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1 produce substantial adverse consequences for cocaine addiction.
2 e their potential pathophysiological role in cocaine addiction.
3 es to diverse types of plasticity, including cocaine addiction.
4 ern of maladaptive behaviors associated with cocaine addiction.
5 receptors that are involved in the action of cocaine addiction.
6 stitute a risk factor for the development of cocaine addiction.
7 cluding heroin and prescription opioids, and cocaine addiction.
8 promoting long-term resistance to relapse to cocaine addiction.
9 er impair executive function and learning in cocaine addiction.
10 th cue exposure therapy for the treatment of cocaine addiction.
11 for the development of relapse treatment of cocaine addiction.
12 gene silencing, is involved in regulation of cocaine addiction.
13 tial treatment for both cocaine overdose and cocaine addiction.
14 tion-related behaviors in an animal model of cocaine addiction.
15 al morphology and behavior that may underlie cocaine addiction.
16 provide evidence for a key role of miRNAs in cocaine addiction.
17 be important in regulating vulnerability to cocaine addiction.
18 ls, MPH did not improve treatment outcome in cocaine addiction.
19 of miRNAs that are likely to play a role in cocaine addiction.
20 ich may provide a new rationale for treating cocaine addiction.
21 t individuals with combined heroin and crack cocaine addiction.
22 lasticity associated with the development of cocaine addiction.
23 tment of disrupting mitochondrial fission in cocaine addiction.
24 g GLT1 as a potential therapeutic target for cocaine addiction.
25 long-term behavioral changes associated with cocaine addiction.
26 herapeutic option in the treatment of severe cocaine addiction.
27 et for drug development for the treatment of cocaine addiction.
28 eceptors, within brain regions implicated in cocaine addiction.
29 e likely to be therapeutically beneficial in cocaine addiction.
30 s potential medications for the treatment of cocaine addiction.
31 ting changes in neuronal function underlying cocaine addiction.
32 ontal cortex (mPFC) plays a critical role in cocaine addiction.
33 target for the development of treatments for cocaine addiction.
34 g-term depression, associative learning, and cocaine addiction.
35 dentify clusters of genes that contribute to cocaine addiction.
36 havioral and molecular mechanisms underlying cocaine addiction.
37 vide tools for the study of the mechanism of cocaine addiction.
38 sses for regulating at least some aspects of cocaine addiction.
39 ral associations, including vulnerability to cocaine addiction.
40 and has been hypothesized to play a role in cocaine addiction.
41 target for prospective pharmacotherapies for cocaine addiction.
42 a range of neurological disorders including cocaine addiction.
43 to adaptive changes in the brain related to cocaine addiction.
44 in long-lasting relapse risk associated with cocaine addiction.
45 ons in patients with Parkinson's disease and cocaine addiction.
46 f early childhood stress in vulnerability to cocaine addiction.
47 sporter plays a key role in the mechanism of cocaine addiction.
48 ity to cocaine and may thereby contribute to cocaine addiction.
49 e social-emotional functional alterations in cocaine addiction.
50 complexes may be efficacious treatments for cocaine addiction.
51 paper describes an immunological approach to cocaine addiction.
52 apeutic cocaine vaccine for the treatment of cocaine addiction.
53 r agonists as a possible pharmacotherapy for cocaine addiction.
54 may be useful pharmacotherapeutic agents for cocaine addiction.
55 ntial as an agonist therapy for treatment of cocaine addiction.
56 ovel therapeutic target for the treatment of cocaine addiction.
57 a promising drug target for the treatment of cocaine addiction.
58 , may render individuals more susceptible to cocaine addiction.
59 norectic and a candidate pharmacotherapy for cocaine addiction.
60 ay have translational potential for treating cocaine addiction.
61 icant barrier to the successful treatment of cocaine addiction.
62 n may be valuable tools for the treatment of cocaine addiction.
63 tagonizing 5-HT1A autoreceptors for treating cocaine addiction.
64 harmacological strategy for the treatment of cocaine addiction.
65 of addiction endophenotypes, especially for cocaine addiction.
66 tify and develop novel pharmacotherapies for cocaine addiction.
67 ers including depression, visceral pain, and cocaine addiction.
68 f opiate and nicotine addiction, but not for cocaine addiction.
69 mphetamine addictions, but not for heroin or cocaine addiction.
70 be a therapeutic target for the treatment of cocaine addiction.
71 idates for the development of treatments for cocaine addiction.
72 zheimer's disease, Huntington's disease, and cocaine addiction.
73 tionale supporting sleep-based therapies for cocaine addiction.
74 have therapeutic utility in the treatment of cocaine addiction.
75 te sleep-based therapeutic opportunities for cocaine addiction.
76 including stroke, motor neuron disease, and cocaine addiction.
77 support a personalized treatment approach to cocaine addiction.
78 ription of specific genes that contribute to cocaine addiction.
79 ent a novel drug target for the treatment of cocaine addiction.
80 mor growth and invasion, viral infection and cocaine addiction.
81 te alterations in the glutamate signaling in cocaine addiction.
82 havior and may be useful in the treatment of cocaine addiction.
83 provide novel therapeutic opportunities for cocaine addiction.
84 d inform the development of therapeutics for cocaine addiction.
85 t to the pathophysiologic characteristics of cocaine addiction.
