1,720,980 research outputs found
Dopaminergic D-1 receptors: essential role in morphine-induced hypermotility
No full textAdministration of morphine HCl (20 mg/kg SC) to male C57Bl/6 mice evoked hypermotility. Pretreatment with low doses of the specific D-1 antagonist SCH 23390 (0.006, 0.012, 0.025 mg/kg SC) dose-dependently inhibited morphine-evoked hypermotility. The results suggest that dopamine is the essential mediator of opiate hypermotility and indicate that D-1 receptors play an important role in this effect
Permissive role of D-1 receptor stimulation for the expression of D-2 mediated behavioral responses: a quantitative phenomenological study in rats.
No full textThe syndrome of behavioral stimulation induced in male Sprague-Dawley rats by two dopaminergic agents was studied by distinguishing specific behavioral items and quantifying them in terms of their incidence. The specific D-2 agonist LY 171555 elicited yawning, genital grooming, exploratory behavior, downward sniffing and licking but failed to induce gnawing even at high doses. On the other hand, the D-1/D-2 agonist apomorphine elicited the full stereotyped syndrome including gnawing. Depletion of endogenous dopamine (DA) by alpha-methyltyrosine (alpha-MT) prevented the ability of LY 171555 to elicit all the items of behavioral stimulation including the stereotyped ones (sniffing and licking). In contrast, the ability of apomorphine to induce stereotypies was not reduced by depletion of endogenous DA by alpha-MT pretreatment. Blockade of D-1 receptors with SCH 23390 abolished the capacity of both LY 171555 and apomorphine to elicit all the items of behavioral stimulation. In alpha-MT pretreated rats, administration of low doses of the D-1 agonist SKF 38393 (2.5 mg/kg s.c.) reinstated the ability of LY 171555 to elicit behavioral stimulation and eventually conferred the ability of inducing gnawing. The results support the hypothesis that stimulation of D-1 receptors exerts a permissive role for the expression of behavioral stimulation following D-2 receptor stimulation. Endogenous DA appears to provide sufficient D-1 input to permit full expression of yawning, genital grooming, exploratory behavior, downward sniffing and licking following D-2 stimulation; pharmacological stimulation of D-1 in addition to D-2 receptors seems however necessary for full expression of the highest rank stereotypy item, gnawing
Permissive role of D-1 receptor stimulation by endogenous dopamine for the expression of postsynaptic D-2-mediated behavioural responses. Yawning in rats.
No full textLow doses of BHT 920, LY 171555 and (+)3PPP, three dopamine agonists selective for D-2 receptors, induced yawning in rats. This effect was reduced by the selective D-1 antagonist SCH 23390 but the antagonism did not exceed a 50% reduction from the control values. In contrast, the selective D-2 antagonist (-)sulpiride completely abolished agonist-induced yawning. A 6 h reserpine pretreatment (5 mg/kg i.p.), which depletes brain dopamine (DA) by about 95%, reduced agonist-induced yawning by an extent similar to SCH 23390; in the reserpinized rats, SCH 23390 completely lost the property of blocking agonist-induced yawning while (-)sulpiride retained it. Two 5HT receptor antagonist, ketanserin and metergoline failed to influence agonist-induced yawning. The reportedly selective D-1 agonist, SKF 38393, failed to induce yawning in normal rats as well as in rats pretreated with reserpine 6 or 16 h earlier. If one excludes that SCH 23390 and the D-2 agonists interact with the same DA-receptors, the data are consistent with the possibility that stimulation of D-1 receptors by endogenous DA plays a permissive-facilitatory role for the behavioural expression of D-2 receptor activation
Antagonism of apomorphine-induced yawning by SCH 23390: evidence against the autoreceptor hypothesis
No full textThe ability of apomorphine to induce yawning (YWG) in normal and reserpinized rats and its interaction with SCH 23390, a potent and specific D-1 receptor antagonist, was studied. Apomorphine was more potent in inducing YWG in reserpine-pretreated as compared to control rats. SCH 23390, in low doses (0.05 mg/kg SC), was able to significantly reduce the YWG evoked by apomorphine both in control and in reserpine-pretreated rats. The results indicate that D-1 receptors contribute to YWG elicited by apomorphine and contradict the idea that this effect is mediated by DA autoreceptors
SKF 38393 potentiates yawning induced by LY 171555: further evidence against the autoreceptor hypothesis of yawning.
