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1 stsynaptic blockade of calcium channels (for gabapentin).
2 le and ropinirole) and alpha2 delta ligands (gabapentin).
3  that was also reversed by pre-incubation in gabapentin.
4 e pain during neuropathy that is reversed by gabapentin.
5 or for the anti-epileptic and analgesic drug gabapentin.
6 h amitriptyline, carbamazepine, diazepam and gabapentin.
7 e taking the placebo and in some patients on gabapentin.
8  domain of thrombospondin-2 was prevented by gabapentin.
9 d research, were extensively used to promote gabapentin.
10 ad complete resolution of nausea when taking gabapentin.
11 , after she was placed on the anticonvulsant gabapentin.
12 rmine the specificity of hBCATc for the drug gabapentin.
13 4 patients enrolled in an open-lbel trial of gabapentin.
14 dorsal horn neurons that could be blocked by gabapentin.
15 with highest correlations for acesulfame and gabapentin.
16  from slices that had been pre-incubation in gabapentin.
17 CaV2.2 and alpha2delta-1 is not disrupted by gabapentin.
18 pine and have been successfully treated with gabapentin.
19 ts noted improvement in symptoms when taking gabapentin.
20 effects more potently and efficaciously than gabapentin.
21 e half were pre-incubated in aCSF containing gabapentin.
22 of newer antidepressants and three trials of gabapentin.
23 ome reporting for trials of off-label use of gabapentin.
24 (hazard ratio [HR] 0.78 [95% CI 0.63-0.97]), gabapentin (0.65 [0.52-0.80]), and topiramate (0.64 [0.5
25  carbamazepine was significantly better than gabapentin (0.75 [0.63-0.90]), and estimates suggest a n
26 , double-blind study was designed to compare gabapentin (1,200-2,400 mg/day) (n=75 patients) with pla
27                                              Gabapentin (1,200-2,400 mg/day) is safe and efficacious
28 ed a masked, crossover, therapeutic trial of gabapentin (1,200mg/day) versus memantine (40 mg/day) fo
29  the first time that the alpha2delta ligands gabapentin [1-(aminomethyl)cyclohexaneacetic acid] and p
30                     Subjects received either gabapentin (1200 mg/day) or matched placebo.
31 95; 95% CI, -1.44 to -0.47), and 2 trials of gabapentin (-2.05; 95% CI, -2.80 to -1.30).
32 y whereas intrathecal morphine (1microg) and gabapentin (200microg) partially reversed thermal and me
33 ed to be higher in patients taking high-dose gabapentin (3,300-3,600 mg/day) than in those taking sta
34 is, we did an open-label study in which oral gabapentin 300 mg thrice daily was given for every other
35 900 mg) and 347 at 8 weeks (113 placebo, 114 gabapentin 300 mg, and 120 gabapentin 900 mg).
36 71 participants at 4 weeks (119 placebo, 123 gabapentin 300 mg, and 129 gabapentin 900 mg) and 347 at
37 shes per day were randomly assigned placebo, gabapentin 300 mg/day, or gabapentin 900 mg/day by mouth
38 43) and 31% (16 to 46) in the group assigned gabapentin 300 mg; and 49% (42 to 56) and 46% (34 to 58)
39                                              Gabapentin (50mg/kg, i.p.) significantly reduced vlPAG n
40 (119 placebo, 123 gabapentin 300 mg, and 129 gabapentin 900 mg) and 347 at 8 weeks (113 placebo, 114
41 (113 placebo, 114 gabapentin 300 mg, and 120 gabapentin 900 mg).
42 56) and 46% (34 to 58) in the group assigned gabapentin 900 mg.
43  assigned placebo, gabapentin 300 mg/day, or gabapentin 900 mg/day by mouth in three divided doses fo
44                               We conducted a gabapentin (900 mg) challenge in healthy human subjects
45 m of this study was to assess the effects of gabapentin, a drug effective in neuropathic pain patient
46 e oligonucleotides to knock down Cavbeta and gabapentin, a drug that binds to and inhibits alpha2delt
47 ng pain; thus, there is a rationale to study gabapentin, a drug that increases the threshold to exper
48                                              Gabapentin, a drug useful in several neurological and ps
49 micked the effect of conditioned medium, and gabapentin, a high-affinity antagonist of TSP binding to
50                Blocking Cavalpha2delta1 with gabapentin, a ligand for the Cavalpha2delta1 proteins, o
51 s in nucleus accumbens, we demonstrated that gabapentin, a specific alpha2delta-1 antagonist, prefere
52 enaline reuptake inhibitors, pregabalin, and gabapentin; a weak recommendation for use and proposal a
53 sis, and medications such as venlafaxine and gabapentin.Additional information is available at: www.a
54 a provide complementary new information that gabapentin administered systemically and spinally can ef
55 verage 5.6%) and between day (average 4.8%), gabapentin administration was associated with an average
56  may account for the differential effects of gabapentin after chronic ethanol.