86 e tendencies and relationships may pre-exist cocaine addiction.
87 a period of heightened propensity to develop cocaine addiction.
88 date could facilitate control of behavior in cocaine addiction.
89 ere are no FDA-approved medications to treat cocaine addiction.
90 ovel therapeutic target for the treatment of cocaine addiction.
91 g, making it a promising pharmacotherapy for cocaine addiction.
92 agonism as a viable therapeutic strategy for cocaine addiction.
93 Administration-approved pharmacotherapy for cocaine addiction.
94 ortant target for cue-exposure therapies for cocaine addiction.
95 against cocaine be a viable prophylaxis for cocaine addiction?
97 rticipation of thalamic dopamine pathways in cocaine addiction, a possibility that merits further inv
99 subjective effects is a cardinal symptom of cocaine addiction and a DSM-V criterion for substance ab
100 e a novel role for G9a in promoting comorbid cocaine addiction and anxiety and suggest that increased
102 ld be considered for their potential role in cocaine addiction and hippocampal-mediated relapse after
103 icroRNA let-7d, which has been implicated in cocaine addiction and other neurological disorders, targ
106 a critical step in developing treatment for cocaine addiction and preventing cardiac complications.
110 ing efforts to find effective treatments for cocaine addiction and suggest the application of this pr
111 on resting-state functional connectivity in cocaine addiction and tested whether resting-state funct
113 be advantageous in immunopharmacotherapy for cocaine addiction, and for emergency cases of drug overd
115 al, predict choice to view cocaine images in cocaine addiction; and (ii) whether such behaviour predi
118 Whether these two prominent features of cocaine addiction are related to each other and are medi
119 ussed with respect to the role of the BLA in cocaine addiction as well as previous studies characteri
120 cleus accumbens (NAc) has been implicated in cocaine addiction because (1) cocaine reinforcement is m
121 ent a novel pharmacotherapeutic approach for cocaine addiction because it may simultaneously function
123 l-molecule therapeutic is available to treat cocaine addiction, but enzyme-based therapy to accelerat
124 g cocaine self-administration contributes to cocaine addiction by acting to facilitate subsequent coc
125 eking behavior, a defining characteristic of cocaine addiction, can be precipitated by contextual cue
128 Abnormal function in reward circuitry in cocaine addiction could predate drug use as a risk facto
130 Methylphenidate has been used to mediate cocaine addiction due to its lower pharmacokinetics, whi
131 There is evidence for sex differences in cocaine addiction from both clinical and preclinical stu
132 armacotherapeutic actions of amphetamine for cocaine addiction go beyond that of replacement therapy.
135 isastrous medical and social consequences of cocaine addiction have made the development of an antico
136 armacological approaches to the treatment of cocaine addiction have thus far been disappointing, and
140 1.6 million people who meet the criteria for cocaine addiction in the United States, and there are cu
148 sequences on behavior.SIGNIFICANCE STATEMENT Cocaine addiction is a neuropsychiatric disorder that is
149 etically tractable model system for studying cocaine addiction is already providing new clues that ma
164 Relapse, a major problem in the treatment of cocaine addiction, is proposed to result in part from ne
166 bits is not necessary for the development of cocaine addiction-like behavior in rats.SIGNIFICANCE STA
170 ining CM with bupropion for the treatment of cocaine addiction may significantly improve outcomes rel
173 f acupuncture as a stand-alone treatment for cocaine addiction or in contexts in which patients recei
174 nsisted of all adults with a heroin or crack cocaine addiction, or both, who started pharmacological
175 D3/D4 receptors as potential treatments for cocaine addiction, particularly in combination with enri
181 al responses to cocaine in all phases of the cocaine addiction process (induction, maintenance, and r
183 In addition to serving as a therapy for cocaine addiction-related diseases, enhanced bioscavengi
188 logical basis of sex-specific differences in cocaine addiction resides in the disparate regulation of
189 oimaging studies have shown that people with cocaine addiction retain some degree of control over dru
190 s a key role in determining vulnerability to cocaine addiction, reveal new molecular regulators that
191 sing therapeutic target for the treatment of cocaine addiction, schizophrenia, Parkinson's disease, a
192 ossibility that the behaviors characterizing cocaine addiction, such as craving-induced relapse, may
193 gene and protein expression associated with cocaine addiction suggest the existence of a mechanism t
194 h rate of comorbidity between depression and cocaine addiction suggests shared molecular mechanisms a
197 lying the vulnerability of impulsive rats to cocaine addiction that localize to the OFC, infralimbic
198 network interactions have been identified in cocaine addiction, the association between these brain n
199 asingly more at risk for the consequences of cocaine addiction, the need to establish better-tailored
201 ver, the actual therapeutic use of a CocH in cocaine addiction treatment is limited by its short biol
202 ed at these complexes may have potential for cocaine addiction treatment.SIGNIFICANCE STATEMENT Toler
205 patients with schizophrenia, depression, or cocaine addiction, using functional magnetic resonance i
206 evel effects of methylphenidate; severity of cocaine addiction was assessed by interview and question
208 ocaine-induced increases in actin cycling in cocaine addiction was examined using the reinstatement o
209 velop a pharmacotherapy for the treatment of cocaine addiction, we embarked on synthesizing novel mol
210 ne oxidase inhibitor selegiline for treating cocaine addiction, we required a method for measuring ur
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