ライフサイエンスコーパス: binge

1 alcohol diet without or with weekly alcohol binge.

2 cted (nonhazardous: 13.6% vs 2.5%; hazardous/binge: 18.2% vs 3.1%; alcohol-related diagnosis: 22.1% v

3 ected (nonhazardous: 6.7% vs 1.4%; hazardous/binge: 9.5% vs 3.0%; alcohol-related diagnosis: 19.0% vs

4 The first alcohol binge activates mTORC1 in NAc D1+ neurons and increases

5 on translocation within both regions reduced binge alcohol consumption in a manner requiring intact g

6 A 30-day history of binge alcohol drinking (for example, 4-5 g kg(-1) per 2

7 Despite the fact that binge alcohol drinking (intake resulting in blood alcoho

8 Repeated cycles of binge alcohol drinking and abstinence are key components

9 ATEMENT We examined the relationship between binge alcohol drinking and spike timing-dependent plasti

10 th the NAc and CeA is a major contributor to binge alcohol drinking and to the genetic propensity to

11 ration after a history of repeated cycles of binge alcohol drinking and withdrawal.

12 ptor (Y1R) activation in the BNST suppressed binge alcohol drinking by enhancing inhibitory synaptic

13 Binge alcohol drinking elevated p(Ser729)-PKCepsilon lev

14 ons between NPY and CRF in the regulation of binge alcohol drinking in both mice and monkeys.

15 Specifically, a mouse paradigm that mimics binge alcohol drinking in humans produced a robust reduc

16 Binge alcohol drinking is a tremendous public health pro

17 role of dopamine in mediating the effects of binge alcohol drinking on synaptic plasticity of NAc MSN

18 sed drinking in the dark (DID) as a model of binge alcohol drinking to assess its effects on spike ti

19 Binge alcohol drinking, a behavior characterized by rapi

20 (STDP), the manner by which STDP responds to binge alcohol drinking, and its sensitivity to dopamine

21 These results indicate that chronic-plus-binge alcohol exposure inhibits the granulopoietic respo

22 To study the effect of chronic-plus-binge alcohol exposure on the granulopoietic response, a

23 st of neutrophils isolated from chronic plus binge alcohol fed mice or from human blood, and decrease

24 CBD on liver injury induced by chronic plus binge alcohol feeding in mice.

25 ive coping behaviors in real life, including binge alcohol intake, emotional eating, and frequency of

26 tory of a highly prevalent form of drinking, binge alcohol intake, influences enzyme priming or the f

27 homelessness, incarceration, substance use, binge alcohol use, depression, and not achieving a suppr

28 Collectively, these data indicate binge alcohol-induced increases in Group1 mGluR signalin

29 tes and marijuana) predicted all 3 levels of binge and extreme binge drinking.

30 The transition to binge and hazardous drinking occurred for 29% and 18% of

31 t approach, human young (18-25 years) social binge and non-binge drinkers were tested for motor impul

32 eatment, CBT was more effective in relieving binging and purging than psychoanalytic psychotherapy an

33 nce of SPP1, chronic ASH mice without weekly binge begin to develop AH.

34 Binge compared with nonbinge drinking (defined as report

35 sitive correlation between the propensity to binge drink alcohol and constitutive p(Ser729)-PKCepsilo

36 e alcohol drinking in nondependent rats that binge drink alcohol and in alcohol-dependent rats.

37 the amygdala (CeA) in nondependent rats that binge drink alcohol and in alcohol-dependent rats.

38 binge eating was associated with starting to binge drink frequently, while both overeating and binge

39 e, which may contribute to the propensity to binge drink.

40 Here, we focus on binge drinkers (BD), characterized by repeated episodes

41 Compared with non-bingers (NBD; n=22), binge drinkers (BD, n=22) showed robust impairments in a

42 We further assessed 32 young binge drinkers and 36 abstinent subjects with alcohol us

43 that subthalamic connectivity differentiates binge drinkers and individuals with alcohol use disorder

44 man young (18-25 years) social binge and non-binge drinkers were tested for motor impulsivity and att

45 of binge drinking among those who were never binge drinkers, and (3) the onset of hazardous drinking

46 We further showed that binge drinkers, like those with alcohol use disorders, h

47 Results were similar after excluding binge drinkers.

48 rdous drinking (14.2 [5.91-34.0]), hazardous/binge drinking (18.9 [7.98-44.8]), and alcohol-related d