57 ined treatment v 49%; 95% CI, 26% to 58% for gabapentin alone) and scores (56%; 95% CI, 26% to 71% fo
58 ined treatment v 60%; 95% CI, 33% to 73% for gabapentin alone).
59 ctively alleviate hot flashes, compared with gabapentin alone, in patients with inadequate hot flash
60  weaned off the antidepressant and receiving gabapentin alone.
61 ntrathecal administration of 10-30 microg of gabapentin also produced a significant effect on the mec
62                                The effect of gabapentin, an anticonvulsant drug that is also effectiv
63                            Pretreatment with gabapentin, an inhibitor of the alpha2delta1 subunit, bl
64                Eighty-four patients received gabapentin and 70 (83%) completed the study; 81 received
65 d for treatment of neuropathic pain, such as gabapentin and amitriptyline.
66 enytoin proved ineffective, while valproate, gabapentin and carbamazepine varied in their potencies,
67                                              Gabapentin and duloxetine reversed mechanical hyperalges
68      Side effects included unsteadiness with gabapentin and lethargy with memantine.
69 ast potential interaction is associated with gabapentin and levetiracetam.
70 l antiepileptic agents, including valproate, gabapentin and phenytoin, reduced the ability of astrocy
71  target of the potent neuropathic analgesics gabapentin and pregabalin (alpha2delta-1 and alpha2delta
72                        The therapeutic drugs gabapentin and pregabalin (PGB), which are both alpha(2)
73 ostherpetic neuralgia compared with placebo, gabapentin and pregabalin are associated with a modest i
74                                              Gabapentin and pregabalin are structurally related compo
75                           The interaction of gabapentin and pregabalin with conventional antiepilepti
76  effectiveness of the alpha-2-delta ligands (gabapentin and pregabalin) and the norepinephrine/seroto
77 ponsive to a variety of therapies, including gabapentin and topiramate.
78 ly comparable to what has been reported with gabapentin and with some newer antidepressants.
79 tremor patients (primidone, propranolol, and gabapentin) and several candidates hypothesized to reduc
80       One hundred thirteen patients received gabapentin, and 89 (78.8%) completed the study; 116 rece
81 lic antidepressants (such as nortriptyline), gabapentin, and a compounded topical gel containing bacl
82        LRP1 regulates alpha2delta binding to gabapentin, and influences calcium channel trafficking a
83 athic rats as compared to the approved drug, gabapentin, and previously published sEH inhibitors.
84  clonidine, soy phyto-oestrogens, vitamin E, gabapentin, and several of the newer antidepressants, wi
85                                              Gabapentin antagonizes the interaction of thrombospondin
86                                              Gabapentin antagonizes thrombospondin binding to alpha2d
87                                              Gabapentin appears to increase human brain GABA levels.
88 sion in the literature regarding efficacy of gabapentin as a candidate addiction therapy.
89                                   The use of gabapentin as an effective analgesic agent for neuropath
90 pha2delta amino acid, R217A, eliminates both gabapentin binding and analgesic efficacy.
91 ison suggests that alpha(2)delta-4 lacks the gabapentin binding motifs characterized for alpha(2)delt
92 2+) -dependent reduction in affinity of (3)H-gabapentin binding to alpha2delta-1.
93                  However, the effect on (3)H-gabapentin binding was not reproduced by the synaptogeni
94 ha2delta-1 might reciprocally influence (3)H-gabapentin binding.
95 pha(2)delta-2; this was confirmed by a [(3)H]gabapentin-binding assay.
96               In vitro studies indicate that gabapentin binds to the alpha(2)delta-1 (hereafter refer
97 ), visual acuity improved significantly with gabapentin, but not with baclofen.
