ライフサイエンスコーパス: dopamine agonist

1 levodopa towards initial monotherapy with a dopamine agonist.

2 unox which is a 5HT-1A agonist and a partial dopamine agonist.

3 oadenosine 3':5'-cyclic monophosphate or the dopamine agonist.

4 experienced improvement with a low dose of a dopamine agonist.

5 f14-deficient mice have reduced responses to dopamine agonists.

6 e expressed after systemic administration of dopamine agonists.

7 izophrenia patients and in rats treated with dopamine agonists.

8 rawing dopaminergic medication, particularly dopamine agonists.

9 17% of patients with Parkinson's disease on dopamine agonists.

10 catechol-O-methyltransferase inhibitors, or dopamine agonists.

11 mic women who are resistant or intolerant to dopamine agonists.

12 reatment of prolactinomas is mainly based on dopamine agonists.

13 on's disease controls were tested ON and OFF dopamine agonists.

14 simultaneous administration of serotonin and dopamine agonists.

15 prolactinomas, initial therapy is generally dopamine agonists.

16 ress disruptions in zebrafish PPI induced by dopamine agonists.

17 up to 14% of Parkinson's disease patients on dopamine agonists.

18 exacerbations in headache were observed with dopamine agonists.

19 ine (Spearman's rho 0.22, p=0.005) and ergot dopamine agonists (0.24, p=0.006) but not correlated wit

20 mals occurred when dopamine or a long-acting dopamine agonist (2-amino-6, 7-dihydroxy-1, 2, 3, 4-tetr

21 sias decreases as a result of initial use of dopamine agonists; (2) surgery, primarily in the form of

22 Treatment of intact rats with the full D(1) dopamine agonist A-77636 induced Fos-like immunoreactivi

23 intermittent, sensitizing regimen of the D1 dopamine agonist ABT-431 dramatically enhances working m

24 Dopamine agonist administration induces changes in firin

25 Dopamine agonists also increase striatal prediction erro

26 NMe-Phe4, Glyo15-enkephalin and the indirect dopamine agonist amphetamine induced a marked increase i

27 nal response to subsequent administration of dopamine agonist, an effect called 'priming'.

28 Thirty-eight patients were treated with a dopamine agonist and 95 with l-dopa (median l-dopa equiv

29 ate receptor, which also acts as an indirect dopamine agonist and at sigma sites, can induce a long l

30 d following combined adenosine antagonist-D1 dopamine agonist and combined D1 dopamine agonist-D2 dop

31 otic derivative of morphine, which acts as a dopamine agonist and is clinically used to treat "off-st

32 Dopamine agonists and antagonists have opposite effects

33 ly, pharmacological evidence shows that both dopamine agonists and antidopaminergics can improve bipo

34 Dopamine agonists and drugs that block dopamine metaboli

35 ans should warn patients prior to initiating dopamine agonists and enquire about these behaviors duri

36 el was evaluated using several high-affinity dopamine agonists and m- and p-tyramine, two compounds w

37 ng, we investigated the relationship between dopamine agonists and risk taking in patients with Parki

38 NT FINDINGS: Existing medical agents such as dopamine agonists and somatostatin ligand receptors are

39 Right-handed PD patients treated with dopamine agonists and/or levodopa, and age- and educatio

40 locomotor responses to cocaine (an indirect dopamine agonist) and to D2 but not to D1 receptor agoni

41 inhibitors of dopamine-metabolizing enzymes, dopamine agonists, and extended release dopamine formula

42 past decade and include carbidopa/levodopa, dopamine agonists, and monoamine oxidase type B (MAO-B)

43 administering medications (benzodiazepines, dopamine agonists, and/or dantrolene) or electroconvulsi

44 binding affinities of dopamine, three known dopamine agonists (antiparkinsonian), and seven known an

45 ts primed with three injections of the D1/D2 dopamine agonist apomorphine (0.5 mg/kg) permitted a cha

46 the climbing behavior in rats induced by the dopamine agonist apomorphine (600 microg/kg) with an ED(

47 hese prepulse effects were eliminated by the dopamine agonist apomorphine (in rats).

