ライフサイエンスコーパス: dopamine agonist

1 levodopa towards initial monotherapy with a dopamine agonist.

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

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

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

5 exacerbations in headache were observed with dopamine agonists.

6 This risk is magnified by dopamine agonists.

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

8 e expressed after systemic administration of dopamine agonists.

9 izophrenia patients and in rats treated with dopamine agonists.

10 17% of patients with Parkinson's disease on dopamine agonists.

11 prolactinomas, initial therapy is generally dopamine agonists.

12 rawing dopaminergic medication, particularly dopamine agonists.

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

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

15 reatment of prolactinomas is mainly based on dopamine agonists.

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

17 simultaneous administration of serotonin and dopamine agonists.

18 faced an even higher ICD risk when receiving dopamine agonists.

19 ress disruptions in zebrafish PPI induced by dopamine agonists.

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

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

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

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

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

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

26 Dopamine agonist administration induces changes in firin

27 Previous small trials of dopamine agonists after stroke provide equivocal evidenc

28 Dopamine agonists also increase striatal prediction erro

29 treatment compared with MAO-B inhibitors or dopamine agonists among people with PD who experienced m

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

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

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

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

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

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

36 Dopamine agonists and antagonists have opposite effects

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

38 Dopamine agonists and drugs that block dopamine metaboli

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

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

41 as migraine preventives in both sexes, while dopamine agonists and prolactin/ prolactin receptor anti

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

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

44 as octreotide, lanreotide and pasireotide), dopamine agonists and the growth hormone receptor antago

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

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

47 inergic medications (eg, carbidopa-levodopa, dopamine agonists), and slower disease progression.

48 mbinations of medications, i.e., Levodopa, a dopamine agonist, and other PD medications, as possible

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

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

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

52 opioids, psychostimulants, anticonvulsants, dopamine agonists, antidepressants, antipsychotics, misc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 Levodopa and the dopamine agonists are effective symptomatic treatments f

68 Dopamine agonists are inexpensive oral agents but, altho

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

70 However, an important question is whether dopamine agonists are most beneficial for patients with

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

72 Dopamine agonists are the preferred treatment for both s

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

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

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

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

77 mone receptor antagonist pegvisomant and the dopamine agonist cabergoline on biochemical control, cli

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

79 Monoamine oxidase-B inhibitors and dopamine agonists can be reserved as potential adjunct t

80 Dopamine agonists can be used as an alternative initial

81 tment by the dopamine precursor levodopa and dopamine agonists can improve motor symptoms, no disease

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

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

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

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

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

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

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

89 e, total levodopa equivalent daily dose, and dopamine agonist (DA) and antidepressant medication use.

90 We investigated the association between dopamine agonist (DA) exposure and conversion to neovasc

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

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

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

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

95 Some patients treated with dopamine agonists develop pathological behaviours, such

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

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

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

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

100 Although dopamine agonist dose did modulate pupillary responses t

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

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

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

104 Dopamine agonists enhance sensitivity to risk in patient

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

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

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

108 cident gambling disorder were treatment with dopamine agonists (Frequency ratio 1.4, p=0.058), monoam

109 years) of follow-up, the participants in the dopamine agonist group had a mean PDQ-39 mobility score

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

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

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

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

114 Dopamine agonists have gained popularity as first-line m

115 Furthermore, dopamine agonists have shown to improve time estimation

116 Dopamine agonists improved headache in 25% and exacerbat

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

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

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

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

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

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

123 The efficacy of dopamine agonists in treating major depressive disorder

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

125 g complexes with selective and non-selective dopamine agonists, including two currently used anti-Par

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

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

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

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

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

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

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

133 Dopamine agonists, involving selective or mixed D1 and D

134 Apomorphine, a dopamine agonist, is a highly effective therapeutic to p

135 Rotigotine (RTG), a dopamine agonist, is currently administered as a transde

136 Dopamine agonists lead to a substantial improvement in m

137 equivalent daily dose total (LEDD-total) and dopamine agonists (LEDD-DA).

138 Open-label dopamine agonist, MAO-B inhibitor, or COMT inhibitor.

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

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

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

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

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

144 Delayed administration of pramipexole, a dopamine agonist, mitigates lethality in bacterial sepsi

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

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

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

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

149 mend initiation of therapy with low doses of dopamine agonists or a(2)d ligands in severe forms.

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

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

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

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

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

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

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

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

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

159 The dopamine agonist pramipexole (PPX) can increase impulsiv

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

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

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

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

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

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

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

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

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

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

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

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

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

173 Dopamine agonist-related ventral striatal hypoactivity t

174 of virtually all antidepressants is enhanced dopamine agonist responsiveness.

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

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

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

178 Dopamine agonists should thus be used cautiously in depr

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

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

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

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

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

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

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

186 Treatment with dopamine agonists such as pramipexole or ropinirole allo

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

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

189 Apomorphine is a dopamine agonist that is used for the management of Park

190 enting RE, we tested methylphenidate(MPH), a dopamine agonist that promotes PFC-dependent learning an

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

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

193 tudies, reveal the conserved binding mode of dopamine agonists, the unique pocket topology underlying

194 nd/or gambling disorders can be triggered by dopamine agonist therapies used to treat Parkinson's dis

195 Dopamine agonist therapy may therefore be potentiating r

196 dverse effects and options for withdrawal of dopamine agonist therapy, as well as indications for sur

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

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

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

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

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

202 Main predictors for other ICDs were dopamine agonist treatment (frequency ratio 1.6, p=0.003

203 Ds that had previously been identified, like dopamine agonist treatment and raise additional attentio

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

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

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

207 k remained significant after controlling for dopamine agonist use (HR = 1.97, 95% CI = 1.33-2.9, p <

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

209 e also evaluated this effect controlling for dopamine agonist use as a time-dependent variable and fo

210 by other known factors, such as decreases in dopamine agonist use.

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

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

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

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

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

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

217 When dopamine agonists were compared with MAO-B inhibitors on

218 n patients with impulse control disorders on dopamine agonists were excluded from the analysis.

219 Dopamine agonists were shown to be effective for treatme

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

221 ,5,1-ij]quinolin-5-amine [(R)-3] is a potent dopamine agonist when tested in animals but surprisingly