98  drugs reduced median eye speed (p < 0.001), gabapentin by 32.8% and memantine by 27.8%, and improved
99 so determined electrophysiologically whether gabapentin causes displacement of beta subunits from Ca(
100         GABA was elevated in patients taking gabapentin compared with 14 complex partial epilepsy pat
101                                              Gabapentin compared with placebo also significantly impr
102                               In conclusion, gabapentin did not provide a significant therapeutic adv
103 ubunit but not in the presence of beta4b; 3) gabapentin does not affect Ca(v)2.1 voltage-dependent ga
104                                              Gabapentin does not seem to have direct Ca2+ channel blo
105 nued on their current antidepressant without gabapentin) during which time they completed validated d
106                                              Gabapentin effects on glutamate are not known.
107                  In this report, we examined gabapentin effects on trafficking and voltage-dependent
108                                              Gabapentin effects were blocked in the presence of a spe
109 in; 7.2 (5.9-9.21) for gabapentin, including gabapentin extended release and enacarbil; and 10.6 (7.4
110 panies to develop and publish articles about gabapentin for the medical literature, and planning to s
111 dies has evaluated newer antidepressants and gabapentin for treating hot flashes.
112 inary support for the safety and efficacy of gabapentin for treatment of cannabis dependence that mer
113 that opioids, tramadol, benzodiazepines, and gabapentin (for radiculopathy) are effective for pain re
114 y of a calcium channel/GABA modulating drug, gabapentin, for the treatment of cannabis dependence.
115 e examined reporting practices for trials of gabapentin funded by Pfizer and Warner-Lambert's subsidi
116                                              Gabapentin (GBP) and S(+)-3-isobutyl-gamma-aminobutyric
117     The antiepileptic and antiallodynic drug gabapentin (GBP) binds to the alpha2delta-1 and alpha2de
118 he effects of electroacupuncture (EA) versus gabapentin (GP) for hot flashes among survivors of breas
119      Confusion was also more frequent in the gabapentin group (7 [8%] vs 1 [1.2%]; P = .06).
120     During the first 6 weeks, the naltrexone-gabapentin group had a longer interval to heavy drinking
121 res of pain were significantly better in the gabapentin group than in the placebo group.
122 omparable in the 2 groups (15 [13.3%] in the gabapentin group vs 11 [9.5%] in the placebo group).
123 pentin group were dizziness (20 [24%] in the gabapentin group vs 4 [4.9%] in the control group; P<.00
124 oup; P<.001) and somnolence (19 [23%] in the gabapentin group vs 5 [6%] in the control group; P = .00
125 rienced significantly more frequently in the gabapentin group were dizziness (20 [24%] in the gabapen
126  and infection were all more frequent in the gabapentin group, but withdrawals were comparable in the
127 rexone-alone group but not in the naltrexone-gabapentin group, while a history of alcohol withdrawal
128 iated with better response in the naltrexone-gabapentin group.
129 intent-to-treat analysis, subjects receiving gabapentin had a statistically significant reduction in
130                                    Moreover, gabapentin had no effect on reinstatement of sucrose see
131                 These findings indicate that gabapentin has a measurable antinociceptive effect and a
132                                              Gabapentin has come into clinical use as adjunctive ther
133 he alpha-2-delta receptor modulators such as gabapentin have shown early promising results in multimo
134  The risk of suicidal acts was increased for gabapentin (hazard ratio [HR], 1.42; 95% confidence inte
135                                              Gabapentin impairs the T-cell receptor-driven calcium re
136 racetamol and opiates in 97% of patients and gabapentin in 45% of patients.
137 e beneficial effect of Cavbeta antisense and gabapentin in allergic airway inflammation.
138 nstitutional trial to assess the efficacy of gabapentin in controlling hot flashes in women with brea
139         To assess the efficacy and safety of gabapentin in patients with fibromyalgia.
140  Intraperitoneal injection of 30-60 mg/kg of gabapentin in resiniferotoxin-treated rats significantly
141 CaV2.2 cell-surface expression is reduced by gabapentin in the presence of wild-type alpha2delta-1 (b
142 ould be employed when considering the use of gabapentin in transplant recipients, especially when com
143 oes not alter cP450 enzymes (lamotrigine and gabapentin) in monotherapy for 6 months or more were fol
144 (6.5-9.4) for pregabalin; 7.2 (5.9-9.21) for gabapentin, including gabapentin extended release and en
145                                              Gabapentin increased the amplitudes of evoked GABA recep
146  (fMRI) in normal volunteers, we studied the gabapentin-induced modulation of brain activity in respo
147                                              Gabapentin infused directly into the CeA also blocked de
148 use selective inhibition of alpha2delta-1 by gabapentin infusion into wild-type VMH significantly inc
149 v)2.1 Ca2+ channels in X. laevis oocytes; 2) gabapentin inhibition occurs in the presence of the Ca2+
150 endent on beta-subunit concentration; and 5) gabapentin inhibition of Ca(v)2.1 trafficking can be rev
151    Our principal findings are as follows: 1) gabapentin inhibits trafficking of recombinant Ca(v)2.1
152 e.g., capsaicin), antiepileptic drugs (e.g., gabapentin), injection of other agents (e.g., botulinum
153 esence of wild-type alpha2delta-1 (but not a gabapentin-insensitive alpha2delta-1 mutant), the intera
154                       The alpha2delta ligand gabapentin interacts with alpha2delta-1, and inhibits ca
155 minophen are preferred analgesic agents, and gabapentin is a contextual third choice, in neurocritica
156 y target pathological channels; for example, gabapentin is a ligand of alpha2delta voltage-activated
157                                              Gabapentin is a nonhormonal agent that also can reduce h
158                                              Gabapentin is a structural analog of GABA that has antic
159  concentrations predict clinical efficacy of gabapentin is an area worthy of exploration.
