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  • 1
    Electronic Resource
    Electronic Resource
    Extracellular Concentrations of Dopamine and Metabolites in the Rat Caudate After Oral Administration of a Novel Catechol-O-Methyltransferase Inhibitor Ro 40–7592 (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effect of the systemic administration of a novel, orally active, catechol-O-methyltransferase (COMT) inhibitor, Ro 40–7592, on the in vivo extracellular concentrations of dopamine (DA) and its metabolites, dihydroxy-phenylacetic acid (DOPAC) and homovanillic acid (HVA), was studied by transcerebral microdialysis in the dorsal caudate of freely moving rats. Ro 40–7592 (at doses of 3.0, 7.5, and 30 mg/kg p.o.) elicited a marked and long-lasting reduction of HVA, and at doses of 7.5 and 30 mg/kg, an increase of DOPAC output, but it failed to increase DA output. The administration of L-β-3,4-dihydroxyphenylalanine (L-DOPA, 20 and 50 mg/kg p.o.) with a DOPA decarboxylase inhibitor (benserazide) increased both HVA and DOPAC output, but failed to modify significantly extracellular DA concentrations in dialysates; in contrast, combined administration of L-DOPA + benserazide with Ro 40–7592 (30 mg/ kg p.o.) resulted in a significant increase in DA output. Ro 40–7592 prevented the L-DOPA-induced increase in HVA output and markedly potentiated the increase in DOPAC output. To investigate to what extent the increase in extra cellular DA concentrations was related to an exocitotic release, tetrodotoxin (TTX) sensitivity was tested. Addition of TTX to Ringer, although abolishing DA output in the absence of L-DOPA, partially reduced it in the presence of L-DOPA + Ro 40–7592 and even more so after L-DOPA without the COMT inhibitor. The results of the present study suggest that metabolism through COMT regulates extracellular concentrations of DA formed from exogenously administered L-DOPA but not of endogenous DA. Therefore, inhibition of COMT results in a potentiation of L-DOPA effects not only by inhibition of its peripheral metabolism (conversion to 3-methoxy-DOPA), but also by inhibition of the metabolism of its active metabolite, DA, in the brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08907.x
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  • 2
    Electronic Resource
    Electronic Resource
    Dopaminergic Regulation of Striatal Acetylcholine Release: The Critical Role of Acetylcholinesterase Inhibition (1998)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 70 (1998), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: This study examined the effects of different levels of acetylcholinesterase (AChE) inhibition on dopaminergic regulation of striatal acetylcholine (ACh) release as estimated by in vivo brain microdialysis. Systemic administration of d-amphetamine (2 or 10 mg/kg) increased the striatal output of ACh when the AChE inhibitor neostigmine (0.1 µM) was present in the perfusion fluid. In contrast, when the same experiments were conducted at 0.01 µM neostigmine, d-amphetamine failed to affect (2 mg/kg) or significantly decreased (10 mg/kg) striatal ACh output. The inhibitory action of the D2 receptor agonist quinpirole (0.2 mg/kg) was significantly greater at 0.01 µM than at 0.1 µM neostigmine. Similarly, there was a nonsignificant trend for the D2 antagonist raclopride (1 mg/kg) to stimulate ACh release to a greater extent at the low neostigmine concentration. In contrast, the stimulant effects of systemic administration of the D1 agonist A-77636 (1.46 mg/kg) on striatal ACh release were the same at the two neostigmine concentrations. These results demonstrate that the concentration of an AChE inhibitor in the perfusion solution can quantitatively and even qualitatively influence the manner in which dopaminergic agents regulate ACh overflow in the striatum. On comparing the present results with earlier reports concerning the effects of d-amphetamine on tissue concentrations of ACh, it is tentatively concluded that a low neostigmine concentration is the more physiologically relevant condition. Under such conditions, at moderate doses d-amphetamine does not appear to alter striatal ACh release, with this likely being due to the opposing actions of D1 and D2 receptors. Nevertheless, until the endogenous interstitial concentrations of striatal ACh can be measured by other methods, the physiological relevance of ACh microdialysis studies in the striatum will remain uncertain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1998.70031088.x
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  • 3
    Electronic Resource
    Electronic Resource
    5HT3 receptor antagonists block morphine- and nicotine-but not amphetamine-induced reward (1989)
    Springer
    Psychopharmacology 97 (1989), S. 175-178 
    Details
    ISSN: 1432-2072
    Keywords: Serotonin ; Morphine ; Nicotine ; Amphetamine ; Reward ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of two potent and specific antagonists of 5HT3 receptors, ICS 205-930 and MDL 72222, on the reinforcing properties of amphetamine, morphine and nicotine was studied in rats. Durg-induced reinforcement was assessed by measuring drug-conditioned place preference. ICS 205-930 and MDL 72222 dose-dependently reduced the place preference induced by morphine (1.0 mg/kg SC). At doses of 0.030 mg/kg SC the two antagonists completely blocked morphine-induced place preference while doses of 0.015 mg/kg SC significantly reduced it. ICS 205-930 and MDL 72222 at doses of 0.030 mg/kg SC also prevented the place preference induced by nicotine (0.6 mg/kg SC). In contrast, ICS 205-930 and MDL 72222 up to doses of 0.030 mg/kg SC failed to modify the place preference elicited by amphetamine (1.0 mg/kg SC). The results indicate that 5HT3 receptors are specifically involved in the reinforcing properties of morphine and nicotine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00442245