49 at least a 4.0-percentage-point increase in binge drinking (95% confidence interval: 0.9, 7.0) and a

50 OR], 1.69 [95% CI, 1.17-2.44]), the onset of binge drinking (AOR, 1.38 [95% CI, 1.08-1.77]), and the

51 -0.259, SE = 0.132, P = .049) and growth of binge drinking (beta = -0.244, SE = 0.073, P = .001), du

52 year), hazard ratios were increased for ever binge drinking (HR = 1.29, 95% CI: 1.15, 1.45) or blacki

53 -1.08]; P = .14) and effects on the risks of binge drinking (odds ratio [OR], 0.84 [99.17% CI, 0.67-1

54 ed with other risk-taking behaviors, such as binge drinking (P < .001 and P = .006, respectively), un

55 mong those who never drank, (2) the onset of binge drinking among those who were never binge drinkers

56 lcohol use has been studied extensively, but binge drinking among youth in the United States is not y

57 documented clinical relevance to adolescent binge drinking and alcoholism in humans to test whether

58 al relevance of PKCepsilon translocation for binge drinking and determination of potential upstream s

59 he sera of healthy individuals after alcohol binge drinking and in mice after binge or chronic alcoho

60 lcohol-induced steatosis in a mouse model of binge drinking as acute ethanol (EtOH) intoxication has

61 sive symptoms and initiation of drug use and binge drinking at least monthly.

62 Binge drinking at the traditionally defined 5+ drinking

63 e importance of assessing multiple levels of binge drinking behavior and their predictors among youth

64 To assess the short-time effects of a binge drinking episode on CB1R availability, 20 healthy

65 with an increased frequency of drinking and binge drinking episodes in adolescents.

66 reinforce evidence-based counseling against binge drinking even at the earliest stages of pregnancy.

67 -0.176, SE = 0.073, P = .02), and growth in binge drinking frequency (beta = -0.183, SE = 0.092, P =

68 o enhance physique were more likely to start binge drinking frequently (2.06; 1.58-2.69) and using dr

69 Our data show that acute alcohol binge drinking in healthy volunteers results in increase

70 inge drinking, and 5.6% reported 15+ extreme binge drinking in the last 2 weeks.

71 The prevalence of binge drinking in the United States is rising.

72 Teen binge drinking is associated with low frontal white matt

73 Binge drinking may be an early indicator of vulnerabilit

74 R modulator, LM11A-31, significantly reduced binge drinking of alcohol.

75 Adolescent binge drinking or adult dependence induction reduced the

76 4-hour, 2-bottle choice drinking in the dark binge drinking or limited access 2-bottle choice.

77 pproaches within the context of two distinct binge drinking procedures, drinking in the dark and sche

78 In follow-up studies we found that binge drinking reduced myelin density in the mPFC in ado

79 The best predictors for high binge drinking score were premature responding in the Sx

80 exceeded medical guidelines for acute harm (binge drinking) and chronic harm (heavy drinking).

81 for alcohol consumption (units per week and binge drinking) from Scottish Health Surveys done in 199

82 of 20.2% of high school seniors reported 5+ binge drinking, 10.5% reported 10+ extreme binge drinkin

83 + binge drinking, 10.5% reported 10+ extreme binge drinking, and 5.6% reported 15+ extreme binge drin

84 t concentrations seen in blood alcohol after binge drinking, and diminished ALDH1a1 leads to enhanced

85 , current health insurance coverage, asthma, binge drinking, and physical activity) was not substanti

86 ing after adjustment for weekly consumption, binge drinking, BMI, and smoking.

87 Binge drinking, defined as reaching a blood alcohol leve

88 al confounders (age, sex, smoking, heavy and binge drinking, diabetes, use of preventive dental servi

89 inhibit TLR4 or MCP-1 expression nor reduce binge drinking, identifying a neuronal TLR4/MCP-1 signal

90 assified as nonhazardous drinking, hazardous/binge drinking, or alcohol-related diagnosis.

91 use problems (frequent alcohol use, frequent binge drinking, prescription drug misuse, and over-the-c

92 the amygdala to examine both idiopathic and binge drinking-induced changes in constitutive PKCepsilo

93 aches to examine the functional relevance of binge drinking-induced changes in glutamate receptors, t

94 sodes of excessive alcohol drinking known as binge drinking.

