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1.
Pharmacological interactions between serotonin and dopamine on behavior in the squirrel monkey 总被引:2,自引:1,他引:1
The behavioral effects of GBR 12909, a selective dopamine uptake inhibitor, were determined in squirrel monkeys trained to
respond under a fixed-interval (FI) schedule of stimulus termination and a second-order schedule of IV drug self-administration.
Intermediate doses of GBR 12909 increased FI response rate markedly, and the highest dose decreased response rate below control
values. The 5HT uptake inhibitors, alaproclate and fluoxetine, and the 5HT agonist, quipazine, attenuated the behavioral-stimulant
effects of GBR 12909, whereas the 5HT2A/2C antagonist, ritanserin, enhanced the behavioral-stimulant effects of the lowest dose. GBR 12909 reliably maintained self-administration,
and ritanserin increased response rate maintained by the highest dose. The dopamine agonist, quinpirole, increased FI response
rate in only one of three subjects, and ritanserin enhanced the behavioral-stimulant effects of quinpirole in that subject.
The dopamine agonist, apomorphine, only decreased FI response rate, and ritanserin did not alter its behavioral effects. The
pharmacological profile of GBR 12909 administered alone and in combination with selective 5HT drugs in the present study was
similar to that obtained previously with cocaine, further demonstrating that 5HT can reliably modulate the behavioral effects
of psychomotor stimulants with prominent dopaminergic actions.
Received: 9 July 1996 / Final version: 22 November 1996 相似文献
2.
Inbred mouse strains have different numbers of midbrain dopaminergic neurons; for example, BALB/cJ mice have 20–25% more neurons than CBA/J mice. As the number of cells decrease, for example in Parkinson's disease and in animals with midbrain dopaminergic cell lesions, the activity of their remaining cells increases. The purpose of the present experiment was to determine whether the functional properties of dopaminergic neurons in the ventral tegmental area (nucleus A10) differ in inbred mouse strains which possess different numbers of cells. The firing rate and autoreceptor sensitivity of A10 dopaminergic cells were examined in the in vitro slice preparation in BALB/cJ, C3H/HeJ, CBA/J, and DBA/2J mouse strains. It was observed that the autoreceptors on mouse dopaminergic neurons exhibit pharmacological properties of dopamine autoreceptors; activation of the autoreceptor produced a marked inhibition (50–70%) in cell firing rate by quinpirole (10−8 M), LY-141865 (10−7 M), (+)-3-(3-hydroxyphenyl)-N-n-propyl-piperidine (10−6 M), propyl-norapomorphine (10−5 M) and dopamine (10−4 M), and this inhibition was blocked or reversed by specific dopamine D2 receptor antagonists [(−) sulphide and spiroperidol, 10−6 M]. The baseline firing rates of the A10 cells did not differ among the four inbred strains [range 2.5 ± 0.2 (C3H/HeJ)−3.4 ± 0.3 (CBA/J) spikes/s ±SEM], and there was no significant difference in autoreceptor sensitivity among the mouse strains as assessed either by superfused dopamine (inhibitory dose 50% ≈150 μM), or by superfused quinpirole (inhibitory dose 50% ≈10 nM). These data indicate that differences in A10 cell numbers of 30% do not significantly influence the baseline firing rate or autoreceptor sensitivity of the cells. 相似文献
3.
Enhanced stimulus-reward learning by intra-amygdala administration of a D3 dopamine receptor agonist
The amygdala is considered to be a critical neural substrate underlying the formation of stimulus-reward associations, and
is known to receive substantial innervation from dopaminergic neurons located within the ventral mesencephalon. However, relat-
ively little is known about the function of the mesoamygdaloid dopamine projection in stimulus-reward learning. Recently,
we have found post-session intra-amygdala microinjections of d-amphetamine to enhance appetitive Pavlovian conditioning as assessed in a discriminative approach task. In the present study,
we have examined the effects of dopamine receptor agonists possessing relative selectivity for the D1, D2 and D3 receptor subtypes in order to examine more fully the role of the mesoamygdaloid dopamine projection in stimulus-reward learning.
Thus, subjects were trained to associate an initially neutral stimulus (CS+) with 10% sucrose reward (US). A second, control stimulus (CS−) was also presented but never paired with sucrose reward. In order to measure specifically the conditioned response to CS+/CS− presentation, responding during CS and US presentations was measured separately. Immediately following each training session,
subjects received bilateral intra-amygdala infusion of 0.1, 1 or 10 nmol/side of SKF-38393, quinpirole or 7-OH-DPAT. Infusions
of SKF-38393 or quinpirole were without effect on CS+ approach. However, post-session intra-amygdala infusions of 7-OH-DPAT enhanced selectively CS+ approach in a dose-dependent fashion. No dose of any drug affected CS−approach, US behaviours, or measures of extraneous behaviour. Subsequent acquisition of a novel conditioned instrumental response
was also unaffected. Thus, the present data indicate a selective involvement of the D3 dopamine receptor subtype in the modulation of stimulus-reward learning by the mesoamygdaloid dopamine projection.
Received: 12 December 1996 / Final version: 9 April 1997 相似文献
4.
