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1  extinction responding, and reinstatement of drug seeking.
2 f the plasticity responsible for relapse and drug seeking.
3  may have a role in the lack of control over drug seeking.
4 tinction and cocaine-primed reinstatement of drug seeking.
5 neurons is a critical component of sustained drug seeking.
6  controlling stress-induced reinstatement of drug seeking.
7 fects of drugs of abuse and reinstatement of drug seeking.
8 ted cocaine priming-induced reinstatement of drug seeking.
9 rat model of stress-induced reinstatement of drug seeking.
10 in the neural circuitry for reinstatement of drug seeking.
11 nd not all stressors induce reinstatement of drug seeking.
12 ations of neurons within these regions drive drug seeking.
13 tor 2 (HCRT-R2) signaling in compulsive-like drug seeking.
14  cocaine intake and blocked reinstatement of drug seeking.
15 ss-, drug-, and cue-induced reinstatement of drug seeking.
16  activity of neurons that would later encode drug seeking.
17  striatal circuits in a manner that promotes drug seeking.
18 ntation of the aversive delay cue reinstated drug seeking.
19 is functionally important for suppressing of drug seeking.
20 l striatum is thought to assume control over drug seeking.
21 ne and ceftriaxone) can decrease measures of drug seeking.
22 y involved in reward learning and relapse of drug seeking.
23 forms of motivated behavior and pathological drug seeking.
24 n the neural circuits controlling relapse to drug seeking.
25 ntrol over behavior and increased compulsive drug seeking.
26  driven by insensitivity to costs imposed on drug seeking.
27 ased positive reinforcement into maladaptive drug seeking.
28 wal to facilitate relapse to compulsive-like drug seeking.
29 altering the projection's ability to inhibit drug seeking.
30 riod of abstinence and a subsequent test for drug seeking.
31 ly involved in the development of compulsive drug seeking.
32 e association between environmental cues and drug seeking.
33 in blocking cocaine-induced reinstatement to drug seeking.
34 use affects t-SP associated with cue-induced drug seeking.
35  more sensitive than males to stress-induced drug seeking.
36 thout affecting cue-induced reinstatement of drug seeking.
37 at plays a critical role in reinstatement of drug seeking.
38 duced alterations to these genes may augment drug-seeking.
39  cocaine and stress-induced reinstatement of drug-seeking.
40 ated in drug-taking and the reinstatement of drug-seeking.
41 dministration (SA) underlie reinstatement of drug-seeking.
42 s imperative to BDNF's suppressive effect on drug-seeking.
43 neural system that initiates and encodes the drug-seeking act, surprisingly little is known about the
44 nisms: the ability of drug cues to reinforce drug-seeking actions following a period of extinction tr
45  CeM output neurons, and decreased incubated drug seeking after 15 forced abstinence days.
46 drug craving (the time-dependent increase in drug seeking after cessation of drug self-administration
47 act of drug use on the ability to extinguish drug seeking after changes in expected outcomes.
48          Knockdown of Drp1 in D1-MSNs blocks drug seeking after cocaine self-administration, while en
49 celerates extinction and reduces cue-induced drug seeking after cocaine self-administration.
50 recently developed a rat model of relapse to drug seeking after food choice-induced voluntary abstine
51 1 receptor signaling played a larger role in drug seeking after IntA.
52 the learned preference, the reinstatement of drug seeking after operant drug self-administration and
53 s on the epigenetic mechanisms of relapse to drug seeking after prolonged abstinence.
54 y incubation of drug craving and cue-induced drug seeking after prolonged voluntary abstinence, mimic
55 unting evidence indicates that resumption of drug seeking after voluntary abstinence recruits neural
56 rain regions, is essential for resumption of drug seeking after voluntary abstinence.
57 nister heroin as adolescents show attenuated drug-seeking after abstinence, compared with adults.
