending on the two scene-environments (X and Y). After experiencing this task repeatedly, the monkeys became able to switch the choice of object when the scene-environment changed unexpectedly. When we blocked the inhibitory input from fast-spiking interneurons (FSIs) to medium spiny projection neurons (MSNs) in the striatum tail by locally injecting IEM-1460, the monkeys became unable to learn scene-selective object values. We then studied the mechanism of the FSI-MSN connection. Before and during this learning, FSIs responded to the scenes selectively, but were insensitive to object values. In contrast, MSNs became able to discriminate the objects (i.e., stronger response to good objects), but this occurred clearly in one of the two scenes (X or Y). This was caused by the scene-selective inhibition by FSI. As a whole, MSNs were divided into two groups that were sensitive to object values in scene X or in scene Y. These data indicate that the local network of striatum tail controls the learning of object values that are selective to the scene-environment. This mechanism may support our flexible switching behavior in various environments.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    RVK:
    RVK:
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2021
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  • 7
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 227, No. 4693 ( 1985-03-22), p. 1494-1496
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    RVK:
    RVK:
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 1985
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    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
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