An innocuous sensory event (a prestimulus) that briefly precedes a startle-eliciting stimulus (SES) will reduce the amplitude
of the subsequently elicited reflex. In three experiments brief silent periods in otherwise continuous noise (gaps) were used
as prestimuli to investigate the effects of the D1 dopamine receptor agonist (±)-SKF-38393 (SKF) and the dopamine D2 receptor group agonist (−)-quinpirole hydrochloride on gap inhibition of the rat’s acoustic startle reflex. Gap durations
of 4 and 50 ms were analyzed. Quinpirole (0–1.6 mg/kg) had a biphasic effect on gap inhibition. Lower doses increased gap
inhibition, an effect that peaked at the 0.4 mg/kg dose. For higher doses, inhibition returned to control levels for the 4-ms
long gap, but remained elevated for the 50-ms long gap. SKF had no effect on gap inhibition, and haloperidol (0.2 mg/kg) reversed
the quinpirole-induced increase of gap inhibition. These data implicate the D2 dopamine receptor group in gap inhibition of startle modulation. The results are discussed in terms of the effects of catecholamine
agonists on attention.
Received: 25 July 1995/Final version: 28 April 1997 相似文献
5.
Neurophysiological investigation of effects of the D-1 agonist SKF 38393 on tonic activity of substantia nigra dopamine neurons 总被引:1,自引:0,他引:1
The effects of the D-1 agonist SKF 38393 on tonic activity of rat substantia nigra pars compacta dopamine neurons were studied using extracellular, single-unit recording techniques. Unlike nonselective D-1/D-2 dopamine agonists or the D-2 agonist quinpirole, SKF 38393 did not inhibit dopamine neuronal activity when applied iontophoretically or when administered intravenously in doses up to 20 mg/kg to chloral hydrate-anesthetized rats. Moreover, pretreatment with SKF 38393 did not alter the inhibitory response of these neurons to apomorphine or the D-2 agonist quinpirole. However, in locally anesthetized, gallamine-treated, artificially respired rats, dopamine cell activity was significantly altered by i.v. administration of SKF 38393; firing rate increases and decreases were observed. Administration of the inactive enantiomer of SKF 38393, S-SKF 38393, did not induce similar changes in parallel experiments. These results support the idea that unlike D-2 autoreceptor stimulation, D-1 receptor stimulation does not exert a direct local effect on dopamine neurons in the substantia nigra pars compacta and suggest that D-1 receptor stimulation at sites postsynaptic to the dopamine cells may indirectly affect the activity of some dopamine neurons through long-loop feedback mechanisms. 相似文献
6.
Robert D. Hienz Troy J. Zarcone Danielle A. Pyle Joseph V. Brady 《Psychopharmacology》1997,134(1):38-45
The effects of cocaine and quinpirole were studied in baboons to determine whether quinpirole, a relatively selective D2/D3 dopamine agonist, produced effects similar to those of cocaine on perceptual and motor processes. To measure perceptual and
motor function, three baboons were trained to discriminate differences between a standard vowel and four other synthetic vowels;
response accuracy as well as response latencies, or ”reaction times”, were measured following drug administrations. Cocaine
reduced reaction times in two baboons, and did not affect reaction times in a third; on the other hand, quinpirole lengthened
reaction times in a dose-dependent manner in all baboons. Cocaine and quinpirole also differed in the time course to produce
the maximal reaction time effect following drug administration. Cocaine and quinpirole did not differ consistently in their
perceptual effects, as indicated by similar changes in d′, a signal-detection index of discriminability. These distinct profiles of effects for cocaine and quinpirole suggest differing
neurochemical actions for these two drugs.
Received: 10 August 1996 /Final version: 16 May 1997 相似文献
7.
Functional coupling between heterologously expressed dopamine D(2) receptors and KCNQ channels 总被引:1,自引:0,他引:1
Ljungstrom T Grunnet M Jensen BS Olesen SP 《Pflügers Archiv : European journal of physiology》2003,446(6):684-694
Activation of KCNQ potassium channels by stimulation of co-expressed dopamine D2 receptors was studied electrophysiologically in Xenopus laevis oocytes and in mammalian cells. To address the specificity of the interaction between D2-like receptors and KCNQ channels, combinations of KCNQ1–5 channels and D2-like receptors (D2L, D3, and D4) were investigated in Xenopus oocytes. Activation of either receptor with the selective D2-like receptor agonist quinpirole (100 nM) stimulated all the KCNQ currents, independently of the subunit combination, indicating a common pathway of receptor-channel interaction. The KCNQ4 current was investigated in further detail and was increased by 19.9±1.6% (n=20) by D2L receptor stimulation. The effect could be mimicked by injection of GTPS and prevented by injection of Bordetella pertussis toxin, indicating that channel stimulation was mediated via a G protein of the Gi/o subtype. Cells of the human neuroblastoma line SH-SY5Y were co-transfected transiently with KCNQ4 and D2L receptors. Stimulation of D2L receptors increased the KCNQ4 current (n=6) as determined in whole-cell patch-clamp recordings. The specificity of the dopaminergic activation of the KCNQ channels was confirmed by co-expression of other neuronal K+ channels (BK, KV1.1, and KV4.3) with the D2L receptor in Xenopus oocytes. None of these K+ channels responded to stimulation of the D2L receptor. In the mammalian brain, dopamine D2 receptors and KCNQ channels co-localise postsynaptically in several brain regions, so modulation of neuronal excitability by dopamine release could in part be mediated via an effect on KCNQ channels. 相似文献
8.
