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1 use affects t-SP associated with cue-induced drug seeking.
2 nd not all stressors induce reinstatement of drug seeking.
3 ations of neurons within these regions drive drug seeking.
4 tor 2 (HCRT-R2) signaling in compulsive-like drug seeking.
5 ss-, drug-, and cue-induced reinstatement of drug seeking.
6  activity of neurons that would later encode drug seeking.
7  striatal circuits in a manner that promotes drug seeking.
8 ntation of the aversive delay cue reinstated drug seeking.
9 thout affecting cue-induced reinstatement of drug seeking.
10 is functionally important for suppressing of drug seeking.
11 l striatum is thought to assume control over drug seeking.
12 ne and ceftriaxone) can decrease measures of drug seeking.
13 at plays a critical role in reinstatement of drug seeking.
14 y involved in reward learning and relapse of drug seeking.
15 forms of motivated behavior and pathological drug seeking.
16 ntrol over behavior and increased compulsive drug seeking.
17 -making circuits that manifest as compulsive drug seeking.
18 cues, including cue-induced reinstatement of drug seeking.
19 r learning and memory, as well as relapse to drug seeking.
20 lar processes engaged in the early stages of drug seeking.
21  extinction responding, and reinstatement of drug seeking.
22  training, or just before cocaine-reinstated drug seeking.
23 RF) regulation of neurocircuitry involved in drug seeking.
24  more sensitive than males to stress-induced drug seeking.
25 f the plasticity responsible for relapse and drug seeking.
26  may have a role in the lack of control over drug seeking.
27 neurons is a critical component of sustained drug seeking.
28  controlling stress-induced reinstatement of drug seeking.
29 fects of drugs of abuse and reinstatement of drug seeking.
30 ted cocaine priming-induced reinstatement of drug seeking.
31 rat model of stress-induced reinstatement of drug seeking.
32 in the neural circuitry for reinstatement of drug seeking.
33 dministration (SA) underlie reinstatement of drug-seeking.
34 s imperative to BDNF's suppressive effect on drug-seeking.
35 egulated over 120 min during cocaine-induced drug-seeking.
36 interoceptive effects of cocaine that impact drug-seeking.
37  cocaine and stress-induced reinstatement of drug-seeking.
38 ated in drug-taking and the reinstatement of drug-seeking.
39 neural system that initiates and encodes the drug-seeking act, surprisingly little is known about the
40 nisms: the ability of drug cues to reinforce drug-seeking actions following a period of extinction tr
41  transmission in the emergence of compulsive drug seeking after a long cocaine-taking history.
42 act of drug use on the ability to extinguish drug seeking after changes in expected outcomes.
43          Knockdown of Drp1 in D1-MSNs blocks drug seeking after cocaine self-administration, while en
44 y incubation of drug craving and cue-induced drug seeking after prolonged voluntary abstinence, mimic
45 nister heroin as adolescents show attenuated drug-seeking after abstinence, compared with adults.
46 striatum, a structure that mediates habitual drug seeking, also mediates punished cocaine seeking.
47 tes cocaine priming-induced reinstatement of drug seeking, an animal model of relapse, in male Spragu
48 rder associated with compulsive drug taking, drug seeking and a loss of control in limiting intake, r
49 ersistent maladaptive memories that maintain drug seeking and are resistant to extinction are a hallm
50 ation sessions were designed to measure both drug seeking and drug taking.
51  chronic disease characterized by compulsive drug seeking and episodes of relapse despite prolonged p
52 19 d after the last session, cocaine-induced drug seeking and extracellular levels of glutamate and d
53     Drug addiction is marked by pathological drug seeking and intense drug craving, particularly in r
54  assess measures of relapse/reinstatement of drug seeking and long-term effects on cognitive function
55 ess) on cognitive performance and relapse to drug seeking and may contribute to the impairments that
56 ng is a possible site of shared signaling in drug seeking and potentiated reinstated sucrose seeking,
57 the development and intensity of cue-induced drug seeking and provides evidence for potential biomark
58 n of this activity could prevent cue-induced drug seeking and relapse long after treatment.