95 t against severe intoxication in response to binge drinking.

96 inhibited target gene expression and blunted binge drinking.

97 and personality as important antecedents of binge drinking.

98 predicted all 3 levels of binge and extreme binge drinking.

99 hold (5 drinks) often used in definitions of binge drinking.

100 We found that the first binge-drinking alcohol session produced enduring enhance

101 otionality, which were associated with fewer binge-drinking days and fewer alcohol related problems.

102 ng drinking limit guidelines in adults or on binge-drinking episodes or social consequences of alcoho

103 r symptoms over time associated with greater binge-drinking frequency.

104 f response to alcohol, would predict rate of binging during an individual alcohol consumption session

105 Binge eating afflicts approximately 5% of US adults, tho

106 Obese subjects with binge eating also have impaired discrimination of subjec

107 in the Arab region; and increasing rates of binge eating and bulimia nervosa in Hispanic and Black A

108 uses evolved protective mechanisms including binge eating and increased metabolic efficiency and fat

109 Secondary endpoints related to binge eating and medical parameters, safety, and treatme

110 petitive responses in psychopathology; e.g., binge eating and opiate or alcohol abuse, disorders in w

111 ore, results suggested that higher levels of binge eating and overeating in males at age 13 y likely

112 Furthermore, higher levels of binge eating and overeating may cause higher BMI in late

113 MI at age 7 y likely causes higher levels of binge eating and overeating, weight and shape concerns,

114 major significant genetic factor underlying binge eating and provide a behavioral paradigm for futur

115 choanalytic psychotherapy (N=34) had stopped binge eating and purging (odds ratio=13.40, 95% confiden

116 ychoanalytic psychotherapy group had stopped binge eating and purging (odds ratio=4.34, 95% CI=1.33-1

117 sdexamfetamine, SGAs, and topiramate reduced binge eating and related psychopathology, and lisdexamfe

118 ically significant effects in the context of binge eating and weight regain prevention requires furth

119 ustify whether classification of obesity and binge eating as an addictive disorder is merited.

120 Overeating and binge eating assessed via questionnaire every 12 to 24 m

121 than health education at reducing objective binge eating at the 12-mo follow-up (P < 0.05).

122 8 weeks), lisdexamfetamine responders (</=1 binge eating day per week for 4 consecutive weeks and CG

123 Change from baseline in binge eating days/week at weeks 11-12 (primary efficacy

124 eatment differences for change from baseline binge eating days/week at weeks 11-12 significantly favo

125 g/day) was superior to placebo in decreasing binge eating days/week from baseline and improving binge

126 disorder criteria and had moderate to severe binge eating disorder (>/=3 binge-eating days per week f

127 were depression (19% [95% CI, 14%-25%]) and binge eating disorder (17% [95% CI, 13%-21%]).

128 l survey, the average lifetime prevalence of binge eating disorder (BED) was 2%.

129 dexamfetamine dimesylate (LDX) vs placebo in binge eating disorder (BED) was evaluated in two multice

130 subjects with (n = 30) and without (n = 30) binge eating disorder (BED) were compared with matched h

131 ents the criterion standard for treatment of binge eating disorder (BED), most individuals do not hav

132 ide the United States on the epidemiology of binge eating disorder (BED).

133 n phenotypes: pathological gambling (PG) and binge eating disorder (BED).

134 The Internet and Binge Eating Disorder (INTERBED) study is a prospective,

135 d bulimia nervosa and more likely to exhibit binge eating disorder and eating disorder not otherwise

136 ating and obesity, emphasizing binge eating, binge eating disorder and food addiction as useful conce

137 sa and bulimia nervosa; and the inclusion of binge eating disorder as a formal diagnosis.

138 y of research also supports the inclusion of binge eating disorder as a formal diagnosis.

139 sorder and 2.9% had partial or full-criteria binge eating disorder but no association with the outcom

140 Our findings support a distinct subtype of binge eating disorder in obesity with similarities in ri

141 n the anticipation of rewards, subjects with binge eating disorder show greater risk-taking, similar

142 Neither depression nor binge eating disorder was consistently associated with d

143 or attention deficit hyperactivity disorder, binge eating disorder, cocaine addiction, obesity, and t

144 trol disorders, including gambling disorder, binge eating disorder, compulsive sexual behaviour, and

145 pled with a lack of control over eating, and binge eating disorder, the Diagnostic and Statistical Ma

146 tablished treatments for bulimia nervosa and binge eating disorder, with stepped-care approaches show

147 rgery patients-in particular, depression and binge eating disorder.