58 tes cocaine priming-induced reinstatement of drug seeking, an animal model of relapse, in male Spragu
59 ersistent maladaptive memories that maintain drug seeking and are resistant to extinction are a hallm
60  is characterized by a compulsive pattern of drug seeking and consumption and a high risk of relapse
61 erable individuals to engage in pathological drug seeking and drug taking that can remain a lifelong
62 ation sessions were designed to measure both drug seeking and drug taking.
63  chronic disease characterized by compulsive drug seeking and episodes of relapse despite prolonged p
64 ression in the NAc is sufficient to decrease drug seeking and increase dendritic spine density, where
65     Drug addiction is marked by pathological drug seeking and intense drug craving, particularly in r
66  assess measures of relapse/reinstatement of drug seeking and long-term effects on cognitive function
67 or (D3R) is involved in the reinstatement of drug seeking and motivation for drugs of abuse.
68 ng is a possible site of shared signaling in drug seeking and potentiated reinstated sucrose seeking,
69 the development and intensity of cue-induced drug seeking and provides evidence for potential biomark
70 n of this activity could prevent cue-induced drug seeking and relapse long after treatment.
71 -associated Pavlovian-conditioned stimuli on drug seeking and relapse, and evidence for impairments i
72 rnical/lateral hypothalamus, is critical for drug seeking and relapse, but it is not clear how the ci
73 ce of glutamatergic signaling in the NAc for drug seeking and relapse, here we examined its role in m
74  of NAc toward a motivational state favoring drug seeking and relapse.
75 s may underlie the persistence of compulsive drug seeking and relapse.
76 sentation of drug-associated cues can elicit drug seeking and relapse.
77 ng a novel method of preventing cue-elicited drug seeking and relapse.
78 prefrontal cortical to striatal control over drug seeking and taking as well as a progression from th
79 addictive behaviors that underlie compulsive drug seeking and taking in humans.
80 es of drug abuse and may drive the increased drug seeking and taking that characterize the transition
81 ncluding escalation of drug intake, punished drug seeking and taking, intermittent drug access, choic
82  evaluated the potential for compulsive-like drug seeking and taking, using intravenous self-administ
83  in neural networks that underlie compulsive drug seeking and taking.
84 gh impulsivity predicts loss of control over drug seeking and taking.
85 FSI-embedded circuit in regulating NAc-based drug seeking and taking.
86 low drug-associated cues to drive compulsive drug seeking and taking.
87 eficits that likely contribute to persistent drug seeking and the high rates of relapse.
88 ced negative affect, a hallmark of continued drug seeking and use in human addicts.
89 ted cocaine priming-induced reinstatement of drug seeking and was associated with increased GluA2 Q/R
90 s such as cocaine or amphetamine can promote drug-seeking and -taking behavior.
91  such as nucleus accumbens (NAcc), promoting drug-seeking and -taking behavior.
92 onse may implicate VPdl in the processing of drug-seeking and drug-taking behavior via projections to
93 o and marijuana dependence as reinforcers of drug-seeking and drug-taking behavior.
94  processes, promoting compulsive patterns of drug-seeking and drug-taking behavior.
95 presses drug self-administration, relapse to drug seeking, and brain responses to drug-associated cue
96 n, cocaine-associated cue-induced relapse to drug seeking, and cocaine-enhanced extracellular DA in t
97 zed by impaired hedonic capacity, compulsive drug seeking, and high stress.
98 ntributes specifically to cocaine-reinstated drug seeking, and identifies this protein as a target fo
99 e drug self-administration, reinstatement of drug seeking, and incubation of drug craving.
100 chronic disorder characterized by compulsive drug seeking, and involves repetitive cycles of compulsi
101 l and opioid self-administration, relapse to drug seeking, and plays a role in emotional responses.
102 heroin reward, drug-induced reinstatement of drug seeking, and reescalation of compulsive heroin self
103 aine addiction is associated with compulsive drug-seeking, and exposure to the drug or to drug-associ
104  significantly more pronounced in compulsive drug-seeking animals.
105  a dorsal striatal system mediating habitual drug seeking are also summarized.
106 udies on the relationship of neurogenesis on drug seeking are limited.
