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1 roved working memory with the a2A-NA agonist Guanfacine.
2 ng might decrease the beneficial efficacy of guanfacine.
3 s of alpha(2A)AR evoked by clonidine than by guanfacine.
4 sulted in loss of the beneficial response to guanfacine.
5 entify the molecular target of the action of guanfacine.
6 d for modafinil, atomoxetine, clonidine, and guanfacine.
7 e remediation and social skills training (15 guanfacine, 13 placebo).
8 o receive either daily placebo (12 M/7 F) or guanfacine (2 or 3 mg) (15 M/6 F) for 3 weeks.
9                           Here, we show that guanfacine, a noradrenergic agonist that modulates dorso
10                                              Guanfacine, a noradrenergic alpha2a agonist, reduced tob
11 ic animals responded to both amphetamine and guanfacine, an alpha2A adrenergic receptor agonist.
12      Lastly, inhibiting cAMP generation with guanfacine, an alpha2A-noradrenergic agonist, normalized
13                                         Both guanfacine and cognitive remediation plus social skills
14 tex and identify the molecular substrate for guanfacine and novel therapeutic interventions.
15                Interfering with this role by guanfacine and similar clinically used drugs can have la
16 s with schizotypal personality disorder, and guanfacine appears to be a promising pharmaceutical augm
17                                              Guanfacine appears to be a safe and effective treatment
18                             Extended-release guanfacine appears to be safe and effective for reducing
19 t into the impact of dose on the efficacy of guanfacine as a treatment for stress-induced relapse of
20                            The modal dose of guanfacine at week 8 was 3 mg/day (range: 1-4 mg/day), a
21                   Systemic administration of guanfacine blocked the increase in immobility in respons
22                                              Guanfacine both excited and inhibited aspects of Guansem
23 tudies show that alpha2A-AR agonists such as guanfacine can restore dlPFC network firing and cognitiv
24 on-Improvement scale) was 50% (15 of 30) for guanfacine compared with 9.4% (3 of 32) for placebo.
25 ive remediation, social skills training, and guanfacine demonstrated statistically significant improv
26                                              Guanfacine did, however, reduce sympathetic tone as well
27          Importantly, we found that low-dose guanfacine does not increase BNST activity, but prevents
28  In an initial dose-testing phase we found a Guanfacine dose that increased performance accuracy, dec
29                  Monkeys treated with higher guanfacine doses also appeared less disinhibited, sugges
30 is hypothesis by stimulating alpha2ARs using Guanfacine during attentional set shifting in male nonhu
31                                     Although guanfacine engages alpha(2a)-AR autoreceptors, it also a
32     In slices from these mice, we found that guanfacine enhanced, rather than suppressed, optogenetic
33                        The alpha2-AR agonist guanfacine enhances prefrontal cortical functions in rat
34 und that two alpha(2) ligands, clonidine and guanfacine, exhibit differential abilities in activating
35 l translation from animals to humans include guanfacine for the treatment of ADHD and related PFC dis
36 o the successful translation of prazosin and guanfacine for treating stress-related disorders.
37 igh doses of the alpha-2A adrenergic agonist guanfacine (GFC) to aged monkeys has been shown to impro
38 , we test this hypothesis using clonidine or guanfacine (GFC), another alpha-2 agonist, in a model of
39 d hyperactivity index improved by 27% in the guanfacine group and 21% in the placebo group, not a sig
40                                          The guanfacine group showed a 43.6% decline in scores on the
41                          For subjects in the guanfacine group, blood pressure declined in the first 4
42         Tic severity decreased by 31% in the guanfacine group, compared to 0% in the placebo group.
43 sed by 22% and omission errors by 17% in the guanfacine group, compared with increases of 29% in comm
44 ctivated by the alpha(2a)-AR partial agonist guanfacine ("Guansembles") in the bed nucleus of the str
45                                              Guanfacine had no effect on PTSD symptoms, subjective sl
46 )-adrenergic receptor (alpha(2a)-AR) agonist guanfacine has been investigated as a potential treatmen
47 and stress-induced craving in human studies, guanfacine has not been reported to decrease relapse rat
48 he effects of the alpha2 adrenergic agonist, guanfacine HCl, on responses to stress and drug cue in a
49  a precision medicine approach, we evaluated guanfacine immediate release (GIR), an alpha(2A) recepto
50              But it has been unclear whether Guanfacine improves specific attention and learning mech
51                                         Oral guanfacine in the treatment of ADHD had no effect on ocu
52   The findings suggest further evaluation of guanfacine in the treatment of cocaine use disorder with
53 s study evaluated the efficacy and safety of guanfacine in treating children with tic disorders and a
54                                              Guanfacine-induced normalization of dopamine signaling m
55                     The local application of guanfacine into either the prelimbic cortex or the ventr
56                             Extended-release guanfacine is approved for children with attention defic
57  This information is particularly timely, as guanfacine is currently the focus of large clinical tria
58 dopamine (bromocriptine) and norepinephrine (guanfacine) manipulations did not improve performance or
59 ine and CRF, and point to an action by which guanfacine may reduce negative affective responses.