148 ference in the number of days with objective binge eating episodes (OBEs) during the previous 28 days

149 the anticipation of losses, obesity without binge eating had a similar pattern to other substance-us

150 We assessed binge eating in closely related C57BL/6 mouse substrains

151 Cyfip2 as a major genetic factor underlying binge eating in heterozygous knockout mice on a C57BL/6N

152 pin-releasing factor (CRF) in stress-induced binge eating in our model.

153 e of CRF receptors in BNST in stress-induced binge eating in our rat model.

154 (12-41) decreased frustration stress-induced binge eating in rats with a history of food restriction.

155 Binge eating is a highly heritable trait associated with

156 Binge eating is associated with obesity and has been con

157 marijuana and other drug use, we found that binge eating is uniquely predictive of incident overweig

158 Compulsive, binge eating of highly palatable food constitutes a core

159 Infrequent binge eating or purging or overeating without a loss of

160 rts to integrate these models by focusing on binge eating phenotypes as the subgroup of obese individ

161 drink frequently, while both overeating and binge eating predicted starting to use marijuana and oth

162 etrograde endocannabinoid signaling, whereas binge eating resulted in the downregulation of a gene se

163 lts with body mass index >/= 30 kg m(-2) and binge eating scale scores >/= 19 received 1-week single-

164 acebo in its effects on weight, fat mass and binge eating scores.

165 r monetary incentives linked alcohol use and binge eating severity.

166 x correlated negatively with alcohol use and binge eating severity.

167 ome to inform molecular mechanisms mediating binge eating susceptibility and establishment.

168 on a C57BL/6N background that showed reduced binge eating toward a wild-type C57BL/6J-like level.

169 Neither overeating nor binge eating was associated with starting to binge drink

170 tations, including starvation resistance and binge eating when food becomes available.

171 isition in disorders involving both natural (binge eating) and artificial (methamphetamine) rewards,

172 and motivational processing of food, and in binge eating, a behaviour strongly linked to obesity.

173 neural circuitry of restrictive food choice, binge eating, and the contribution of specific serotonin

174 n disordered eating and obesity, emphasizing binge eating, binge eating disorder and food addiction a

175 In fully adjusted models, binge eating, but not overeating, was associated with in

176 Binge eating, recurrent and persistent episodes of overe

177 The neuronal substrate for binge eating, which can at times lead to obesity, is not

178 eating days/week from baseline and improving binge eating-related key secondary endpoints.

179 ress-induced drug seeking, in stress-induced binge eating.

180 onal psychotherapy further reduced objective binge eating.

181 ing, unhealthy weight-control behaviors, and binge eating.

182 ction, may also be effective in ameliorating binge eating.

183 tify quantitative trait loci associated with binge eating.

184 el pharmacological treatment for compulsive, binge eating.

185 We assessed the change in binge-eating (BE) behaviors measured as days per week (b

186 derate to severe binge eating disorder (>/=3 binge-eating days per week for 14 days before open-label

187 mary outcome variable, time to relapse (>/=2 binge-eating days per week for 2 consecutive weeks and >

188 Binge-eating disorder (BED) is characterized by recurrin

189 Binge-eating disorder (BED), a public health problem ass

190 l or food, in alcohol use disorders (AUD) or binge-eating disorder (BED), suggest a disturbance in ex

191 The best treatment options for binge-eating disorder are unclear.

192 Eligible adults met DSM-IV-R binge-eating disorder criteria and had moderate to sever

193 Binge-eating disorder is characterized by excessive, unc

194 he characteristic symptomatology observed in binge-eating disorder.

195 as a potential pharmacological treatment for binge-eating disorder.

196 f efficacy in adults with moderate to severe binge-eating disorder.

197 and topiramate reduced weight in adults with binge-eating disorder.

198 ramate also increased abstinence and reduced binge-eating frequency and related psychopathology.