107                      These effects of ZIP on drug seeking are specific, as we did not see any effect
108                Chronic stress and compulsive drug-seeking are two examples of dysregulated states of
109 ted to decrease consumption, withdrawal, and drug-seeking associated with several drugs of abuse and
110 a long-lasting disruption of context-induced drug seeking (at least 30 days).
111             In the development of addiction, drug seeking becomes habitual and controlled by drug-ass
112 d subsequent enhanced locomotor response and drug seeking behavior after repeated cocaine administrat
113 t stimulus-control over both drug taking and drug seeking behavior and are difficult to extinguish.
114                                              Drug seeking behavior and chronic drug use are associate
115 inence from cocaine self-administration, and drug seeking behavior was measured.
116 ing the released glutamate from synapses and drug seeking behavior.
117 e with the ability of multiple cues to drive drug-seeking behavior after just one reactivation and tr
118 with OCT3 mediates corticosterone effects on drug-seeking behavior and establish OCT3 function as an
119 e neuroadaptations underlying stress-induced drug-seeking behavior and may be useful in the treatment
120 cleus accumbens (NAc) facilitate conditioned drug-seeking behavior and primarily originate from media
121                 Behavioral manifestations of drug-seeking behavior are causally linked to alterations
122 footshock stress did not by itself reinstate drug-seeking behavior but potentiated reinstatement in r
123                                 Furthermore, drug-seeking behavior continued to require dopamine neur
124 nderpin difficulties in learning to suppress drug-seeking behavior during abstinence.
125 n about the role that astrocytes may play in drug-seeking behavior for commonly abused substances.
126              The influence of social cues on drug-seeking behavior has garnered attention recently, b
127 s been shown to facilitate the extinction of drug-seeking behavior in a manner resistant to reinstate
128 (2) priming- or cue-induced reinstatement of drug-seeking behavior in abstinent subjects (models of r
129                              To better model drug-seeking behavior in addicts, we first developed a n
130 adolescence increases the risk of relapse to drug-seeking behavior in adulthood.
131 potent of the analogues successfully reduced drug-seeking behavior in an animal model of drug-relapse
132 atement, and nicotine-associated cue-induced drug-seeking behavior in P-rats.
133                          We modeled flexible drug-seeking behavior in rats by requiring animals to so
134  we tested whether an estrogen could augment drug-seeking behavior in response to an ordinarily subth
135                        We observed decreased drug-seeking behavior on ED1 following 10 mg/kg S-propra
136 pproach to facilitate learned suppression of drug-seeking behavior that may aid drug abstinence.
137 ia and hyperkatifeia, which drive pronounced drug-seeking behavior via processes of negative reinforc
138 the effect of the introduction of the ADF on drug-seeking behavior was examined.
139                                     However, drug-seeking behavior was significantly higher in concur
140           This is the first work to modulate drug-seeking behavior with astrocyte-specific DREADDs.
141 ed memories.SIGNIFICANCE STATEMENT Continued drug-seeking behavior, a defining characteristic of coca
142 lect depression, the propensity to engage in drug-seeking behavior, and drug craving.
143 e-associated cue was sufficient to reinstate drug-seeking behavior, despite the continued presence of
144 (vGluT2) neurons have contrasting effects on drug-seeking behavior, our data may indicate a complex r
145 kg, i.p.) alone were sufficient to reinstate drug-seeking behavior, pretreatment with E2 potentiated
146 comotor-activating effects of cocaine and on drug-seeking behavior, rats receiving methyl supplementa
147               Although estrogens can enhance drug-seeking behavior, they do not directly induce reins
148 of GRIA1, a glutamatergic gene implicated in drug-seeking behavior, verified the increased enrichment
149 rimed, but not cue-induced, reinstatement of drug-seeking behavior, whereas inhibition of SNr GABA ne
150 ration, and cocaine-induced reinstatement of drug-seeking behavior, whereas R-MOD inhibited cocaine-i
151 th the ability of a drug-paired cue to drive drug-seeking behavior.