48 Three priming injections with the D1/D2 dopamine agonist apomorphine permits a challenge with th

49 of the mice to the locomotor effects of the dopamine agonist apomorphine, the psychostimulants cocai

50 ction of motor deficits was prevented by the dopamine agonist apomorphine.

51 dose (600 microgram/kg) of the non-selective dopamine agonist apomorphine.

52 ing the behavioral effects in animals of the dopamine agonist apomorphine.

53 eferences were tested after injection of the dopamine agonist, apomorphine (APO), or vehicle.

54 nhibition (PPI) of the startle reflex by the dopamine agonists, apomorphine (APO) and D-amphetamine (

55 el was evaluated at both receptors using the dopamine agonists, apomorphine and 7-OH-DPAT.

56 rant behavior maintained by food or a direct dopamine agonist are similarly affected.

57 The most frequently used dopamine agonists are bromocriptine and cabergoline.

58 Levodopa and the dopamine agonists are effective symptomatic treatments f

59 Dopamine agonists are inexpensive oral agents but, altho

60 Short-acting pulsatile dopamine agonists are more likely to induce dyskinesia t

61 Most currently used dopamine agonists are selective for D2-like receptors, w

62 Dopamine agonists are the preferred treatment for both s

63 quent testing with food, cocaine or a direct dopamine agonist as reinforcers, fixed ratio and progres

64 otes generation of spinal motor neurons, and dopamine agonists augment this process.

65 s and augmented locomotor response to direct dopamine agonists both in intact and in dopamine-deplete

66 the reinforcing effects of cocaine and other dopamine agonists, but not food or opioids, in mice.

67 in men; they are generally treated with the dopamine agonists cabergoline and bromocriptine.

68 Dopamine agonists can be used as an alternative initial

69 ential for this diagnosis and treatment with dopamine agonists can provide benefit.

70 ensitizing course of quinpirole, a D(2)/D(3) dopamine agonist, can be modified by the MAO(A) inhibito

71 We tested the hypothesis that a D1 dopamine agonist could stimulate acetylcholine release d

72 s suggest that combining rehabilitation with dopamine agonists could enhance both the saliency of the

73 Our novel multifunctional dopamine agonists D-519 and D-520 exhibited significant

74 The dopamine agonist, D-amphetamine, biased the rats toward

75 tagonist-D1 dopamine agonist and combined D1 dopamine agonist-D2 dopamine agonist treatment.

76 n the analysis, 86% started DRT, 40% were on dopamine agonists (DA), 19% reported incident ICD behavi

77 om dopaminergic medication use, particularly dopamine agonists (DAA).

78 d an association between ICDs and the use of dopamine agonists (DAs), particularly at greater dosages

79 Ropinirole, which is a non-ergot dopamine agonist derivative, exerts therapeutic benefits

80 ive responsiveness of D1 striatal neurons to dopamine agonists develops, indicated by the induction o

81 ive treatment of adenomas with octreotide or dopamine agonists did not change the apoptotic index sig

82 ergent synthesis was developed for the novel dopamine agonist dinapsoline.

83 We examined the effects of the indirect dopamine agonist (dopamine reuptake inhibitor) GBR-12909

84 induction of dyskinesia, and both D1 and D2 dopamine agonist drugs are able to initiate dyskinetic m

85 There is evidence that partial D2-like dopamine agonists (e.g., terguride) may not affect D2-li

86 o involve mechanisms other than stimulant or dopamine agonist effects.