59 -associated Pavlovian-conditioned stimuli on drug seeking and relapse, and evidence for impairments i
60 rnical/lateral hypothalamus, is critical for drug seeking and relapse, but it is not clear how the ci
61 ce of glutamatergic signaling in the NAc for drug seeking and relapse, here we examined its role in m
62 s may underlie the persistence of compulsive drug seeking and relapse.
63 sentation of drug-associated cues can elicit drug seeking and relapse.
64 ng a novel method of preventing cue-elicited drug seeking and relapse.
65 prefrontal cortical to striatal control over drug seeking and taking as well as a progression from th
66 s suggest that the development of compulsive drug seeking and taking depends on dorsostriatal mechani
67 addictive behaviors that underlie compulsive drug seeking and taking in humans.
68 es of drug abuse and may drive the increased drug seeking and taking that characterize the transition
69  evaluated the potential for compulsive-like drug seeking and taking, using intravenous self-administ
70 FSI-embedded circuit in regulating NAc-based drug seeking and taking.
71  in neural networks that underlie compulsive drug seeking and taking.
72 gh impulsivity predicts loss of control over drug seeking and taking.
73 low drug-associated cues to drive compulsive drug seeking and taking.
74 al-directed becomes habitual after prolonged drug seeking and taking.
75 eficits that likely contribute to persistent drug seeking and the high rates of relapse.
76                                              Drug seeking and the vulnerability to relapse occur when
77 ced negative affect, a hallmark of continued drug seeking and use in human addicts.
78 ted cocaine priming-induced reinstatement of drug seeking and was associated with increased GluA2 Q/R
79  such as nucleus accumbens (NAcc), promoting drug-seeking and -taking behavior.
80 s such as cocaine or amphetamine can promote drug-seeking and -taking behavior.
81 ge-type intake of fat and the development of drug-seeking and -taking behaviors, suggesting that a hi
82 xt of prior findings of SB 334867 effects on drug-seeking and drug-consuming behaviors.
83                                   Compulsive drug-seeking and drug-taking are important substance-abu
84 onse may implicate VPdl in the processing of drug-seeking and drug-taking behavior via projections to
85 o and marijuana dependence as reinforcers of drug-seeking and drug-taking behavior.
86  processes, promoting compulsive patterns of drug-seeking and drug-taking behavior.
87 s are essential driving force for compulsive drug-seeking and drug-taking behaviors in the developmen
88 the acquisition of maladaptive instrumental (drug-seeking and drug-taking) and pavlovian (cue-drug as
89 pal localized cue-motivated reinstatement of drug-seeking and/or cognitive deficits observed during w
90 n, cocaine-associated cue-induced relapse to drug seeking, and cocaine-enhanced extracellular DA in t
91 zed by impaired hedonic capacity, compulsive drug seeking, and high stress.
92 ntributes specifically to cocaine-reinstated drug seeking, and identifies this protein as a target fo
93 e drug self-administration, reinstatement of drug seeking, and incubation of drug craving.
94 heroin reward, drug-induced reinstatement of drug seeking, and reescalation of compulsive heroin self
95  significantly more pronounced in compulsive drug-seeking animals.
96  a dorsal striatal system mediating habitual drug seeking are also summarized.
97 udies on the relationship of neurogenesis on drug seeking are limited.
98 hich time-dependent increases in cue-induced drug seeking are observed after withdrawal from intraven
99                Chronic stress and compulsive drug-seeking are two examples of dysregulated states of
100 f adult-born neural and glial progenitors in drug seeking associated with the different stages of the
101 teral striatum, on the other hand, disrupted drug seeking at all stages of training.
102 a long-lasting disruption of context-induced drug seeking (at least 30 days).
103             In the development of addiction, drug seeking becomes habitual and controlled by drug-ass
104 heroin dependence and their association with drug seeking behavior.
