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1 est in this target as potential treatment of cocaine addiction.
2 shows promise as a treatment for people with cocaine addiction.
3 d inform the development of therapeutics for cocaine addiction.
4 t to the pathophysiologic characteristics of cocaine addiction.
5 e tendencies and relationships may pre-exist cocaine addiction.
6 a period of heightened propensity to develop cocaine addiction.
7 date could facilitate control of behavior in cocaine addiction.
8 ere are no FDA-approved medications to treat cocaine addiction.
9 ovel therapeutic target for the treatment of cocaine addiction.
10 g, making it a promising pharmacotherapy for cocaine addiction.
11 agonism as a viable therapeutic strategy for cocaine addiction.
12  Administration-approved pharmacotherapy for cocaine addiction.
13 ortant target for cue-exposure therapies for cocaine addiction.
14 es to diverse types of plasticity, including cocaine addiction.
15 ern of maladaptive behaviors associated with cocaine addiction.
16 receptors that are involved in the action of cocaine addiction.
17 stitute a risk factor for the development of cocaine addiction.
18 cluding heroin and prescription opioids, and cocaine addiction.
19 promoting long-term resistance to relapse to cocaine addiction.
20 er impair executive function and learning in cocaine addiction.
21 th cue exposure therapy for the treatment of cocaine addiction.
22 gene silencing, is involved in regulation of cocaine addiction.
23 tial treatment for both cocaine overdose and cocaine addiction.
24 tion-related behaviors in an animal model of cocaine addiction.
25 al morphology and behavior that may underlie cocaine addiction.
26 provide evidence for a key role of miRNAs in cocaine addiction.
27  be important in regulating vulnerability to cocaine addiction.
28 ls, MPH did not improve treatment outcome in cocaine addiction.
29  of miRNAs that are likely to play a role in cocaine addiction.
30 ich may provide a new rationale for treating cocaine addiction.
31 t individuals with combined heroin and crack cocaine addiction.
32 lasticity associated with the development of cocaine addiction.
33 g GLT1 as a potential therapeutic target for cocaine addiction.
34 long-term behavioral changes associated with cocaine addiction.
35 herapeutic option in the treatment of severe cocaine addiction.
36 et for drug development for the treatment of cocaine addiction.
37 eceptors, within brain regions implicated in cocaine addiction.
38 e likely to be therapeutically beneficial in cocaine addiction.
39 tial inroads for therapeutic intervention in cocaine addiction.
40 s potential medications for the treatment of cocaine addiction.
41 ting changes in neuronal function underlying cocaine addiction.
42 ontal cortex (mPFC) plays a critical role in cocaine addiction.
43 target for the development of treatments for cocaine addiction.
44 g-term depression, associative learning, and cocaine addiction.
45 dentify clusters of genes that contribute to cocaine addiction.
46 havioral and molecular mechanisms underlying cocaine addiction.
47 vide tools for the study of the mechanism of cocaine addiction.
48 sses for regulating at least some aspects of cocaine addiction.
49 ral associations, including vulnerability to cocaine addiction.
50  relapse to drug use is a primary symptom of cocaine addiction.
51  and has been hypothesized to play a role in cocaine addiction.
52 target for prospective pharmacotherapies for cocaine addiction.
53  a range of neurological disorders including cocaine addiction.
54 rget for pharmacotherapies designed to treat cocaine addiction.
55  to adaptive changes in the brain related to cocaine addiction.
56 in long-lasting relapse risk associated with cocaine addiction.
57 ons in patients with Parkinson's disease and cocaine addiction.
58 f early childhood stress in vulnerability to cocaine addiction.
59 sporter plays a key role in the mechanism of cocaine addiction.
60 ity to cocaine and may thereby contribute to cocaine addiction.
61 produce substantial adverse consequences for cocaine addiction.
62 paper describes an immunological approach to cocaine addiction.
63 apeutic cocaine vaccine for the treatment of cocaine addiction.
64 r agonists as a possible pharmacotherapy for cocaine addiction.
65 e their potential pathophysiological role in cocaine addiction.
66 may be useful pharmacotherapeutic agents for cocaine addiction.
67 lso offer a route towards gene therapies for cocaine addiction.
68 e social-emotional functional alterations in cocaine addiction.
69 g to study transcription factors involved in cocaine addiction.
70 g preclinical evidence for its impairment in cocaine addiction.
71 implicated noradrenergic (NA) dysfunction in cocaine addiction.
72  have therapeutic value for the treatment of cocaine addiction.
73 rstanding of molecular mechanisms underlying cocaine addiction.
74 ay have translational potential for treating cocaine addiction.
75 d maladaptive drug-related attention bias in cocaine addiction.
76 ntibody research to aid in the fight against cocaine addiction.