87 Dopamine agonists enhance sensitivity to risk in patient

88 (DEX; 10(-6) M) as early as e15.5, while the dopamine agonist ergocryptine (ERG; 10(-6) M) did not al

89 yskinesias after intermittent treatment with dopamine agonists following dopamine depletion are all c

90 Strong evidence supports using levodopa and dopamine agonists for motor symptoms at all stages of Pa

91 nd patients who had started treatment with a dopamine agonist had developed these treatment complicat

92 Initiating therapy with a long-acting dopamine agonist has been shown to delay the onset and r

93 Methamphetamine (MAP), an indirect dopamine agonist, has been shown to produce a leftward s

94 Dopamine agonists have been shown to play a role in sele

95 Dopamine agonists have gained popularity as first-line m

96 Furthermore, dopamine agonists have shown to improve time estimation

97 Dopamine agonists improved headache in 25% and exacerbat

98 e clarified the relative roles of l-dopa and dopamine agonists in early Parkinson disease and shown t

99 Converging data suggest dopamine agonists in ICDs appear to enhance learning fro

100 , we show data consistent with the idea that dopamine agonists in susceptible individuals with Parkin

101 mparable to the highest levels obtained with dopamine agonists in the basal ganglia.

102 imally exposed by repeated administration of dopamine agonists in the postpubertal period (D1 priming

103 by a reduction in the downstream effects of dopamine agonists in these models.

104 D2 family dopamine agonists, including low doses of the D3-preferr

105 Quinpirole (10 microM), a D2 dopamine agonist, increased rod-cone coupling, whereas s

106 provide a model for enhanced sensitivity to dopamine agonist-induced disruption of PPI.

107 Strain differences in sensitivity to dopamine agonist-induced disruption of prepulse inhibiti

108 ell, cell-based functional assay to quantify dopamine agonist-induced ERK phosphorylation in D2- and

109 king D(5) dopamine receptors were tested for dopamine agonist-induced phosphoinositide signaling both

110 Caffeine attenuated dopamine agonist-induced striatal c-Fos expression.

111 This switch is suggested to underlie dopamine-agonist-induced dyskinetic movements that devel

112 Dopamine agonists, involving selective or mixed D1 and D

113 Dopamine agonists lead to a substantial improvement in m

114 sults provide a potential explanation of why dopamine agonists may lead to an unconscious bias toward

115 sensitivity to the PPI-disruptive effects of dopamine agonists may provide insight into the genetic b

116 ntadine, anticholinergics, beta-blockers, or dopamine agonists) may be initiated first to avoid levod

117 We have previously reported that specific dopamine agonists mediate protection against apoptosis i

118 ogical perspective, the effects of selective dopamine agonists mimic the anti-inflammatory effects of

119 Methylphenidate hydrochloride, an indirect dopamine agonist, normalizes task-related regional brain

120 , similar to the exaggerated responsivity to dopamine agonists observed in many schizophrenia patient

121 sted the effects of an opioid antagonist and dopamine agonist on the ability of a salient white noise

122 patients with early PD to test the effect of dopamine agonists on clinical and neuroimaging markers o

123 ations have developed, adjuvant therapy with dopamine agonists or entacapone can reduce off time and

124 ld improvement in motor function compared to dopamine agonists or levodopa.

125 ment with levodopa, SKF 38393 (D1-preferring dopamine agonist), or quinpirole (D2-preferring agonist)

126 initiation of levodopa therapy, the role of dopamine agonists, particularly ropinirole and pramipexo

127 ssants fenfluramine and dexfenfluramine, the dopamine agonists pergolide and cabergoline, and more re

128 C-propyl-norapomorphine ((11)C-NPA) is a new dopamine agonist PET radiotracer that holds potential fo

129 (11)C-N-propylnorapomorphine ((11)C-NPA), a dopamine agonist PET tracer, in human subjects and deter

130 vivo pharmacological profile for an indirect dopamine agonist pharmacotherapy for treating cocaine, m

131 iac surgery, anticoagulation, treatment with dopamine agonists, pituitary stimulation testing, and pr

132 The dopamine agonist pramipexole (PPX) can increase impulsiv

133 In models of dopaminergic neuronal loss, the dopamine agonist pramipexole has exhibited neuroprotecti

134 Previous studies suggest that the dopamine agonist pramipexole may possess antidepressant

135 phy (PET), [15O]water, and the D3-preferring dopamine agonist pramipexole to identify D3-mediated reg

136 target for drugs effective in RLS, including dopamine agonists (pramipexole and ropinirole) and alpha