105 e with the ability of multiple cues to drive drug-seeking behavior after just one reactivation and tr
106 with OCT3 mediates corticosterone effects on drug-seeking behavior and establish OCT3 function as an
107 e neuroadaptations underlying stress-induced drug-seeking behavior and may be useful in the treatment
108 cleus accumbens (NAc) facilitate conditioned drug-seeking behavior and primarily originate from media
109                 Behavioral manifestations of drug-seeking behavior are causally linked to alterations
110 footshock stress did not by itself reinstate drug-seeking behavior but potentiated reinstatement in r
111 xciting new possibility is the extinction of drug-seeking behavior by manipulation of epigenetic mech
112                                 Furthermore, drug-seeking behavior continued to require dopamine neur
113 nderpin difficulties in learning to suppress drug-seeking behavior during abstinence.
114 l conditioned stimulus in rats and influence drug-seeking behavior during abstinence.
115 tly extinguished and spontaneous recovery of drug-seeking behavior following presentation of previous
116 n about the role that astrocytes may play in drug-seeking behavior for commonly abused substances.
117                           Cocaine can elicit drug-seeking behavior for drug-predicting stimuli, even
118                        Traditional models of drug-seeking behavior have shown that exposure to associ
119 s been shown to facilitate the extinction of drug-seeking behavior in a manner resistant to reinstate
120 (2) priming- or cue-induced reinstatement of drug-seeking behavior in abstinent subjects (models of r
121                              To better model drug-seeking behavior in addicts, we first developed a n
122 adolescence increases the risk of relapse to drug-seeking behavior in adulthood.
123 potent of the analogues successfully reduced drug-seeking behavior in an animal model of drug-relapse
124             Because stress also precipitates drug-seeking behavior in cocaine addicts, we also postul
125 atement, and nicotine-associated cue-induced drug-seeking behavior in P-rats.
126                          We modeled flexible drug-seeking behavior in rats by requiring animals to so
127 -striatal addiction circuitry and attenuated drug-seeking behavior in rats.
128 g that musical contextual cues can reinstate drug-seeking behavior in rats.
129  we tested whether an estrogen could augment drug-seeking behavior in response to an ordinarily subth
130        Recent studies show yohimbine-induced drug-seeking behavior is attenuated by orexin receptor 1
131                        We observed decreased drug-seeking behavior on ED1 following 10 mg/kg S-propra
132 session, a drug-priming injection reinstated drug-seeking behavior only in rats that in the past had
133 pproach to facilitate learned suppression of drug-seeking behavior that may aid drug abstinence.
134             Although such cues may influence drug-seeking behavior through multiple routes, it is the
135 the effect of the introduction of the ADF on drug-seeking behavior was examined.
136           This is the first work to modulate drug-seeking behavior with astrocyte-specific DREADDs.
137 ed memories.SIGNIFICANCE STATEMENT Continued drug-seeking behavior, a defining characteristic of coca
138 lect depression, the propensity to engage in drug-seeking behavior, and drug craving.
139 e-associated cue was sufficient to reinstate drug-seeking behavior, despite the continued presence of
140 oned behaviors, such as conditioned fear and drug-seeking behavior, is a process of active learning,
141 kg, i.p.) alone were sufficient to reinstate drug-seeking behavior, pretreatment with E2 potentiated
142 comotor-activating effects of cocaine and on drug-seeking behavior, rats receiving methyl supplementa
143               Although estrogens can enhance drug-seeking behavior, they do not directly induce reins
144 of GRIA1, a glutamatergic gene implicated in drug-seeking behavior, verified the increased enrichment
145 ration, and cocaine-induced reinstatement of drug-seeking behavior, whereas R-MOD inhibited cocaine-i
146 discover new therapeutic candidates to treat drug-seeking behavior.
147  drug users, and are thought to facilitate a drug-seeking behavior.
148 d effects on an addict's emotional state and drug-seeking behavior.
149 ortex (mPFC) is implicated in the relapse of drug-seeking behavior.
150 muli, such cues can instigate and invigorate drug-seeking behavior.
151 C) that promote behavioral sensitization and drug-seeking behavior.
152 e memory processes involved in extinction of drug-seeking behavior.
153 d heroin self-administration and cue-induced drug-seeking behavior.
154 ecific HDAC is involved in the extinction of drug-seeking behavior.
