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  • 1
    Electronic Resource
    Electronic Resource
    Antidepressant Treatments, Including Sibutramine Hydrochloride and Electroconvulsive Shock, Decrease β1 but Not β2-Adrenoceptors in Rat Cortex (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The β1 and β2-adrenoceptor populations in rat cortex were individually quantified by labelling all of the receptors with [3H]dihydroalprenolol and displacing with iso-prenaline (200 μM) or CGP 20712A (l-{2-[(3-carbamoyl-4-hydroxy)phenoxy]ethylamino}-3-[4-(l-methyl-4-trifluoro-methyl-2-imidazolyl)phenoxy]-2-propanol methanesul-phonate; 100 nM) to define total β-adrenoceptors and β1-adrenoceptors, respectively. Binding parameters for β2-adrenoceptors were calculated by the difference. Oral administration of the monoamine reuptake inhibitors sibutramine HC1 (3 mg/kg), amitriptyline (10 mg/kg), desipramine (10 mg/kg), or zimeldine (10 mg/kg) for 10 days decreased the total number of β-adrenoceptors present in rat cortex. This effect was entirely due to a reduction in the number of β1-adrenoceptors. Similarly, 10 days of treatment with the monoamine oxidase inhibitor tranylcypromine (10 mg/kg p.o.) or five electroconvulsive shocks (ECSs; 200 V, 2 s) spread over this period also down-regulated β-adrenoceptors by reducing the content of the βsubtype. By contrast, treatment with clenbuterol (5 mg/kg p.o.) for 10 days reduced the number of cortical β-adrenoceptors by an effect on the β2-adre-noceptor population. The effects of short-term treatment with these drugs were also investigated, and, using the doses shown above, the results of 3 days of administration or a single ECS were determined. Sibutramine HC1 and desipramine were alone in producing a reduction in number of β-adrenoceptors after 3 days. Once again, this was exclusively due to a loss of β1-adrenoceptors. Together, the results show that antidepressants with disparate pharmacological actions all down-regulated β-adrenoceptors through the neuronal β1-adrenoceptor subtype. In addition, sibutramine HC1 and desipramine produced this attenuation very rapidly. However, clenbuterol treatment reduced the number of β2-adrenoceptors, and its reported antidepressant activity is, therefore, unlikely to be mediated via this mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07389.x
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  • 2
    Electronic Resource
    Electronic Resource
    An investigation of the role of 5-hydroxytryptamine in the attenuation of presynapticα 2-adrenoceptor-mediated responses by antidepressant treatments (1990)
    Springer
    Psychopharmacology 101 (1990), S. 100-106 
    Details
    ISSN: 1432-2072
    Keywords: 5-Hydroxytryptamine-noradrenaline interactions ; α 2-Adrenoceptor-mediated behaviour ; Sedation ; Hypoactivity ; Clonidine ; Antidepressant effects ; Desipramine ; ECS ; Mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Changes in the function of presynapticα 2-adrenoceptors in the brain were assessed by rating the hypoactivity (sedation) response of mice to clonidine (0.1 mg/kg). A single injection of 5,7-dihydroxytryptamine (5,7-DHT, 75 µg ICV) or administration ofp-chlorophenylalanine (PCPA; 200 mg/kg) daily for 11–15 days produced 62–77% reductions in brain 5-HT concentrations and marked supersensitivity of 5-HT2 receptor function, as indicated by the enhancement of the head-twitch response to 5-methoxy-N,N-dimethyltryptamine (2 mg/kg). Clonidine-induced hypoactivity was moderately enhanced after 5,7-DHT lesioning, but not after repeated PCPA injection. In addition, 5,7-DHT lesioning prevented the adaptive attenuation of thisα 2-adrenoceptor-mediated response produced by daily injection of desipramine (10 mg/kg) for 14 days, but had no effect on the reduction caused by five electroconvulsive shocks (ECS, 200 V, 2 s) spread over 10 days. In contrast, repeated PCPA treatment did not prevent the reduction of clonidine-induced hypoactivity produced by repeated desipramine or ECS administration. Together, these results indicate that 5-HT (or possibly a cotransmitter contained within 5-hydroxytryptamine neurones) influences presynapticα 2-adrenoceptor function. Furthermore, an intact 5-HT neuronal input is a prerequisite for the attenuation of clonidine-induced hypoactivity by desipramine, but not ECS. The probable explanation for a contrasting requirement for a functional 5-HT input is that desipramine and ECS induce this common adaptive response by different pharmacological mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02253725
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  • 3
    Electronic Resource
    Electronic Resource
    Monosodium glutamate induced lesions of the arcuate nucleus. I. Endocrine deficiency and ultrastructure of the median eminenceSupported by USDHS Program Project Grant NS-11462. (1976)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 186 (1976), S. 185-196 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Monosodium glutamate was administered daily on days 5 through 10 postnatally at a dose of 2.5 mg/gm body weight. Counts of remaining perikarya in the arcuate nucleus of adult mice indicated approximately an 80% decrease in the number of perikarya. The arcuate lesion resulted in endocrine deficits; reproductive capacity was reduced, animals were smaller in stature and obese, and the weights of the anterior pituitary, ovaries and testes were significantly decreased while adrenals were unaffected. Light microscopic studies revealed no significant changes in thickness or general histological appearance of the median eminence. At the electron microscope level, there were no alterations in the number of nerve terminals or dense core vesicles per unit area in the contact zone. These observations suggest that afferents to the median eminence from the arcuate nucleus may form a relatively small portion of its total nerve terminal population.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1091860205
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    Paper (German National Licenses)
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