160       This mechanism may help to explain why gabapentin is both effective and selective in the treatm
161                           The anticonvulsant gabapentin is effective in reducing the subjective pain
162                                              Gabapentin is effective in the control of hot flashes at
163                                              Gabapentin is effective in the treatment of pain and sle
164 activation, thus supporting the concept that gabapentin is more effective in modulating nociceptive t
165                                              Gabapentin is well established as an effective treatment
166          Despite the therapeutic efficacy of gabapentin, its molecular and cellular mechanisms of act
167 nd marketed in the United States: felbamate, gabapentin, lamotrigine, and topiramate.
168 iepileptic drugs selected for discussion are gabapentin, lamotrigine, felbamate, vigabatrin, and topi
169                    In contrast, the new AEDs gabapentin, lamotrigine, levetiracetam, tiagabine, topir
170 xploratory analysis suggests that the use of gabapentin, lamotrigine, oxcarbazepine, and tiagabine, c
171  randomly assigned to receive carbamazepine, gabapentin, lamotrigine, oxcarbazepine, or topiramate.
172  randomly assigned to receive carbamazepine, gabapentin, lamotrigine, oxcarbazepine, or topiramate.
173                                              Gabapentin, marketed for the treatment of seizures and n
174                    Our findings suggest that gabapentin may be an effective treatment for many patien
175                              We suggest that gabapentin may cause acute renal dysfunction by a mechan
176 xcitatory synapse formation and suggest that gabapentin may function therapeutically by blocking new
177                                              Gabapentin may reduce these symptoms and help prevent ea
178 neration antipsychotics, iliac fascia block, gabapentin, melatonin, lower levels of intraoperative pr
179                                     In vivo, gabapentin microinjected in the nucleus accumbens core a
180         This preliminary evidence shows that gabapentin might have a role in treatment of chemotherap
181                                              Gabapentin monotherapy appears to be efficacious for the
182 uli was sensitive to systemic treatment with gabapentin, morphine and the cannabinoid WIN 55,212-2, b
183 addition, IB-MECA was equally efficacious as gabapentin (Neurontin) or amitriptyline, but respectivel
184 rough litigation concerning the promotion of gabapentin (Neurontin, Pfizer, Inc., New York, New York)
185 tructurally and pharmacologically related to gabapentin (Neurontin; Pfizer Inc., New York, NY).
186  in turn, dependence reverses the effects of gabapentin on CeA neurons, and suggest that gabapentin r
187          Here, we investigated the effect of gabapentin on GABAergic transmission in CeA slices, on e
188 potential effect of systemic and intrathecal gabapentin on tactile allodynia induced by resiniferotox
189 -controlled trial was to study the effect of gabapentin on the perception of pruritus and its behavio
190 ents with downbeat nystagmus will respond to gabapentin or baclofen.
191 endent processes with Cavalpha2delta1 ligand gabapentin or genetic Cavalpha2delta1 knockdown blocks T
192 n period to a maximum dosage of 3600 mg/d of gabapentin or matching placebo.
193  Patients were randomized to the study drug (gabapentin or placebo) at a starting dose of 300 mg oral
194 Hot flashes can be managed with venlaxafine, gabapentin, or-potentially-stress management.
195 he SF-36 and POMS also significantly favored gabapentin (P< or =.01).
196 d sleep interference showed improvement with gabapentin (P<.001).
197 tion have shown improvements with oestrogen, gabapentin, paroxetine, and clonidine, but little or no
198       Topiramate, onabotulinum toxin type A, gabapentin, petasites and tizanidine are among the agent
199  and thromboembolic stroke patients, whereas gabapentin/pregabalin were favored in subarachnoid hemor
200 rs of the glutamatergic system, riluzole and gabapentin, prolong survival.