155   The ventral pallidum (VP) is necessary for drug-seeking behavior.
156 craving") that instigates and/or invigorates drug-seeking behavior.
157 ological responses, craving, withdrawal, and drug-seeking behavior.
158 the study of anxiogenesis and stress-induced drug-seeking behavior.
159 ility of drug-predictive cues to precipitate drug-seeking behavior.
160 utamate signaling plays an essential role in drug-seeking behavior.
161 sducing stimuli into salient cues that drive drug-seeking behavior.
162 tic disorders or predispose an individual to drug-seeking behavior.
163  activation in drug-induced reinstatement of drug-seeking behavior.
164 y contribute to cue-induced drug craving and drug-seeking behavior.
165 indings that have important implications for drug-seeking behavior.
166 this crucial circuitry to promote compulsive drug-seeking behavior.
167 th the ability of a drug-paired cue to drive drug-seeking behavior.
168 ired CSs intact and able to continue driving drug-seeking behavior.
169    It also failed to induce reinstatement of drug-seeking behavior.
170 hin the DG that could directly contribute to drug-seeking behavior.
171 ivational states that instigate and maintain drug-seeking behavior.
172 avior and may have a role in the etiology of drug-seeking behavior.
173 ian memories that can precipitate relapse to drug-seeking behavior.
174   Addiction involves an inability to control drug-seeking behavior.
175 opeptide released into the VTA that promotes drug-seeking behaviors and potentiates excitatory synapt
176             Overall, these data suggest that drug-seeking behaviors are, in part, attributable to a D
177 ketamine doses used were capable of inducing drug-seeking behaviors as measured by place preference c
178 ions and in the mediation of drug-taking and drug-seeking behaviors in animal models of addiction.
179 t process in both development and relapse of drug-seeking behaviors in drug addiction.
180 ms by which stress triggers reinstatement of drug-seeking behaviors is particularly pertinent to nico
181 iors, arousal, sleep-wakefulness regulation, drug-seeking behaviors, and learning and memory.
182  hippocampal neurogenesis and drug-taking or drug-seeking behaviors, but the lack of a causative link
183  training would facilitate the extinction of drug-seeking behaviors, thus reducing relapse.
184  differences in extinction and incubation of drug-seeking behaviors.
185 g modulator that potentially plays a role in drug-seeking behaviors.
186 at regulates orexin neuronal activity during drug-seeking behaviors.
187 modulating gene expression that may subserve drug-seeking behaviors.
188 onergic state underlying depression-like and drug-seeking behaviors.
189 l raphe nucleus that mediates depressive and drug-seeking behaviors.
190 med in regions involved in the extinction of drug-seeking behaviors.
191 and new approaches are emerging to treat the drug seeking behaviour and craving associated with relap
192 eference and METH- or cue-induced relapse to drug-seeking behaviour in mice.
193 nterventions to enhance insight may decrease drug-seeking behaviour, especially in urine negative coc
194  and examined its potential association with drug-seeking behaviour.
195 a (LHb) has been implicated in regulation of drug-seeking behaviours through aversion-mediated learni
196 a (LHb) has been implicated in regulation of drug-seeking behaviours through aversion-mediated learni
197 PH and amphetamine on dopamine responses and drug-seeking behaviours, without altering cocaine effect
198 mbic cortex stimulation decreased compulsive drug-seeking behaviours.
199  characterized by repetitive drug taking and drug seeking, both tightly controlled by cannabinoid CB1
200 eral striatum selectively disrupted punished drug seeking but did not affect unpunished drug seeking,
201 cal evidence has shown to predict compulsive drug seeking but has not yet been studied in humans.
202 ial prefrontal cortex (vmPFC) in conditioned drug seeking, but specific knowledge of the temporal rol
203 rained rodents mGluR5 stimulation reinstates drug seeking by activating nNOS, but activating mGluR5 d
204 ine craving is observed after suppression of drug seeking by adverse consequences (punishment).