199 lso showed flexibility in foraging patterns, binge-eating less and using feeders more when they exper

200 We developed recently a binge-eating model in which female rats with a history o

201 e opioid system and food-related behavior in binge-eating obese individuals, these results support a

202 antagonist GSK1521498 on eating behaviour in binge-eating obese subjects.

203 Risk of binge-eating relapse over 6 months was lower in particip

204 PC1 ('binge-eating'), accounting for 38% of variation, capture

205 GAs (MD, -3.84 [CI, -6.55 to -1.13]) reduced binge-eating-related obsessions and compulsions, and SGA

206 d disorders, eg, substance-use disorders and binge-eating.

207 ide a potential mechanism for severe cocaine binge episodes, which occur even after sustained abstine

208 Chronic plus binge ethanol feeding acts synergistically to induce liv

209 Chronic-binge ethanol feeding leads to high blood alcohol levels

210 Utilizing the Gao-binge ethanol feeding protocol, matched mLipin-1KO mice

211 C57BL/6-Ly5.1 mice were fed chronic plus binge ethanol to create a model of ALD.

212 sion in an effortful T-maze task following a binge exposure to methamphetamine, and no such changes i

213 vioral addictions, and eating disorders with binge features.

214 Simulations demonstrated the ability to binge-feed increased cumulative consumption (16-32%) and

215 l infiltration and injury induced by chronic-binge feeding in mice and may also contribute to the pat

216 We found that after chronic plus binge feeding of Lieber-DeCarli liquid diet in male C57B

217 The degree of binge-feeding by bull trout in the field was slightly re

218 nd food availability influence the degree of binge-feeding by comparing field observations with labor

219 Binge-feeding has important implications for energy budg

220 fied mice, with the exception of the chronic binge-feeding model.

221 sis), but this phenomenon of hyperphagia (or binge-feeding) is largely overlooked.

222 , moderate drinkers (60-229 drinks/year) who binged had a higher risk (HR = 1.25, 95% CI: 1.08, 1.44)

223 Weekly binge in this new hybrid feeding model shifts chronic AS

224 Binge-induced changes in VTA CRF system protein and mess

225 identify the premorbid transcriptome and the binge-induced transcriptome to inform molecular mechanis

226 mGluR1, mGluR5 and PLC inhibitors to reduce binge intake depended upon intact Homer2 expression as r

227 hat the efficacy of mGluR1 blockade to lower binge intake involves a pathway independent of PLC activ

228 PLC inhibitors all dose-dependently reduced binge intake, without influencing sucrose drinking.

229 nd development of drug-seeking habits in the binge/intoxication stage involve changes in dopamine and

230 Low, moderate to high, or binge-level alcohol exposure in the first trimester or t

231 es, midface, chin, and parietal region), and binge-level exposure in the first trimester (chin).

232 were associated with the rate of achieving a binge-level exposure.

233 Early binge-like alcohol drinking may promote the development

234 hol typically begins during adolescence when binge-like consumption of large quantities is common.

235 the precise behavioral mechanisms underlying binge-like drinking and its consequences on striatal syn

236 semble only partially contributed to alcohol-binge-like drinking in nondependent rats.

237 kout (KO) mice selectively increased ethanol binge-like drinking, without affecting ethanol metabolis

238 might facilitate the acquisition of ethanol binge-like drinking.

239 toxicating blood alcohol levels (BALs) after binge-like drinking.

240 nt models of chronic, dependence-driven, and binge-like drinking.

241 gnature for genetic risk for high intensity, binge-like drinking.

242 RF2R signaling, and CRF2R activation reduces binge-like drinking; 2) inhibiting VTA-projecting BNST C

243 g VTA-projecting BNST CRF neurons attenuates binge-like drinking; and 3) binge-like ethanol drinking

244 Memantine dose-dependently decreased binge-like eating and fully blocked food-seeking behavio

245 he present results show that OSU6162 reduces binge-like eating behavior and attenuates the impact of

246 thereby activating these neurons to suppress binge-like eating behavior and suggest ERalpha and/or SK

247 strogen replacement substantially suppresses binge-like eating behavior in ovariectomized female mice

248 he SK current in the DRN markedly suppressed binge-like eating in female mice.

249 gens to the DRN and substantially suppressed binge-like eating in ovariectomized female mice.