The effects on schedule-controlled operant behavior of the D2 receptor agonist, quinpirole, and the D1 agonist, SKF 38393, were assessed alone and in combination with selective dopamine-receptor antagonists. Squirrel monkeys (Saimiri sciureus) were trained to press a response key under fixed-interval and fixed-ratio schedules of food reinforcement. The fixed-interval schedule maintained relatively low rates of responding that increased up to food presentation. The fixed-ratio schedule maintained relatively constant high rates of responding. Quinpirole increased rates and disrupted the temporal pattern of responding under the fixed-interval schedule at doses (0.1–1.0 mg/kg) that decreased rates of responding under the fixed-ratio schedule. Under the fixed-interval schedule, the D2 antagonists, spiperone (0.003–0.006 mg/kg) and haloperidol (0.003–0.01 mg/kg), and the D1 antagonist, SCH 23390 (0.03 mg/kg), shifted the quinpirole dose-effect curve to the right. The maximal effects of quinpirole were decreased at the highest doses of the antagonists. However, only spiperone antagonized effects of quinpirole on the rates of responding under the fixed-ratio schedule. The D1 agonist, SKF 38393, dose-dependently (1.0–10.0 mg/kg) decreased rates of responding under both schedules. Those effects were not antagonized by any doses studied of either spiperone (0.003 mg/kg) or SCH 23390 (0.003–0.3 mg/kg). Rather, both antagonists enhanced the effects of SKF 38393. The present study suggests significant differences between the effects of D1 and D2 agonists on schedule-controlled behavior, and differences in the antagonist actions of the D2 antagonists haloperidol and spiperone. Further, the selective dopamine D1 agonist, SKF 38393, has behavioral effects that cannot be antagonized by either a D1 or D2 antagonist, suggesting that some other mechanism has a significant role in mediating its behavioral effects. 相似文献
9.
Post-training administration of theN-methyl-d-aspartate (NMDA) antagonists CPP (0.5 and 1.0 mg/kg) and MK-801 (0.25 and 0.5 mg/kg) impaired, in a dose dependent fashion, the one-trial inhibitory avoidance response in NMRI mice. The D1 dopamine (DA) agonist SKF 38393 (10 and 20 mg/kg) and the D2 agonist quinpirole (0.5 and 1.0 mg/kg) instead facilitate the response in the same behavioral paradigm. Sub-chronic blockade of NMDA receptors with MK-801 (0.25 mg/kg once a day for 14 days) did not change the response to both competitive (CPP) and non-competitive (MK-801) NMDA antagonists. The same chronic treatment with MK-801 induced an increased response to both SKF 38393 and quinpirole. These data suggest that repeated administration of MK-801 induce an upregulation of both D1 and D2 DA receptors without affecting NMDA receptors. 相似文献
10.
Rationale: The purpose of the present investigation was to evaluate the effects of the D3 agonist (±)-7-hydroxy-dipropylaminotetralin (7-OH-DPAT), various dopamine (DA) agonists and DA antagonists on the antinociceptive
effects of μ opioids. Methods: Antinociception was assessed using a warm-water tail-withdrawal procedure in rats. Results: The μ opioids morphine (0.3–10 mg/kg) and dezocine (0.03–3.0 mg/kg) produced dose-dependent increases in antinociception
with maximal effects obtained at the higher doses tested. Pretreatment with the putative D3 agonist 7-OH-DPAT (1.0–10 mg/kg) produced a dose-dependent attenuation of the antinociceptive effects of morphine and dezocine.
At the highest dose of 7-OH-DPAT tested, the morphine dose-effect curve was shifted rightward by approximately 1.5 log units
and the dezocine curve by greater than 2.3 log units. The (+)-isomer of 7-OH-DPAT (1.0 and 3.0 mg/kg) also shifted the morphine
dose-effect curve to the right in a dose-dependent manner. The DA D3/D2 agonist (−)-quinpirole (0.1–10 mg/kg) attenuated the effects of morphine, but these effects were small in magnitude, not
dose-dependent and observed only under a limited set of conditions. The DA D2/D3 antagonist spiperone failed to alter the morphine dose-effect curve, but reversed the effects of 7-OH-DPAT on morphine antinociception.
Pretreatment with the DA D1 agonist (±)-SKF38393 (1.0 and 10 mg/kg) and the D1 antagonist (+)-SCH23390 (0.1 and 1.0 mg/kg) failed to alter the morphine dose-effect curve. Conclusion: The finding that 7-OH-DPAT markedly attenuated the effects of morphine and that these effects were reversed with spiperone
suggests that activity at the D3, and possibly the D2, receptor can modulate μ agonist-induced antinociception.
Received: 30 June 1998/Final version: 12 January 1999 相似文献