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  • 1990-1994  (1)
  • 1985-1989  (2)
  • Beta-adrenergic adenylate cyclase  (1)
  • Clonidine  (1)
  • Conditioned reinforcement  (1)
Material
Years
  • 1990-1994  (1)
  • 1985-1989  (2)
Year
Keywords
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Archives of dermatological research 280 (1988), S. 89-92 
    ISSN: 1432-069X
    Keywords: Cyclosporin A ; Beta-adrenergic adenylate cyclase ; Phosphodiesterase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has been known that beta-adrenergic adenylate cyclase response is decreased in psoriatic-involved epidermis. Since the immunosuppressive agent, cyclosporin A, is reported to be effective on psoriasis clinically, the effect of cyclosporin A on beta-adrenergic adenylate cyclase response in pig skin was examined in vitro. Therapeutic serum levels of cyclosporin A (100–400 ng/ml) augmented the beta-adrenergic adenylate cyclase response of the epidermis. Highest levels of cyclosporin A (2–20 μg/ml) did not have any effect on its response. Both low K m and high K m cyclic AMP phosphodiesterases were not affected by cyclosporin A. Therefore, it is suggested that the clinical efficacy of cyclosporin A on psoriasis can be explained partially by its direct effect on the keratinocyte itself.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2072
    Keywords: Clonidine ; Locus coeruleus ; Intracerebral infusion ; Withdrawal ; Naloxone ; Morphine ; 3-Methoxy-4-hydroxyphenylglycol (MHPG) ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Clonidine, an alpha-2-adrenergic agonist, suppresses signs of opiate withdrawal in animals and in man. Electrical or chemical stimulation of the nucleus locus coeruleus (LC) increases noradrenergic activity and brain concentration of the noradrenergic metabolite MHPG, and produces many signs of opiate withdrawal. Thus, clonidine's ability to attenuate withdrawal might be due to the reduction of noradrenergic neuronal activity originating in the LC, but additional alpha-2-adrenergic receptors throughout the body and other mechanisms may also play a role. The present study explored the neuroanatomical and pharmacological selectivity of alpha-2-adrenergic receptors of the LC in the anti-withdrawal action of clonidine. Experiment 1 tested the hypothesis that behavioral and biochemical measures of naloxone-precipitated withdrawal from morphine would be blocked by infusions of clonidine (0.6 or 2.4 μg/μl) into the LC. Significant reductions were observed in the occurrence of diarrhea, ptosis, weight loss and wet-dog shakes. Clonidine also reversed the naloxone-precipitated increase in hippocampus MHPG concentration. In experiment 2 subjects received an LC infusion or IP injection of a non-lipophilic alpha-2-agonist (ST-91), which does not penetrate the blood-brain barrier, or of clonidine into the dorsal parabrachial nucleus (DPB) to test the selectivity of the effects of clonidine infusions into the LC. ST-91 infusions into the LC reduced several of the observed withdrawal signs and increased others (e.g., jumping). Although peripheral injections of ST-91 attenuated some of the checked signs associated with naloxone-precipitated withdrawal, the frequency of wet-dog shakes was not reduced. ST-91 infusions into the LC, but not systemic ST-91 administration, prevented the withdrawal-induced increase in hippocampus MHPG concentration. Clonidine infused lateral to the LC into the DPB did not significantly attenuate withdrawal or reduce hippocampus MHPG levels. These results provide behavioral and biochemical evidence to support the suggestion that clonidine significantly attenuates naloxone-precipitated withdrawal through an interaction with noradrenergic neurons located in the vicinity of the LC.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2072
    Keywords: Conditioned reinforcement ; Dopamine ; Noradrenaline ; d-Amphetamine ; Dorsal noradrenergic bundle ; Nucleus accumbens
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Three experiments examined the behavioural, pharmacological and neural specificity of the previously reported potentiation of responding with conditioned reinforcement following intra-accumbensd-amphetamine, by studying the effects of intraaccumbens dopamine (DA) and noradrenaline, using an acquisition of a new response procedure. In experiment 1, the effects of intra-cerebral DA infusions (5, 20, 50 µg/2 µl) were compared in four conditions: (i) intra-accumbens DA following positive pairing of the conditioned stimulus (CS) and water during training; (ii) as (i) but also following a systemic dose of the DA receptor antagonist alpha-flupenthixol; (iii) intra-accumbens DA following random pairing of the CS and water during training; and (iv) as (i) but with intra-caudate rather than intra-accumbens DA. The results showed that only with intra-accumbens DA in the positive pairing condition was there a significant dose-dependent increase in responding. In experiment 2, the effects of a higher range of doses (20, 100, 200 µg) and smaller infusion volume (5, 25, 50 µg/l µl) of intra-accumbens DA were studied, in comparison with a similar range of doses (5, 25, 50 µg/l µl) of intra-accumbens noradrenaline (NA). Only DA produced a selective, dose-dependent increase in responding with conditioned reinforcement. In experiment 3 neurotoxic lesions of the dorsal noradrenergic bundle (DNAB) using 6-hydroxydopamine producing profound (about 90%) depletion of cortical and nucleus accumbens NA levels had no effect on the increased responding with conditioned reinforcement produced by intra-accumbensd-amphetamine (3, 10, 30 µg/l µl). The results are discussed in terms of the neurochemical mediation of the potentiation of the effects of conditioned reinforcers byd-amphetamine and the role of DA-dependent mechanisms of the nucleus accumbens in reward-related processes.
    Type of Medium: Electronic Resource
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