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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Neurochemical research 24 (1999), S. 1067-1074 
    ISSN: 1573-6903
    Keywords: Adenosine A2 receptors ; NECA binding ; guanine nucleotides ; glutamate analog ; cAMP ; chicks
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Binding properties of the subtypes of adenosine A2 receptors in membrane preparations and the effects of adenosine receptor ligands on cAMP accumulation in slices from the optic tectum of neonatal chicks have been investigated. [3H]2-[4-(2-p-carboxyethyl)phenylamino]-5'-N-ethylcarboxaminoadenosine (CGS 21680), a selective ligand for adenosine A2a receptors, did not bind to optic tectal membranes, as observed with rat striatal membranes. CGS 21680 also did not induce cyclic AMP accumulation in optic tectum slices. However, 5'-N-ethylcarboxamidoadenosine (NECA), 2-chloro-adenosine or adenosine induced a 2.5- to 3-fold increase on cyclic AMP accumulation in this preparation. [3H]NECA binds to fresh non-washed-membranes obtained from optic tectum of chicks, displaying one population of binding sites, which can be displaced by NECA, 8-phenyltheophylline, 2-chloro-adenosine, but is not affected by CGS 21680. The estimated KD value was 400.90 ± 80.50 nM and the Bmax was estimated to be 2.51 ± 0.54 pmol/mg protein. Guanine nucleotides, which modulate G-proteins activity intracellularly, are also involved in the inhibition of glutamate responses by acting extracellularly. Moreover, we have previously reported that guanine nucleotides potentiate, while glutamate inhibits, adenosine-induced cyclic AMP accumulation in slices from optic tectum of chicks. However, the guanine nucleotides, GMP or GppNHp and the metabotropic glutamate receptors agonist, 1S,3R-ACPD did not alter the [3H]NECA binding observed in fresh non-washed-membranes. Therefore, the adenosine A2 receptor found in the optic tectum must be the adenosine A2b receptor which is available only in fresh membrane preparations, and its not modulated by guanine nucleotides or glutamate analogs.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 67 (1996), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Adenosine A1 receptors as well as other components of the adenylate cyclase system have been studied in cultured cerebellar granule cells. No significant changes in adenosine A1 receptor number, assayed by radioligand binding in intact cells, were detected from 2 days in vitro (DIV) until 7 DIV. Nevertheless, a decline in this parameter was detected at 9 DIV. The steady-state levels of α-Gs and α-Gi, detected by immunoblotting, showed similar profiles, increasing from 2 to 5 DIV and decreasing afterward. Forskolin-stimulated adenylate cyclase levels also showed an increase until 5 DIV, decreasing at 7 and 9 DIV. The adenosine A1 receptor analogue cyclopentyladenosine (CPA) was able to inhibit cyclic AMP accumulation at 2, 5, and 7 DIV but failed to do so at 9 DIV. This inhibition was prevented by the specific adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine. The presence of adenosine deaminase in the culture increased adenosine A1 receptor number during the period studied and induced recovery of the inhibitory effect of CPA, lost after 7 DIV. These data suggest that functional expression of adenosine A1 receptors and the other components of the adenylate cyclase system is subjected to regulation during the maturation of cultured cerebellar granule cells and demonstrates a key role for endogenous adenosine in the process.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 59 (1978), S. 71-74 
    ISSN: 1432-2072
    Keywords: Ethanol ; Memory consolidation ; Shuttle avoidance ; Inhibitory avoidance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Ethanol (3 g/kg, given i.p. as a 33% w/v solution), was given to adult Wistar rats 1 min after training in (1) a 50-trial session of shuttle avoidance, using buzzers and shocks, and (2) an inhibitory avoidance experience in a step-through apparatus. The animals were retested 7 days after training in condition (1), and 3 days after training in condition (2). There was no difference in retention scores between the ethanoltreated, saline-treated, or untreated animals. In addition, there was no evidence of an aversive effect of ethanol per se under any of the two training conditions, in spite of the fact that the dose of ethanol used caused a very profound ataxia, and was lethal for 14.3% of the animals (a slightly higher dose, 4 g/kg, is lethal for about 80% of our rats). These data do not favor the hypothesis that an acute administration of ethanol may influence memory consolidation.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 70 (1980), S. 173-177 
    ISSN: 1432-2072
    Keywords: Endogenous opiates ; Beta-endorphin ; Amnesic effects ; Amnesic mechanisms ; Memory consolidation ; Non-associative factors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The endogenous opiate peptide, beta-endorphin (0.4, 1.0, 2.0, and 10.0 μg/kg) was injected IP into rats immediately after training in a shuttle avoidance task, and its effect on memory retention was evaluated in test sessions carried out 24 h later. The drug was found to cause retrograde amnesia, the ED50 being 1.0 μg/kg. Beta-endorphin immunoreactivity was measured in the hypothalamus and rest of the brain of rats submitted to training, or test sessions of shuttle avoidance learning, pseudoconditioning in the shuttle-box, tones alone, or foot-shocks alone. After training in any of the four paradigms, there was a marked (46–60%) depletion of beta-endorphin immunoreactivity in the rest of the brain. No changes were detected in the hypothalamus or after test sessions. The loss of beta-endorphin immunoreactivity may be attributed to release of this substance caused by the stimuli used for training. From the present findings, as well as previous observations on the memory-facilitating influence of the opiate receptor antagonist, naloxone, it is concluded that there is a physiological amnesic mechanism mediated by beta-endorphin (and perhaps other opoid peptides as well), which is triggered by the non-associative factors present in the various forms of learning.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Neurochemical research 23 (1998), S. 211-218 
    ISSN: 1573-6903
    Keywords: Adenosine A1 receptor ; G-protein ; desensitization ; cerebellum ; granule cells ; adenylyl cyclase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Agonist-induced desensitization of adenosine A1 receptor-mediated inhibition of adenylyl cyclase has been studied in cerebellar granule cells. Exposure of cells to the adenosine A1 receptor agonist R-phenylisopropyl adenosine (R-PIA) from 2 to 48 h brings about desensitization of this signal transduction pathway. Associated with the desensitization process, a decrease in radioligand binding performed in intact cells with the adenosine A1 receptor agonist [3H]cyclohexyladenosine (CHA) has been detected. Simultaneously, an increase of adenosine A1 radioligand binding has also been detected in microsomes. A decrease in the steady-state level of α-Gi in both, plasma membrane and microsomes also has been detected during the desensitization process. These data may account for the desensitization of the inhibitory pathway of the adenylyl cyclase in cerebellar granule cells described herein. After a transient increase in adenosine A1 receptor mRNA, no changes were observed in this parameter after 12 hr of treatment with the adenosine A1 agonist R-PIA, suggesting a post-transcriptional regulation of this receptor during long-term desensitization.
    Type of Medium: Electronic Resource
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