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  • 4
    Electronic Resource
    Electronic Resource
    SCH 23390 blocks drug-conditioned place-preference and place-aversion: anhedonia (lack of reward) or apathy (lack of motivation) after dopamine-receptor blockade? (1989)
    Springer
    Psychopharmacology 99 (1989), S. 151-155 
    Details
    ISSN: 1432-2072
    Keywords: Dopamine ; Morphine ; Nicotine ; Diazepam ; Naloxone ; Phencyclidine ; Picrotoxin ; Place-aversion ; Place-preference ; SCH 23390
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The influence of the D1 antagonist SCH 23390 on the motivational properties of rewarding (morphine, nicotine and diazepam) and aversive (naloxone, phencyclidine and picrotoxin) drugs was studied in the rat in a two-compartment place-conditioning paradigm, which included a pre-conditioning test for spontaneous place-preference. The specific D1 dopamine-receptor antagonist SCH 23390 (0.05 mg/kg SC), paired with both compartments or, separately, with the preferred or with the non-preferred compartment, failed to affect the spontaneous unconditioned preference of the animal. Pairing of morphine (1.0 mg/kg SC), nicotine (0.6 mg/kg SC) or diazepam (1.0 mg/kg IP) with the less preferred compartment induced significant preference for that compartment. Pairing of SCH 23390 (0.05 mg/kg SC) with both compartments completely blocked the place-preference induced by morphine, nicotine and diazepam. Naloxone (0.8 mg/kg SC), phencyclidine (2.5 mg/kg SC) or picrotoxin (2.0 mg/kg IP) paired with the preferred compartment elicited place-aversion. Pairing of SCH 23390 (0.05 mg/kg SC) with both compartments abolished also the place-aversion induced by naloxone, phencyclidine and picrotoxin. The results indicate that blockade of dopamine transmission blocks the motivational properties of rewarding as well as aversive stimuli. It is suggested that neuroleptics rather than simply blocking the rewarding impact of positive reinforcers (anhedonia, lack of pleasure) exert a more general influence on conditioned behaviour by blocking the affective impact of negative as well as positive reinforcers (apathy, lack of motivation).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00442800
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  • 5
    Electronic Resource
    Electronic Resource
    Blockade of acquisition of drug-conditioned place aversion by 5HT3 antagonists (1990)
    Springer
    Psychopharmacology 100 (1990), S. 459-463 
    Details
    ISSN: 1432-2072
    Keywords: 5-HT ; 5HT3 antagonist ; Naloxone ; Phencyclidine ; Picrotoxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of two 5HT3 antagonists, ICS 205-930 and MDL 72222, on drug-induced place aversion was studied in a two-compartment apparatus with a procedure including a pre-test for spontaneous preference. Naloxone (0.8 mg/kg SC), phencyclidine (2.5 mg/kg SC) and picrotoxin (2.0 mg/kg IP) paired with the preferred compartment elicited a significant place aversion. ICS 205-930 and MDL 72222 failed to modify spontaneous place preference when paired with both compartments. ICS 205-930 (30 µg/kg SC) paired with the preferred and, in other experiments, with the non-preferred compartment, also failed to modify spontaneous preference. ICS 205-930 (7.5, 15 and 30 µg/kg SC), paired with both compartments, dose-dependently reduced the place aversion induced by naloxone (0.8 mg/kg SC), phencyclidine (2.5 mg/kg SC) and picrotoxin (2.0 mg/kg IP). MDL 72222 (30 µg/kg SC) paired with both compartments had a similar effect. The result indicate that 5HT, via 5HT3 receptors, plays a role in the aversive properties of drug stimuli.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02243996
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  • 6
    Electronic Resource
    Electronic Resource
    Chronic lithium attenuates dopamine D1-receptor mediated increases in acetylcholine release in rat frontal cortex (1996)
    Springer
    Psychopharmacology 125 (1996), S. 162-167 
    Details
    ISSN: 1432-2072
    Keywords: Acetylcholine ; Microdialysis ; Lithium ; Cortex ; Dopamine D1 receptors ; Methylphenidate ; Mania
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of chronic lithium treatment on methylphenidate-, D1 dopamine receptor agonist (A-77636)-, and tactile stimulation-induced increases in frontal cortical acetylcholine release were studied in the rat using in vivo brain microdialysis. Cortical acetylcholine release in control rats was maximally stimulated by methylphenidate (1.25 and 2.5 mg/kg) to 173% and 212% above baseline, respectively. The effect of methylphenidate (2.5 mg/kg) was blocked by pretreatment with the dopamine D1 receptor antagonist SCH 23390 (0.3 mg/kg). Chronic treatment with lithium chloride (3–4 weeks) produced plasma lithium concentrations of 0.45±0.02 meq/l. Chronic lithium significantly reduced increases in cortical acetylcholine release produced by methylphenidate. Stimulation of dopamine D1 receptors with the full D1 receptor agonist A-77636 (0.73 mg/kg) increased cortical acetylcholine release. Chronic lithium significantly reduced this effect of A-77636. In contrast, lithium failed to influence the increases of cortical acetylcholine release produced by tactile stimulation. These results suggest that while lithium does not influence normal, arousal-related increases in cortical acetylcholine release, this ion selectively attenuates dopamine mediated increases and/or abnormally large increase, which in the present circumstances were pharmacologically induced. The relevance of these findings to the antimanic actions of lithium is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02249415
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