No full textThe effect of concurrent D-1 receptor stimulation by SKF 38393 on the expression of yawning elicited by D-2 receptor stimulation with LY 171555 was studied in the rat. A low dose of SKF 38393 (2.5 mg/kg SC), while failed to elicit yawning, potentiated the effectiveness of LY 171555 in eliciting yawning at all the doses tested (12.5, 25 and 50 micrograms/kg SC) and this effect was abolished by SCH 23390 (0.012 mg/kg SC). The results indicate that in analogy with typical post-synaptic dopaminergic effects (hypermotility-stereotypy), yawning elicited by a D-2 agonist is facilitated by concurrent stimulation of D-1 receptors and therefore is consistent with previous evidence that yawning in response to a D-2 agonist is not mediated by autoreceptors
The MEK inhibitor SL327 blocks acquisition but not expression of lithium-induced conditioned place aversion: a behavioral and immunohistochemical study
No full textRationale: Recent evidence involves extracellular signal-regulated kinase (ERK) in positive motivational properties of drugs as determined by conditioned place preference but, to date, its role in conditioned place aversion (CPA) still awaits to be fully characterized. Objectives: The aim of this study was to assess whether activated ERK (pERK) plays a role in the acquisition and/or expression of lithium-induced CPA. Methods: C57BL/6J mice were subjected to lithium (150 mg/kg)-induced CPA. The role of pERK was determined by administering the mitogen-activating extracellular kinase inhibitor, SL327, (a) 25 and 50 mg/kg, before each exposure to the lithium-associated compartment (acquisition), and (b) 25, 50, and 100 mg/kg, before post-conditioning test (expression). To assess whether ERK is activated by acute lithium and, in distinct experiments, during CPA expression, mice were sacrificed, 30 min after lithium, and immediately after post-conditioning test, respectively, for pERK immunohistochemistry. Results: Lithium increased pERK-positive neurons in bed nucleus of stria termialis, in central and basolateral amygdala and elicited significant CPA. SL327 (50 mg/kg) significantly prevented its acquisition. In addition, the post-conditioning test of lithium-conditioned mice determined a significant increase of pERK-positive neurons in the dorsal striatum and SL327 (50 mg/kg), administered before post-conditioning test, while failing at the doses of 25, 50, and 100 mg/kg, to affect lithium-induced CPA expression, completely prevented it. Conclusions: These results indicate that pERK is critical for acquisition, but not expression, of lithium-induced CPA and that its activation in the dorsal striatum, during expression, is not critical for retrieval of the aversive memory
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Dopamine-dependent behavioural stimulation by non-peptide delta opioids BW373U86 and SNC 80: 2. Place-preference and brain microdialysis studies in rats
No full textThe motivational properties of the non-peptide delta-opioid receptor agonists BW373U86 and SNC 80 were investigated using the place-conditioning paradigm. BW373U86 (0.5 1.0 mg/kg s.c.) and SNC 80 (1.25 5.0 mg/kg s.c.) elicited significant preference for the drug-paired compartment, in a dose-related fashion. Naltrindole (5.0 mg/kg s.c.) pretreatment, while failing to modify preference when given alone, completely prevented place-preference induced by BW373U86 (1.0 mg/kg s.c.) and SNC 80 (1.25 mg/kg s.c.). The dopamine D-1 receptor antagonist SCH23390, given at doses that do not affect place-preference (0.012 mg/kg s.c.), completely prevented the place-preference induced by BW373U86 and SNC 80. At the doses effective in eliciting place-preference, BW373U86 and SNC 80 failed to modify extracellular dopamine in the medial nucleus accumbens, while in the dorso-lateral caudate-putamen BW373U86 (1.0 and 2.5 mg/kg s.c.) reduced extracellular dopamine, and this effect was prevented by naltrindole (5.0 mg/kg s.c.). SNC 80, only at the dose of 5 mg/kg s.c., significantly reduced extracellular DA in the dorso-lateral caudate-putamen. The results indicate that stimulation of delta-opioid receptors has incentive properties that might be related to an indirect amplification of post-synaptic dopamine transmissio
- …
