Decrease in hypothalamic epinephrine concentration and other neurochemical changes produced by quinpirole, a dopamine agonist, in rats

Fuller, Ray W.; Hemrick‐Luecke, Susan K.

doi:10.1007/bf01251910

Cited by 30 publications

(10 citation statements)

References 21 publications

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“…In accordance with the literature data (Tsuruta et al, 1981;Fuller and Hemrick-Luecke, 1985;Walters et al, 1987), we have found that quinpirole, an agonist of dopamine D-2 receptors, increases the locomotor activity of rats, the effect being attenuated by (4-)-sulpiride, an antagonist of these receptors.…”

Section: Discussionsupporting

confidence: 90%

“…There is much data to indicate that locomotor hyperactivity is evoked by stimulation of dopamine D-2 receptors (Seeman, 1980;Start and Starr, 1986). Therefore, we decided to study the influence of AD on the effect of quinpirole, a selective agonist of dopamine D-2 receptors (Tsuruta et al, 1981;Fuller and Hemrick-Luecke, 1985). Our initial experiments demonstrated that imipramine and (+)-oxaprotiline, administered repeatedly, increase the locomotor hyperactivity induced by quinpirole (Maj et al, 1989).…”

Section: Introductionmentioning

confidence: 98%

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Antidepressants given repeatedly increase the behavioural effect of dopamine D-2 agonist

Rogóż

Skuza

et al. 1989

J. Neural Transmission

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The effects of single or repeated doses of antidepressant drugs (imipramine, amitriptyline, citalopram, mianserin) on rat locomotor hyperactivity induced by quinpirole, a dopamine D-2 receptor agonist, was investigated. Single doses of antidepressants do not change the effect of quinpirole, but enhance it when they are administered repeatedly. This enhancement is inhibited by (+/-)-sulpiride, a dopamine D-2 receptor antagonist. The results obtained indicate that the enhancement of dopaminergically-stimulated hyperactivity induced by repeated doses of antidepressants is mediated by dopamine D-2 receptors.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 98%

Antidepressants given repeatedly increase the behavioural effect of dopamine D-2 agonist

Rogóż

Skuza

et al. 1989

J. Neural Transmission

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“…Our earlier data suggest that stress-induced anhedonia results from a decreased sensitivity of the D 2 receptors in the nucleus accumbens. Evidence of postsynaptic subsensitivity was provided by a series of experiments assessing the rewarding properties of the DiD 3 agonist, quinpirole (Fuller and Hemrick-Luecke 1985;Sokotoff et al 1990) using the place preference procedure. Responses to quinpirole, administered systemically or directly into the nucleus accumbens, were attenuated or abolished following CMS (Papp et al , 1993.…”

Section: Discussionmentioning

confidence: 99%

Stereospecific reversal of stress-induced anhedonia by mianserin and its (+)-enantiomer

Cheeta

Broekkamp²,

Willner

1994

Psychopharmacology

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Chronic sequential exposure to a variety of mild unpredictable stressors has previously been found to depress the consumption of a dilute (1%) sucrose solution and to inhibit food-induced place preference conditioning. In the present study, using a simplified version of the mild stress procedure, the decreased sucrose intake was reversed by chronic (4 weeks) treatment with the atypical antidepressant mianserin. The racemic compound (+/-)-mianserin (5 mg/kg per day) and one of its enantiomers, (+)-mianserin (2.5 mg/kg) were effective in this model; a lower dose of (+/-)-mianserin (2.5 mg/kg), and the other enantiomer. (-)-mianserin (2.5 mg/kg), were ineffective. Vehicle-treated stressed animals were also subsensitive to food reward in the place conditioning procedure: normal place preference conditioning was reinstated by chronic treatment with (+/-)-mianserin (5 mg/kg) or (+)-mianserin, but not by the lower dose of (+/-)-mianserin (2.5 mg/kg) or by (-)-mianserin. Raclopride (100 micrograms/kg) reinstated the decrease in sucrose intake in stressed animals successfully treated with (+/-)- or (+)-mianserin. The results suggest that (+)-mianserin is the active enantiomer in reversing chronic mild stress-induced anhedonia, and further support the hypothesis of a dopaminergic mechanism of antidepressant action in this paradigm.