152 ired CSs intact and able to continue driving drug-seeking behavior.
153    It also failed to induce reinstatement of drug-seeking behavior.
154 hin the DG that could directly contribute to drug-seeking behavior.
155 ivational states that instigate and maintain drug-seeking behavior.
156 ian memories that can precipitate relapse to drug-seeking behavior.
157   Addiction involves an inability to control drug-seeking behavior.
158 discover new therapeutic candidates to treat drug-seeking behavior.
159  drug users, and are thought to facilitate a drug-seeking behavior.
160 d effects on an addict's emotional state and drug-seeking behavior.
161 ortex (mPFC) is implicated in the relapse of drug-seeking behavior.
162 muli, such cues can instigate and invigorate drug-seeking behavior.
163 C) that promote behavioral sensitization and drug-seeking behavior.
164 e memory processes involved in extinction of drug-seeking behavior.
165 ecific HDAC is involved in the extinction of drug-seeking behavior.
166   The ventral pallidum (VP) is necessary for drug-seeking behavior.
167 craving") that instigates and/or invigorates drug-seeking behavior.
168 t stable rates of responding and conditioned drug-seeking behavior.
169 hereas "novelty-seeking" predicts compulsive drug-seeking behavior.
170 se, such as ethanol, can trigger craving and drug-seeking behavior.
171 io-sexual context appears to enhance further drug-seeking behavior.
172 avior and may have a role in the etiology of drug-seeking behavior.
173 d heroin self-administration and cue-induced drug-seeking behavior.
174 d to cocaine-conditioned cues and relapse to drug seeking behaviors.
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 ms by which stress triggers reinstatement of drug-seeking behaviors is particularly pertinent to nico
179                                        Next, drug-seeking behaviors were measured during cue reactivi
180 blockade of MORs in the VTA counteracted two drug-seeking behaviors, locomotor activity and place pre
181 med in regions involved in the extinction of drug-seeking behaviors.
182 maladaptive plasticity that drives food- and drug-seeking behaviors.
183  differences in extinction and incubation of drug-seeking behaviors.
184 g modulator that potentially plays a role in drug-seeking behaviors.
185  in experience-dependent neuroplasticity and drug-seeking behaviors.
186 and new approaches are emerging to treat the drug seeking behaviour and craving associated with relap
187 e conceptual distinctions between compulsive drug-seeking behaviour and compulsive drug-taking behavi
188 eference and METH- or cue-induced relapse to drug-seeking behaviour in mice.
189 a (LHb) has been implicated in regulation of drug-seeking behaviours through aversion-mediated learni
190 a (LHb) has been implicated in regulation of drug-seeking behaviours through aversion-mediated learni
191 PH and amphetamine on dopamine responses and drug-seeking behaviours, without altering cocaine effect
192 mbic cortex stimulation decreased compulsive drug-seeking behaviours.
193  characterized by repetitive drug taking and drug seeking, both tightly controlled by cannabinoid CB1
194 cal evidence has shown to predict compulsive drug seeking but has not yet been studied in humans.
195 ial prefrontal cortex (vmPFC) in conditioned drug seeking, but specific knowledge of the temporal rol
196 rained rodents mGluR5 stimulation reinstates drug seeking by activating nNOS, but activating mGluR5 d
197 ine craving is observed after suppression of drug seeking by adverse consequences (punishment).
198 umbens (NAS) contributes to the promotion of drug-seeking by drug-predictive cues, it also appears to
199                                   Relapse to drug seeking can be caused by exposure to drug-associate
200   These data demonstrate that stress-induced drug seeking can occur in a terminal environment of low
201 stinence induced by negative consequences of drug seeking can paradoxically potentiate opioid craving
202             Such conditioned responses (e.g. drug seeking) can be diminished either through a passive
203 xible when trying to procure drugs, and thus drug seeking cannot be governed by habit alone.
204          Thus, the facilitated extinction of drug-seeking cannot be explained by adverse effects on p
205 tivity to specific stressors may manifest as drug seeking depends on biological sex.