250 Our results show that RO5256390 blocked binge-like eating in rats responding 1 h per day for a h

251 Estrogen-dependent inhibition of binge-like eating was blocked in female mice specificall

252 ere, the effects of OSU6162 on consummatory (binge-like eating) and appetitive (cue-controlled seekin

253 Administration of GLP-1 alone reduced binge-like eating, but not to the same extent as the GLP

254 t core, microinfusion of memantine decreased binge-like eating.

255 urons immediately (in 2 to 3 seconds) evoked binge-like eating.

256 not prelimbic, subregion of the mPFC-reduced binge-like eating.

257 ed that TAAR1 may have a role in compulsive, binge-like eating; we tested this hypothesis by assessin

258 ntributions of these receptors in modulating binge-like ethanol consumption (n = 89).

259 The effects of binge-like ethanol consumption on the VTA CRF system wer

260 We provide novel evidence that 1) blunted binge-like ethanol consumption stemming from CRF1R block

261 urons attenuates binge-like drinking; and 3) binge-like ethanol drinking alters protein and messenger

262 However, the effects of binge-like ethanol drinking on this system have not been

263 ith high temporal resolution over 6 weeks of binge-like ethanol drinking using the 'drinking in the d

264 f local CRF neurons in the VTA did not alter binge-like ethanol drinking, but inhibition of VTA-proje

265 o-VTA CRF projections is critical in driving binge-like ethanol intake.

266 Using a well-established model of binge-like ethanol treatment of rat pups on postnatal da

267 Repeated binge-like exposure to alcohol during adolescence has be

268 en together, these findings demonstrate that binge-like exposure to alcohol during early to middle ad

269 OSU6162 significantly reduced binge-like intake of chocolate-flavored sucrose pellets

270 istory of intermittent food restriction show binge-like palatable food consumption after 15 min expos

271 0-) were exposed to either a methamphetamine binge (METH+) or saline (METH-), then tested in the atte

272 al Institute on Alcohol Abuse and Alcoholism binge model) or chow diets along with water containing 0

273 ightly up- or down-regulated in this chronic-binge model.

274 Compared with low-level drinkers who never binged, moderate drinkers (60-229 drinks/year) who binge

275 minant states (great tits, males and adults) binged more than subordinate birds (blue tits, females a

276 ter alcohol binge drinking and in mice after binge or chronic alcohol consumption.

277 , which was assessed for harmful patterns of binge or frequent drinking.

278 Binge or moderate alcohol exposure impairs host defense

279 trial fibrillation (AF) following an alcohol binge or the "holiday heart syndrome" is well characteri

280 trocytes, and microglia) following a cocaine binge paradigm.

281 btype analyses (1606 AN restricting; 1445 AN binge-purge) were performed.

282 iagnosis of anorexia nervosa (restricting or binge-purging subtype) and a demonstrated history of chr

283 ein in the gray matter medial to the CCFM of binge rats indicated myelin was damaged on axons in the

284 acute cocaine administration might factor in binge-related escalated consumption.

285 ation between moderate lifetime drinking and binging (relative excess risk due to interaction = 0.33,

286 After 2 weeks of daily alcohol binges, synaptic plasticity was profoundly altered.

287 porter sites may be efficacious in promoting binge termination following relapse.

288 ted during 12 h unlimited access to cocaine (binge), the duration of the withdrawal did not influence

289 N 5-HT neurons as potential targets for anti-binge therapies.

290 d cocaine self-administration during a 24 h "binge." This may suggest dissociation between locomotor

291 l three risk factors had the highest rate of binging throughout the session compared with the lowest

292 1.37) were associated with a higher rate of binging throughout the session.

293 ergic interneurons were subjected to a 3 day binge-type 5% w/w ethanol consumption regimen from embry

294 ession in the VTA tunes ethanol intake under binge-type conditions: the more GIRK3, the less ethanol

295 ntrol deficits associated with addiction and binge-type eating disorders.

296 First, we demonstrate that a time-delimited binge-type ethanol exposure in utero during early gestat

297 , young adult offspring exposed to the 3 day binge-type ethanol regimen exhibited impaired reversal l

298 Our binge-type regimen increased the density of MGE-derived

299 ferences in eating disorder symptoms such as binging, vomiting, or laxative abuse were observed betwe

300 lated cocaine self-administration in a 24 h "binge." VTA CRF continues to influence cocaine seeking i