1994
DOI: 10.1016/0006-2952(94)90323-9
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Effects of dopamine partial-agonist aminoergolines on dopamine metabolism in limbic and extrapyramidal regions of rat brain

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Cited by 5 publications
(2 citation statements)
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“…In the “open-loop” model, it is possible for dopaminergic drugs to modify dopamine synthesis via long-loop feedback pathways; whereas, γ-butyrolactone is used in the “closed-loop” model to inhibit nerve impulse flow, thus dopamine agonists and antagonists can only modify dopamine synthesis through autoreceptor-mediated actions (Walters and Roth, 1976). As expected, γ-butyrolactone, when administered alone, increased dopamine synthesis in the dorsal striatum of adolescent and adult rats (see also Walters and Roth, 1976; Shalaby et al, 1981; Baldessarini et al, 1994; Andersen et al, 1997). Regardless of the model employed, stimulating D 2 autoreceptors with quinpirole inhibited dopamine synthesis in both age groups (Svensson et al, 1991; Andersen et al, 1997; Heidbreder and Baumann 2001; Der-Ghazarian et al, 2010).…”
Section: Discussionsupporting
confidence: 80%
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“…In the “open-loop” model, it is possible for dopaminergic drugs to modify dopamine synthesis via long-loop feedback pathways; whereas, γ-butyrolactone is used in the “closed-loop” model to inhibit nerve impulse flow, thus dopamine agonists and antagonists can only modify dopamine synthesis through autoreceptor-mediated actions (Walters and Roth, 1976). As expected, γ-butyrolactone, when administered alone, increased dopamine synthesis in the dorsal striatum of adolescent and adult rats (see also Walters and Roth, 1976; Shalaby et al, 1981; Baldessarini et al, 1994; Andersen et al, 1997). Regardless of the model employed, stimulating D 2 autoreceptors with quinpirole inhibited dopamine synthesis in both age groups (Svensson et al, 1991; Andersen et al, 1997; Heidbreder and Baumann 2001; Der-Ghazarian et al, 2010).…”
Section: Discussionsupporting
confidence: 80%
“…After 25 min, groups were further subdivided with rats being injected with distilled water or the nerve impulse inhibitor γ-butyrolactone (PD 28, 625 mg/kg; PD 91, 750 mg/kg, i.p.). Although 750 mg/kg γ-butyrolactone is commonly administered to adult rats (Walters and Roth, 1976; Svensson et al, 1991; Baldessarini et al, 1994), a lower dose of the drug was given to PD 28 rats because 750 mg/kg γ-butyrolactone, when combined with haloperidol, frequently causes respiratory failure in younger animals. After an additional 5 min, all rats were injected with the DOPA decarboxylase inhibitor NSD-1015 (100 mg/kg, i.p.).…”
Section: Methodsmentioning
confidence: 99%