206 drug craving (the time-dependent increase in drug seeking during abstinence).
207  access caused time-independent increases in drug seeking during abstinence.
208 etamine sensitization and on drug taking and drug seeking during cocaine self-administration.
209 at the stress associated with non-reinforced drug seeking during early abstinence (on extinction day
210  and beta-adrenoceptor transmission in DH on drug seeking during ED1 by infusing a cocktail of WAY100
211                    Our results indicate that drug seeking during initial abstinence involves 5-HT and
212 ently demonstrated incubation of cue-induced drug-seeking during the initial phase of abstinence, fol
213 and very robust cue-induced reinstatement of drug seeking, especially in a subset of "addiction-prone
214 t was initiated by 10 minutes of cue-induced drug seeking, followed by 45 minutes with contingent coc
215 laboratory has reported a robust increase in drug seeking following a period of withdrawal in chronic
216  appears to play a role in the inhibition of drug-seeking following extinction procedures.
217 mplicated in stress-induced reinstatement of drug seeking for other commonly abused drugs.
218 rved role in stress-induced reinstatement of drug seeking for prototypical substances of abuse.
219 ift over time and experience of control over drug seeking from a limbic cortical-ventral striatal cir
220 e, there is a transition in the control over drug seeking from ventral to anterior dorsal striatum (a
221 chanisms that are important for establishing drug-seeking habits and reinstating them quickly after p
222 witch from controlled drug use to compulsive drug-seeking habits and relapse to these maladaptive hab
223 nal transition from recreational drug use to drug-seeking habits are unknown.
224 nt of incentive salience, and development of drug-seeking habits in the binge/intoxication stage invo
225                   Development of maladaptive drug-seeking habits occurs in conjunction with a ventral
226           It is characterized by maladaptive drug-seeking habits that are maintained despite adverse
227 luntary, recreational drug use to compulsive drug-seeking habits, neurally underpinned by a transitio
228 dopamine levels in the striatum, reinforcing drug-seeking habits.
229 cesses that result ultimately in maladaptive drug-seeking habits.
230 pallidum (VP), a key limbic node involved in drug seeking, has well-established roles in conventional
231 like behavior, including relapse propensity, drug seeking in abstinence, and compulsive (punished) dr
232 e to drug use in humans and reinstatement of drug seeking in animal models of drug relapse.
233                                   Reinstated drug seeking in animal models of relapse relies on gluta
234                  The persistence of punished drug seeking in animals is better explained by greater d
235 ehaviors and stress-induced reinstatement of drug seeking in both conditioned place preference (CPP)
236     We found that p-FAK was increased during drug seeking in both D1 and D2-medium spiny neurons (MSN
237 ve additive or more-than-additive effects on drug seeking in laboratory animals, but, surprisingly, s
238 s in the study of context-induced relapse to drug seeking in rat models.
239 tective agent propentofylline (PPF) modifies drug seeking in rats using a reinstatement model of coca
240 ference, and cocaine-primed reinstatement of drug seeking in rats.
241 e (10 mg/kg) attenuated the reinstatement of drug seeking in rats.
242 with which D1 activity is increased to drive drug seeking in response to contextual cues.
243                 The intensity of cue-induced drug seeking in rodent models correlates with the induct
244  effects of LHb inactivation in control over drug seeking in several cocaine self-administration (SA)
245        Here we use a rat model of compulsive drug seeking in which cocaine seeking persists in a subg
246 e absence of Meth triggered reinstatement of drug-seeking in concurrent animals.
247  negatively impact emotional state and drive drug seeking, in part, by modulating the activity of the
248 cated in stress responses and stress-induced drug seeking, in stress-induced binge eating.
249  female rats, the time-dependent increase in drug seeking (incubation) is critically dependent on the
250 d that nuclear HDAC5 limits reinstatement of drug seeking independent of NPAS4.