201           Safety information was defined for gabapentin, propofol, sevoflurane, the combination of ri
202                                     Systemic gabapentin reduced ethanol intake in dependent, but not
203  the presence of central sensitization; (ii) gabapentin reduced the activation in the brainstem, only
204                            We found that (i) gabapentin reduced the activations in the bilateral oper
205                  Primidone, propranolol, and gabapentin reduced the amplitude (power) of the patholog
206            Overall, our results suggest that gabapentin reduces the number of beta4a-bound Ca(v)2.1 c
207                                            A gabapentin regimen (topical or oral) had been recommende
208  gabapentin on CeA neurons, and suggest that gabapentin represents a potential medication for treatme
209       Collectively, these findings show that gabapentin reverses behavioral measures of ethanol depen
210 d GEPR-9s, and this effect may contribute to gabapentin's effectiveness in anxiety and pain in which
211                                 Importantly, gabapentin's effects on drug seeking were not due to a g
212                                              Gabapentin seems to decrease hot flashes by approximatel
213  Using a rat neuropathic pain model in which gabapentin-sensitive tactile allodynia develops after ti
214                                              Gabapentin significantly reduced APN median eye speed in
215                         Relative to placebo, gabapentin significantly reduced cannabis use as measure
216            Trials were for off-label uses of gabapentin sponsored by Pfizer and Parke-Davis, and docu
217 em, only during central sensitization; (iii) gabapentin suppressed stimulus-induced deactivations, on
218  Spinal administration of the anticonvulsant gabapentin suppresses allodynia by an unknown mechanism.
219 ible acute renal dysfunction after beginning gabapentin therapy for chronic pain due to diabetic neur
220   Mood and quality of life also improve with gabapentin therapy.
221                                              Gabapentin (titrated from 900 to 3600 mg/d or maximum to
222                              The addition of gabapentin to naltrexone improved drinking outcomes over
223 by their ability to inhibit binding of [(3)H]gabapentin to pig brain membranes and for their potency
224                               The ability of gabapentin to suppress this pathway may be important for
225 used to communicate favorable messages about gabapentin to their physician colleagues.
226                                 Lamotrigine, gabapentin, topiramate, and oxcarbazepine are available
227                           Systemic baclofen, gabapentin, tramadol, and morphine dose-dependently atte
228        A significantly greater proportion of gabapentin-treated patients compared with placebo-treate
229                                              Gabapentin-treated patients displayed a significantly gr
230                 By intent-to-treat analysis, gabapentin-treated patients' mean daily pain score at th
231 atistically significant differences favoring gabapentin treatment were observed in measures of qualit
232                                    The three gabapentin trials decreased hot flashes by 35% to 38% co
233           The SSRIs or SNRIs, clonidine, and gabapentin trials provide evidence for efficacy; however
234 normalities with neurological symptoms, with gabapentin-type anticonvulsants, and is among the first
235  mg/day [N=50]), naltrexone (50 mg/day) with gabapentin (up to 1,200 mg/day [N=50]) added for the fir
236 ted a double-blind crossover trial comparing gabapentin (up to 900 mg/day) to baclofen (up to 30 mg/d
237                                              Gabapentin users had increased risk in subgroups of youn
238 signed to receive both an antidepressant and gabapentin versus being weaned off the antidepressant an
239 o or fewer, 0.87, 0.85-0.90), and treatment (gabapentin vs carbamazepine, 0.71, 0.59-0.86; topiramate
240                                  The dose of gabapentin was 1,800 mg per os, in a single administrati
241                             The promotion of gabapentin was a comprehensive and multifaceted process.
242                                              Gabapentin was also associated with significantly greate
243                                              Gabapentin was associated with an increase in mean HSA,
244 or baseline values); only the higher dose of gabapentin was associated with significant decreases in
245 ed whether the combination of naltrexone and gabapentin was better than naltrexone alone and/or place
246             This effect did not endure after gabapentin was discontinued.
247                                              Gabapentin was generally well tolerated.
248 or not the antidepressant was continued when gabapentin was started, there was an approximately 50% m
249 ts with APN, the reduction of nystagmus with gabapentin was substantial and 8 of these elected to con
250      In the 2.3% with demyelinating disease, gabapentin was the most likely second analgesic (50.0%).
251 atistically significant differences favoring gabapentin were reported.
252 the effectiveness of the anticonvulsant drug gabapentin, which is a specific inhibitor of BCATc.
253 ocally perfused pramipexole, ropinirole, and gabapentin, which significantly counteracted optogenetic
254               Some newer antidepressants and gabapentin, within 4 weeks of therapy initiation, decrea
255 lozapine, duloxetine, clonazepam, ramelteon, gabapentin, zonisamide, and yokukansan.

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