77 he understanding of the role of microglia in cocaine addiction.
78 f opiate and nicotine addiction, but not for cocaine addiction.
79 support a personalized treatment approach to cocaine addiction.
80  for the development of relapse treatment of cocaine addiction.
81 tment of disrupting mitochondrial fission in cocaine addiction.
82  complexes may be efficacious treatments for cocaine addiction.
83 ntial as an agonist therapy for treatment of cocaine addiction.
84 ovel therapeutic target for the treatment of cocaine addiction.
85 a promising drug target for the treatment of cocaine addiction.
86 , may render individuals more susceptible to cocaine addiction.
87 norectic and a candidate pharmacotherapy for cocaine addiction.
88 icant barrier to the successful treatment of cocaine addiction.
89 n may be valuable tools for the treatment of cocaine addiction.
90 tagonizing 5-HT1A autoreceptors for treating cocaine addiction.
91 harmacological strategy for the treatment of cocaine addiction.
92  of addiction endophenotypes, especially for cocaine addiction.
93 tify and develop novel pharmacotherapies for cocaine addiction.
94 ers including depression, visceral pain, and cocaine addiction.
95 mphetamine addictions, but not for heroin or cocaine addiction.
96 be a therapeutic target for the treatment of cocaine addiction.
97 idates for the development of treatments for cocaine addiction.
98 zheimer's disease, Huntington's disease, and cocaine addiction.
99 tionale supporting sleep-based therapies for cocaine addiction.
100 have therapeutic utility in the treatment of cocaine addiction.
101 te sleep-based therapeutic opportunities for cocaine addiction.
102  including stroke, motor neuron disease, and cocaine addiction.
103 ription of specific genes that contribute to cocaine addiction.
104 ent a novel drug target for the treatment of cocaine addiction.
105 ression is a potential therapeutic target in cocaine addiction.
106 mor growth and invasion, viral infection and cocaine addiction.
107 te alterations in the glutamate signaling in cocaine addiction.
108 havior and may be useful in the treatment of cocaine addiction.
109  provide novel therapeutic opportunities for cocaine addiction.
110  against cocaine be a viable prophylaxis for cocaine addiction?
111               These findings suggest that in cocaine addiction 1) activation of the corticolimbic rew
112 rticipation of thalamic dopamine pathways in cocaine addiction, a possibility that merits further inv
113  subjective effects is a cardinal symptom of cocaine addiction and a DSM-V criterion for substance ab
114          Although tolerance is a hallmark of cocaine addiction and a DSM-V criterion for substance ab
115 e a novel role for G9a in promoting comorbid cocaine addiction and anxiety and suggest that increased
116                                              Cocaine addiction and depression are comorbid disorders.
117 vestigated as potential therapeutics against cocaine addiction and for cognitive enhancement.
118 ld be considered for their potential role in cocaine addiction and hippocampal-mediated relapse after
119 icroRNA let-7d, which has been implicated in cocaine addiction and other neurological disorders, targ
120                                              Cocaine addiction and overdose have long defied specific
121                  Successful immunotherapy of cocaine addiction and overdoses requires cocaine-binding
122  a critical step in developing treatment for cocaine addiction and preventing cardiac complications.
123 ave therapeutic potential for treating human cocaine addiction and preventing relapse.
124 ecture and molecular neuropathology of human cocaine addiction and provides a framework for translati
125 play an important role in sex differences in cocaine addiction and relapse.
126  is thought to be critical for expression of cocaine addiction and relapse.
127 ing efforts to find effective treatments for cocaine addiction and suggest the application of this pr
128  on resting-state functional connectivity in cocaine addiction and tested whether resting-state funct
129 s in the neuroadaptive cascade that leads to cocaine addiction and withdrawal.
130 be advantageous in immunopharmacotherapy for cocaine addiction, and for emergency cases of drug overd
131  in synaptic plasticity, dopamine signaling, cocaine addiction, and neurodegenerative disorders.
132 tially generalizable to other subgroups with cocaine addiction, and to additional substance use disor
133 eurons modulate numerous distinct aspects of cocaine addiction- and relapse-related behaviors, and po
134 al, predict choice to view cocaine images in cocaine addiction; and (ii) whether such behaviour predi
135                                              Cocaine addiction appears to be associated with a drug-i
136                        Treatment efforts for cocaine addiction are hampered by high relapse rates.
137      Whether these two prominent features of cocaine addiction are related to each other and are medi
138 ussed with respect to the role of the BLA in cocaine addiction as well as previous studies characteri
139 cleus accumbens (NAc) has been implicated in cocaine addiction because (1) cocaine reinforcement is m
140 ent a novel pharmacotherapeutic approach for cocaine addiction because it may simultaneously function
141 ical trials for Parkinsonism, depression and cocaine addiction but lacked efficacy.