251 ing and tested the rats for reinstatement of drug seeking induced by cocaine-paired cues and cocaine
252 spectively, and it also prevented relapse to drug-seeking induced by reexposure to cannabinoids or ca
253 in the dmPFC may be an important mediator of drug seeking initiated by multiple relapse triggers.
254 isorder characterized by a cycle composed of drug seeking, intoxication with drug taking and withdraw
255             Context-induced reinstatement of drug seeking is a well established animal model for asse
256  different animal models in which relapse to drug seeking is assessed after cessation of operant drug
257 ssical incubation of drug craving rat model, drug seeking is assessed after homecage forced abstinenc
258  that propensity to discount cost imposed on drug seeking is associated with dependence severity.
259                                              Drug seeking is associated with the activation of reward
260 ion in ventral pallidum subregional roles in drug seeking is likely to be important for understanding
261 signaling by the aversive stimuli that cause drug seeking is not well characterized.
262                 Loss of control over harmful drug seeking is one of the most intractable aspects of a
263 se studies, context-induced reinstatement of drug seeking is reliably observed in laboratory animals
264 ruitment of prefrontal inhibitory control of drug seeking is still functional after prolonged cocaine
265 of bFGF in this region affects extinction of drug seeking is unknown.
266                           Yet how relapse to drug-seeking is assembled from activity across the mesol
267    Next, we describe recent discoveries that drug-seeking is associated with transient synaptic plast
268 guish neural subpopulations activated during drug-seeking is to examine their projection targets.
269                        We find that habitual drug-seeking isn't necessary for the development of addi
270 regabalin 60 and 90 mg/kg doses demonstrated drug seeking-like behavior, which was significantly bloc
271 fluence on the initiation and maintenance of drug seeking often long into abstinence, especially when
272 ocial choice-induced abstinence on incubated drug seeking on day 15.
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 n voluntary because negative consequences of drug seeking outweigh the desire for the drug.
276 y a neurochemical correlate for a laboratory drug-seeking paradigm that can be administered to treatm
277 ent process consisting of a highly motivated drug-seeking phase that, if successful, is followed by a
278 the course of drug exposure the control over drug seeking progressively devolves to anterior dorsal s
279 del of drug craving and relapse, cue-induced drug seeking progressively increases after withdrawal fr
280 d this projection, which resulted in reduced drug seeking, regardless of the drug-free period.
281 these VP output pathways in reinstatement of drug seeking remain poorly understood.
282 r these VP contributions to reinstatement of drug seeking remain unknown.
283                      In rodents, cue-induced drug seeking requires transient synaptic potentiation (t
284 ths, including maladaptive responses such as drug seeking, social withdrawal, and compulsive behavior
285  from controlled drug use to compulsive-like drug seeking/taking.
286 n imaging of IL-NAc neurons in rats during a drug-seeking test.
287 ere activated during "incubated" cue-induced drug-seeking tests after prolonged withdrawal, with nona
288 rder is attributed to persistent cue-induced drug seeking that intensifies (or "incubates") during dr
289 d significantly contribute to the compulsive drug seeking that is a core component of addiction.
290 anisms underlying goal-directed and habitual drug seeking, the influence of drug-associated Pavlovian
291        Evidence suggests that HCRT may drive drug-seeking through activation of specific brain region
292 al striatal circuit underlying goal-directed drug seeking to a dorsal striatal system mediating habit
293 t extinction and facilitate reinstatement of drug seeking to drive relapse.
294                  We then assessed relapse to drug seeking under extinction conditions after 1 and 21
295 rugs of abuse can evoke powerful craving and drug seeking urges, but effective treatment to suppress
296 on extinction day 1 (ED1)) may contribute to drug seeking via beta-adrenergic and 5-HT neurotransmiss
297 tex (mPFC), suggesting that G-CSF influences drug seeking via glutamatergic mechanisms.
298 on, cocaine priming-induced reinstatement of drug seeking was associated with increased phosphorylati
299                                Nonreinforced drug seeking was positively correlated with changes in s
300         Importantly, gabapentin's effects on drug seeking were not due to a general depression of spo

 
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