60 le pharmacotherapy were randomly assigned to guanfacine (N=29) versus placebo (N=34).
61 5 years [SD=2.25]) were randomly assigned to guanfacine (N=30) or placebo (N=32) for 8 weeks.
62 preference (CPP) and the effects of low dose guanfacine on BNST activity and stress-induced reinstate
63 inally, we evaluated the effects of low-dose guanfacine on BNST cFOS immunoreactivity and stress-indu
64 e findings highlight sex-specific effects of guanfacine on drug craving, anxiety, and negative mood w
65                               The effects of guanfacine on performance of the delayed alternation tas
66  This study aimed to evaluate the effects of guanfacine on the anterior and posterior segments of the
67  extended-release alpha2-adrenergic agonists guanfacine or clonidine (no studies).
68 ssigned to receive 8 weeks of treatment with guanfacine or placebo under double-blind conditions.
69  (the alpha(2A) adrenergic receptor agonist, guanfacine) or repetitive transcranial magnetic stimulat
70            A significant time-by-medication (guanfacine, placebo) interaction was observed for MCCB r
71 d, double-blind, placebo-controlled trial of guanfacine plus cognitive remediation and social skills
72                                              Guanfacine produced inhibition of cAMP-dependent signali
73 ation of alpha(2A)AR with clonidine, but not guanfacine, promotes the interaction of the actin bindin
74                             Six of the hits (guanfacine, quinidine, xylometazoline, oxymetazoline, fe
75 A)-adrenergic receptors (ARs) by the agonist guanfacine reduced cFos expression in these neurons both
76 inically well tolerated alpha(2A)-AR agonist guanfacine reduces activity of these cells in vivo, and
77       We found that the alpha(2A)-AR agonist guanfacine selectively inhibited this PBN input to the B
78                                              Guanfacine significantly attenuated cocaine craving, alc
79                                          One guanfacine subject with sedation withdrew at week 4.
80 non-stimulant drugs, such as atomoxetine and guanfacine, suggest that targeting the norepinephrine (N
81 ated by the centrally acting alpha2a agonist guanfacine, suggesting a role of increased sympathetic t
82 mulations, atomoxetine, and extended-release guanfacine to improve symptoms of ADHD in adolescents.
83 e in baseline BPND from the untreated to the guanfacine-treated condition.
84 e and was compared between the untreated and guanfacine-treated conditions.
85                                         Four guanfacine-treated subjects (13.3%) and four placebo sub
86               A subset (n=12) then underwent guanfacine treatment (3 mg/day for 3 weeks) and the set
87                                              Guanfacine treatment attenuated amphetamine-induced DA r
88 errations was observed at the sixth month of guanfacine treatment in comparison with the baseline exa
89                                      Chronic guanfacine treatment reduced [(11)C]FLB457 BPND in tobac
90 e examination findings at the sixth month of guanfacine treatment.
91 n before and 6 months after the beginning of guanfacine treatment.
92 athetic neurons in response to clonidine and guanfacine, two drugs used for treatment of hypertension
93 double-blind, randomized controlled trial of guanfacine versus placebo for posttraumatic stress disor
94                  After 8 weeks of treatment, guanfacine was associated with a mean improvement of 37%
95                                              Guanfacine was associated with a number of side effects.
96                                              Guanfacine was associated with insignificant decreases i
97  randomized clinical trial, extended-release guanfacine was compared with placebo in children with AS
98                                              Guanfacine was then used in all local injection studies.
99                      The positive effects of guanfacine were associated with extended ability to main
100             Nine of 17 subjects who received guanfacine were blindly rated on the Clinical Global Imp
101                                              Guanfacine, which is an alpha-2 agonist with a higher af
102 ntal exposure to the alpha2 receptor agonist guanfacine, which is commonly used in the pediatric popu
103 Ca(2+) current suppression by clonidine than guanfacine, which paralleled a more marked receptor phos
104 mine release before and after treatment with guanfacine with [(11)C]FLB457, a dopamine D2/D3 receptor
105  faster feature-based reversal learning with Guanfacine with single-subject computational modeling.

 
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