142  be exploited to develop novel therapies for cocaine addiction, but a molecular target has not yet be
143 l-molecule therapeutic is available to treat cocaine addiction, but enzyme-based therapy to accelerat
144 terventions have been explored to counteract cocaine addiction, but to date no market-approved medica
145 g cocaine self-administration contributes to cocaine addiction by acting to facilitate subsequent coc
146 eking behavior, a defining characteristic of cocaine addiction, can be precipitated by contextual cue
147                                              Cocaine addiction continues to be a major health and soc
148                                              Cocaine addiction continues to be a significant public h
149     Abnormal function in reward circuitry in cocaine addiction could predate drug use as a risk facto
150 to control participants, people with chronic cocaine addiction demonstrate reduced utility PEs in the
151              The lack of medication to treat cocaine addiction desperately calls for a treatment deve
152          There is no effective treatment for cocaine addiction despite extensive knowledge of the neu
153     Methylphenidate has been used to mediate cocaine addiction due to its lower pharmacokinetics, whi
154     There is evidence for sex differences in cocaine addiction from both clinical and preclinical stu
155 armacotherapeutic actions of amphetamine for cocaine addiction go beyond that of replacement therapy.
156 zes GluA2 AMPARs at synapses but its role in cocaine addiction has not been examined.
157       Investigation of the role of stress in cocaine addiction has yielded an efficacious combination
158 isastrous medical and social consequences of cocaine addiction have made the development of an antico
159 armacological approaches to the treatment of cocaine addiction have thus far been disappointing, and
160 e required to link D2R to neuroplasticity in cocaine addiction in females.
161                                              Cocaine addiction in humans is associated with long-term
162 ce every 2-4 wk, or longer, for treatment of cocaine addiction in humans.
163  raised much interest because of its role in cocaine addiction in preclinical models.
164 uricular acupuncture is widely used to treat cocaine addiction in the United States and Europe.
165 1.6 million people who meet the criteria for cocaine addiction in the United States, and there are cu
166      A new pharmacokinetic approach treating cocaine addiction involves rapidly metabolizing cocaine
167 mechanisms that lead to comorbid anxiety and cocaine addiction, irrespective of which comes first, is
168                                              Cocaine addiction is a chronic illness characterized by
169                                              Cocaine addiction is a chronic, relapsing disorder chara
170                                              Cocaine addiction is a chronically relapsing brain disea
171                                              Cocaine addiction is a debilitating neuropsychiatric dis
172                                              Cocaine addiction is a disease characterized by chronic
173                                              Cocaine addiction is a long-lasting relapsing illness ch
174                                     Treating cocaine addiction is a major challenge and currently no
175                                              Cocaine addiction is a major problem for which there is
176                                              Cocaine addiction is a major public health problem that
177 sequences on behavior.SIGNIFICANCE STATEMENT Cocaine addiction is a neuropsychiatric disorder that is
178                                              Cocaine addiction is a significant medical and public co
179 etically tractable model system for studying cocaine addiction is already providing new clues that ma
180                                              Cocaine addiction is associated with altered resting-sta
181                                              Cocaine addiction is associated with compulsive drug-see
182                                              Cocaine addiction is associated with disturbed rsFC in s
183                                              Cocaine addiction is characterized by a gradual loss of
184                                              Cocaine addiction is characterized by a progressive incr
185                                              Cocaine addiction is characterized by an impaired abilit
186                                              Cocaine addiction is characterized by long-lasting vulne
187                                              Cocaine addiction is characterized by patterns of compul
188                                              Cocaine addiction is characterized by poor judgment and
189                                              Cocaine addiction is commonly viewed as a disorder of ne
190 he relationship between anxiety symptoms and cocaine addiction is complicated; anxiety can be both a
191                  One of the core symptoms of cocaine addiction is compulsive drug-seeking behavior.
192 ted learning.SIGNIFICANCE STATEMENT Although cocaine addiction is driven in part by the formation of
193 ferences in drug abuse, and a key feature of cocaine addiction is pathologically high motivation for
194               One of the major challenges of cocaine addiction is the high rate of relapse to drug us
195                                              Cocaine addiction is thought to involve persistent neuro
196                                              Cocaine addiction is thought to stem, in part, from neur
197               A major goal of treatments for cocaine addiction is to reduce relapse-associated cravin
198 medium spiny neurons (MSNs), one hallmark of cocaine addiction, is independent of DA signaling.
199 Relapse, a major problem in the treatment of cocaine addiction, is proposed to result in part from ne
200 ral and electrophysiological determinants of cocaine addiction liability.
201 bits is not necessary for the development of cocaine addiction-like behavior in rats.SIGNIFICANCE STA
202 s been identified as a predictive factor for cocaine addiction-like behavior.