205 umbens (NAS) contributes to the promotion of drug-seeking by drug-predictive cues, it also appears to
206                                   Relapse to drug seeking can be caused by exposure to drug-associate
207   These data demonstrate that stress-induced drug seeking can occur in a terminal environment of low
208             Such conditioned responses (e.g. drug seeking) can be diminished either through a passive
209 xible when trying to procure drugs, and thus drug seeking cannot be governed by habit alone.
210          Thus, the facilitated extinction of drug-seeking cannot be explained by adverse effects on p
211                       Continued instrumental drug seeking despite contingent punishment is a core phe
212 etamine sensitization and on drug taking and drug seeking during cocaine self-administration.
213 at the stress associated with non-reinforced drug seeking during early abstinence (on extinction day
214  and beta-adrenoceptor transmission in DH on drug seeking during ED1 by infusing a cocktail of WAY100
215                    Our results indicate that drug seeking during initial abstinence involves 5-HT and
216 ently demonstrated incubation of cue-induced drug-seeking during the initial phase of abstinence, fol
217 and very robust cue-induced reinstatement of drug seeking, especially in a subset of "addiction-prone
218                Addicts repeatedly relapse to drug seeking even after years of abstinence, and this be
219 d drug seeking but did not affect unpunished drug seeking, even after extended training.
220 t was initiated by 10 minutes of cue-induced drug seeking, followed by 45 minutes with contingent coc
221  appears to play a role in the inhibition of drug-seeking following extinction procedures.
222 mplicated in stress-induced reinstatement of drug seeking for other commonly abused drugs.
223 rved role in stress-induced reinstatement of drug seeking for prototypical substances of abuse.
224 ift over time and experience of control over drug seeking from a limbic cortical-ventral striatal cir
225 chanisms that are important for establishing drug-seeking habits and reinstating them quickly after p
226 witch from controlled drug use to compulsive drug-seeking habits and relapse to these maladaptive hab
227 nal transition from recreational drug use to drug-seeking habits are unknown.
228 nt of incentive salience, and development of drug-seeking habits in the binge/intoxication stage invo
229                           The development of drug-seeking habits is implicated in the transition from
230                   Development of maladaptive drug-seeking habits occurs in conjunction with a ventral
231           It is characterized by maladaptive drug-seeking habits that are maintained despite adverse
232 luntary, recreational drug use to compulsive drug-seeking habits, neurally underpinned by a transitio
233 dopamine levels in the striatum, reinforcing drug-seeking habits.
234 cesses that result ultimately in maladaptive drug-seeking habits.
235 like behavior, including relapse propensity, drug seeking in abstinence, and compulsive (punished) dr
236 e to drug use in humans and reinstatement of drug seeking in animal models of drug relapse.
237                                   Reinstated drug seeking in animal models of relapse relies on gluta
238 tress facilitates reinstatement of addictive drug seeking in animals and promotes relapse in humans.
239 ehaviors and stress-induced reinstatement of drug seeking in both conditioned place preference (CPP)
240 ve additive or more-than-additive effects on drug seeking in laboratory animals, but, surprisingly, s
241 ce--and possibly associated behaviours (e.g. drug seeking in natural settings, relapse after treatmen
242 s in the study of context-induced relapse to drug seeking in rat models.
243 tective agent propentofylline (PPF) modifies drug seeking in rats using a reinstatement model of coca
244 e (10 mg/kg) attenuated the reinstatement of drug seeking in rats.
245 with which D1 activity is increased to drive drug seeking in response to contextual cues.
246  effects of LHb inactivation in control over drug seeking in several cocaine self-administration (SA)
247        Here we use a rat model of compulsive drug seeking in which cocaine seeking persists in a subg
248  cortical-nucleus accumbens pathway underlie drug-seeking in animals with a cocaine self-administrati
249  negatively impact emotional state and drive drug seeking, in part, by modulating the activity of the
250 cated in stress responses and stress-induced drug seeking, in stress-induced binge eating.
251 tegrins may contribute to cocaine-reinstated drug-seeking, in part by promoting reduced GluR2 surface
252 d that nuclear HDAC5 limits reinstatement of drug seeking independent of NPAS4.