137 Long-acting dopamine agonists providing continuous, rather than puls

138 tion of 1.0 mg/kg d-amphetamine, an indirect dopamine agonist, quickly restored behavioral activation

139 was observed for prior treatment with the D2 dopamine agonist quinpirole and stimulation of cAMP synt

140 The D(2) dopamine agonist quinpirole or the D(1) dopamine agonist

141 e further compared to those of the D(2)-like dopamine agonist quinpirole using a factorial design in

142 lso shown that pretreatment with the D2-like dopamine agonist quinpirole virtually abolishes RU-24969

143 n effect blocked by pretreatment with the D2 dopamine agonist quinpirole.

144 red and compared to the response of the full dopamine agonist quinpirole.

145 Preclinical studies have demonstrated that dopamine agonists reduce dopamine formation in compariso

146 Dopamine agonist-related ventral striatal hypoactivity t

147 of virtually all antidepressants is enhanced dopamine agonist responsiveness.

148 hat systemic administration of non-selective dopamine agonists results in a pronounced expression of

149 on's disease (PD) patients taking either the dopamine agonist ropinirole or L-DOPA.

150 Here, we investigated whether the dopamine agonist rotigotine would have a beneficial effe

151 In one series of experiments we used the dopamine agonists, SKF 82958 and quinpirole as relativel

152 ropargylxanthine (DMPX: 10 mg/kg) and the D1 dopamine agonist SKF38393 (0.5 mg/kg) to 6-OHDA-lesioned

153 observed after coadministration of D1 and D2 dopamine agonists (SKF38393: 0.5 mg/kg + quinpirole: 0.0

154 D(2) dopamine agonist quinpirole or the D(1) dopamine agonist SKF82958 reversed this contralateral ro

155 moadenosine 3':5'-cyclic monophosphate, or a dopamine agonist, SKF82958.

156 results support the hypothesis that specific dopamine agonists stabilize distinct conformations of th

157 ptors in the dorsal striatum does not affect dopamine agonist-stimulated behaviors or neuropeptide mR

158 Treatment with dopamine agonists such as pramipexole or ropinirole allo

159 ent's treatment to an equivalent dosage of a dopamine agonist that can be administered once daily or

160 ent's treatment to an equivalent dosage of a dopamine agonist that can be administered once daily or

161 d if systemic administration of Piribedil, a dopamine agonist that reduces the sound evoked auditory

162 o results in a sensitization of responses to dopamine agonists that is manifest by increased activati

163 rate amount of PD treatment and can tolerate dopamine agonist therapy.

164 In patients on dopamine agonists, these behaviors as a group are relati

165 Administration of dopamine agonists to 6-hydroxydopamine (6-OHDA) lesioned

166 r neurotensin plays a role in the ability of dopamine agonists to increase extracellular GABA levels.

167 e is increasing interest in the potential of dopamine agonists to provide a neuroprotective effect an

168 istence of dyskinesia induced by levodopa or dopamine agonist treatment.

169 agonist and combined D1 dopamine agonist-D2 dopamine agonist treatment.

170 this supersensitive response with long-term dopamine agonist treatments may provide insights into dy

171 covariates of amantadine use, including both dopamine agonist use and levodopa dosage.

172 We further showed that pramipexiole, a dopamine agonist used to treat human RLS, reduced RLS-li

173 effect was a very long-lasting one since the dopamine agonist was administered 6 weeks after cessatio

174 In contrast, motor stimulation by a D1 dopamine agonist was not attenuated in the KO mice.

175 tion, and IV self-administration of a direct dopamine agonist was robust in the DAT(-/-) mice.

176 ith worsening, whereas treatment with direct dopamine agonists was followed by immediate ambulation,

177 In patients with impulse control disorder, dopamine agonists were associated with enhanced sensitiv

178 he neuroprotective effects of pramipexole, a dopamine agonist, were investigated in 3-acetylpyridine

179 ,5,1-ij]quinolin-5-amine [(R)-3] is a potent dopamine agonist when tested in animals but surprisingly