203 e amygdala of outbred rats with high and low cocaine addiction-like behaviors following prolonged abs
204 molecular adaptations that produce increased cocaine addiction-like behaviors.
205                                In a model of cocaine addiction, mAb 15A10 blocked completely the rein
206                Recent evidence suggests that cocaine addiction may involve progressive drug-induced n
207 ining CM with bupropion for the treatment of cocaine addiction may significantly improve outcomes rel
208 t in both rodent and primate striatum, using cocaine addiction mouse models.
209 peractivity disorder, binge eating disorder, cocaine addiction, obesity, and type 2 diabetes.
210                                The impact of cocaine addiction on GMV, tested by (1) comparing the CU
211 f acupuncture as a stand-alone treatment for cocaine addiction or in contexts in which patients recei
212 an FDA-approved pharmacotherapy specific for cocaine addiction or overdose.
213  no market-approved medications for treating cocaine addiction or relapse exist, and effective interv
214 nsisted of all adults with a heroin or crack cocaine addiction, or both, who started pharmacological
215  D3/D4 receptors as potential treatments for cocaine addiction, particularly in combination with enri
216 1 receptors may represent a novel target for cocaine addiction pharmacotherapies.
217 edited GluA2(Q) represent a novel target for cocaine addiction pharmacotherapies.
218             Disulfiram has been an effective cocaine addiction pharmacotherapy, and one of its possib
219 her consideration of PDM as a candidate anti-cocaine addiction pharmacotherapy.
220 dol has been explored as a possible agent in cocaine addiction pharmacotherapy.
221 al responses to cocaine in all phases of the cocaine addiction process (induction, maintenance, and r
222 genetic and neurobiological contributions to cocaine addiction, provides a rapid approach for generat
223 ew cocaine vaccine (dAd5GNE) in antagonizing cocaine addiction-related behaviors in rats.
224      In addition to serving as a therapy for cocaine addiction-related diseases, enhanced bioscavengi
225 rability of impulsive individuals to develop cocaine addiction remain unknown.
226                                              Cocaine addiction remains a serious problem lacking an e
227 ate how the mPFC is functionally involved in cocaine addiction remains incomplete.
228 ion, a role of the endocannabinoid system in cocaine addiction remains widely inconclusive.
229                                              Cocaine addiction remains without an effective pharmacot
230 logical basis of sex-specific differences in cocaine addiction resides in the disparate regulation of
231 and, an induced plasticity evoked by chronic cocaine addiction resulted in progressive transcriptiona
232 oimaging studies have shown that people with cocaine addiction retain some degree of control over dru
233 s a key role in determining vulnerability to cocaine addiction, reveal new molecular regulators that
234 sing therapeutic target for the treatment of cocaine addiction, schizophrenia, Parkinson's disease, a
235 ossibility that the behaviors characterizing cocaine addiction, such as craving-induced relapse, may
236  gene and protein expression associated with cocaine addiction suggest the existence of a mechanism t
237 h rate of comorbidity between depression and cocaine addiction suggests shared molecular mechanisms a
238 g why women display a more severe profile of cocaine addiction than men.
239  women experiencing a more severe profile of cocaine addiction than men.
240 lying the vulnerability of impulsive rats to cocaine addiction that localize to the OFC, infralimbic
241 network interactions have been identified in cocaine addiction, the association between these brain n
242 asingly more at risk for the consequences of cocaine addiction, the need to establish better-tailored
243 an established role in preclinical models of cocaine addiction, the translational significance of the
244 RIP as a novel target for the development of cocaine addiction therapeutics.
245 ver, the actual therapeutic use of a CocH in cocaine addiction treatment is limited by its short biol
246 l drug repurposing candidates for opioid and cocaine addiction treatment, bridging the gap between tr
247 orthosteric antagonists/inverse agonists for cocaine addiction treatment.
248 ing candidates for further investigation for cocaine addiction treatment.
249 ed at these complexes may have potential for cocaine addiction treatment.SIGNIFICANCE STATEMENT Toler
250      There is a large unmet medical need for cocaine addiction treatments.
251                                     Treating cocaine addiction using dopamine replacement strategies,
252  patients with schizophrenia, depression, or cocaine addiction, using functional magnetic resonance i
253                                       Hence, cocaine addiction vulnerability may be linked to multipl
254 evel effects of methylphenidate; severity of cocaine addiction was assessed by interview and question
255         The results of the study showed that cocaine addiction was associated with a 20% to 22% reduc
256 ocaine-induced increases in actin cycling in cocaine addiction was examined using the reinstatement o
257 velop a pharmacotherapy for the treatment of cocaine addiction, we embarked on synthesizing novel mol
258 ne oxidase inhibitor selegiline for treating cocaine addiction, we required a method for measuring ur

 
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