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“…Moreover, the selective D-2 agonist quinpirole [26] did not increase, and even tended to decrease, plasma OT after administration to the SON. These findings are similar to our earlier observation that basal OT secretion is not increased by systemically administered D-2 agonists [6], In addition, they suggest that activation of the cyclic AMP messenger system, which accompanies D -l, but not D-2 receptor stimula tion [25], is important for the action of DA on OT secre tion.…”

Section: Discussionmentioning

confidence: 99%

Activation of Central D-1 Dopamine Receptors Stimulates Oxytocin Release in the Lactating Rat: Evidence for Involvement of the Hypothalamic Paraventricular and Supraoptic Nuclei

Parker

Crowley

1992

Neuroendocrinology

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The stimulatory effect of dopamine (DA) on the release of oxytocin (OT) in lactating rats is exerted at the D-1 DA receptor subtype. Because the neural loci mediating this effect have not been identified, the objective of the present studies was to test whether OT release in the lactating rat would be elevated after central administration of a D-1 DA receptor agonist into the third ventricle (3V) or directly into either the rostral paraventricular/anterior commissural nucleus area (PVN/ACN), the central paraventricular nucleus area, or the supraoptic nucleus (SON), all of which contain OT neurosecretory cells. Lactating rats were implanted with a stainless steel cannula directed into one of the above areas or into the arcuate-ventromedial region of the medial basal hypothalamus (MBH), or sites dorsal to the PVN/ACN or SON, which served as anatomical controls. After 6-7 days of recovery, each animal received an intra-atrial cannula for sequential blood sampling, and was used in experiments 24 h later. Animals were separated from their litters, and following a period of basal blood sampling, received central microinjections of either vehicle, the D-1 DA receptor agonist SKF-38393, or the D-2 DA receptor agonist quinpirole, and blood samples were removed periodically for 60 min. An injection of angiotensin II (Ang II, 100 ng) was made into each site as a positive control for OT release. Injection of SKF-38393 (12.5 or 50 µg/5 µl) into the 3V resulted in a statistically significant and dose-releated increase in plasma OT concentrations, which was attenuated by intravenous pretreatment with the specific D-1 DA receptor antagonist, SCH-23390 (1.2 mg/kg). Unilateral injection of SKF-38393 (8 µg) into the SON region also produced a significant increase in plasma OT concentrations, while more modest increases followed injection of this agent into the PVN sites. Systemic pretreatment with the D-1 DA antagonist also blocked the effect of SKF-38393 in the SON. Plasma OT concentrations were not significantly changed after administration of SKF-38393 into the MBH or to dorsal control sites, or after any central injections of vehicle or the D-2 agonist quinpirole. Ang II markedly stimulated OT release after administration to 3V, PVN, SON and MBH, but not to the control sites dorsal to the PVN and SON. The present findings extend previous observations that D-1 DA receptors mediate the central dopaminergic stimulation of OT secretion in the lactating rat, and suggest that the SON region may be an important locus for this effect.

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Decrease in hypothalamic epinephrine concentration and other neurochemical changes produced by quinpirole, a dopamine agonist, in rats

Cited by 30 publications

References 21 publications

Antidepressants given repeatedly increase the behavioural effect of dopamine D-2 agonist

Antidepressants given repeatedly increase the behavioural effect of dopamine D-2 agonist

Stereospecific reversal of stress-induced anhedonia by mianserin and its (+)-enantiomer

Activation of Central D-1 Dopamine Receptors Stimulates Oxytocin Release in the Lactating Rat: Evidence for Involvement of the Hypothalamic Paraventricular and Supraoptic Nuclei

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