253 edule) by extinction significantly decreased drug seeking indicating that behavior is goal-directed r
254 ing and tested the rats for reinstatement of drug seeking induced by cocaine-paired cues and cocaine
255 spectively, and it also prevented relapse to drug-seeking induced by reexposure to cannabinoids or ca
256 in the dmPFC may be an important mediator of drug seeking initiated by multiple relapse triggers.
257 isorder characterized by a cycle composed of drug seeking, intoxication with drug taking and withdraw
258             Context-induced reinstatement of drug seeking is a well established animal model for asse
259  different animal models in which relapse to drug seeking is assessed after cessation of operant drug
260        These data suggest that extinction of drug seeking is associated with selective glutamatergic
261                                              Drug seeking is associated with the activation of reward
262 ion in ventral pallidum subregional roles in drug seeking is likely to be important for understanding
263 signaling by the aversive stimuli that cause drug seeking is not well characterized.
264                 Loss of control over harmful drug seeking is one of the most intractable aspects of a
265 se studies, context-induced reinstatement of drug seeking is reliably observed in laboratory animals
266 ruitment of prefrontal inhibitory control of drug seeking is still functional after prolonged cocaine
267 though the neuroanatomical basis of punished drug seeking is unclear, we hypothesize that the sensori
268 of bFGF in this region affects extinction of drug seeking is unknown.
269    Next, we describe recent discoveries that drug-seeking is associated with transient synaptic plast
270 guish neural subpopulations activated during drug-seeking is to examine their projection targets.
271                        We find that habitual drug-seeking isn't necessary for the development of addi
272            Devaluation of the outcome of the drug seeking link (i.e., the drug taking link of the cha
273 ol was most effective in females in reducing drug seeking on ED1, and WAY100635/GR127935 and betaxolo
274 0635/GR127935 was most effective in reducing drug-seeking on ED1, whereas betaxolol/ICI-118 551 was i
275 y a neurochemical correlate for a laboratory drug-seeking paradigm that can be administered to treatm
276 ent process consisting of a highly motivated drug-seeking phase that, if successful, is followed by a
277 del of drug craving and relapse, cue-induced drug seeking progressively increases after withdrawal fr
278 these VP output pathways in reinstatement of drug seeking remain poorly understood.
279 r these VP contributions to reinstatement of drug seeking remain unknown.
280                      In rodents, cue-induced drug seeking requires transient synaptic potentiation (t
281 ths, including maladaptive responses such as drug seeking, social withdrawal, and compulsive behavior
282                                      Using a drug seeking/taking chained schedule of intravenous coca
283  from controlled drug use to compulsive-like drug seeking/taking.
284 ere activated during "incubated" cue-induced drug-seeking tests after prolonged withdrawal, with nona
285 d significantly contribute to the compulsive drug seeking that is a core component of addiction.
286 n rats, the present studies examined whether drug seeking that is initially goal-directed becomes hab
287 anisms underlying goal-directed and habitual drug seeking, the influence of drug-associated Pavlovian
288        Evidence suggests that HCRT may drive drug-seeking through activation of specific brain region
289 al striatal circuit underlying goal-directed drug seeking to a dorsal striatal system mediating habit
290 t extinction and facilitate reinstatement of drug seeking to drive relapse.
291 icotinic acetylcholine receptors (nAChRs) in drug seeking to nicotine and other drugs of abuse.
292                  We then assessed relapse to drug seeking under extinction conditions after 1 and 21
293 rugs of abuse can evoke powerful craving and drug seeking urges, but effective treatment to suppress
294 on extinction day 1 (ED1)) may contribute to drug seeking via beta-adrenergic and 5-HT neurotransmiss
295 or, and amphetamine-induced reinstatement of drug seeking was assessed with particular attention to t
296 on, cocaine priming-induced reinstatement of drug seeking was associated with increased phosphorylati
297                                Nonreinforced drug seeking was positively correlated with changes in s
298         Importantly, gabapentin's effects on drug seeking were not due to a general depression of spo
299                                   Compulsive drug seeking, which is characterized by continued instru
300 nstatement session inhibited cocaine-induced drug-seeking, while RGD microinjection during extinction

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