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1 ort for a neuroimmune mechanism of excessive alcohol drinking.
2 id receptor (MR) activation drive compulsive alcohol drinking.
3 ms mediate environmental changes that affect alcohol drinking.
4 an rhythmicity and explored its relevance to alcohol drinking.
5 y of the ACC during withdrawal and excessive alcohol drinking.
6 essary roles for mGluR5/Homer2/PI3K in binge alcohol drinking.
7 gh alcohol consumption (SHAC) model of binge alcohol drinking.
8 al tegmental area (VTA) negatively regulates alcohol drinking.
9 ng in a genetically selected rodent model of alcohol drinking.
10 e concentrated sweet solutions and excessive alcohol drinking.
11 gets reduces excessive and harmful levels of alcohol drinking.
12 environmental contexts associated with prior alcohol drinking.
13 with Daun02 produced a long-term decrease in alcohol drinking.
14 dependent C57BL/6J mice following 24 days of alcohol drinking.
15 g a potential mechanistic basis for habitual alcohol drinking.
16 ptations gate or drive excessive, compulsive alcohol drinking.
17 also selectively reduced aversion-resistant alcohol drinking.
18 ior and the abstinence-induced escalation of alcohol drinking.
19 gs indicated a protective effect of moderate alcohol drinking (2-30 drinks/month for women and 2-60 d
22 king period was terminated by 20 min of free alcohol drinking access that achieved significant blood
23 the authors investigated whether history of alcohol drinking affected risks of NHL and multiple myel
25 reclinical animal models of either excessive alcohol drinking, alcohol-seeking, or relapse-like drink
26 he first time that Grm7 is a risk factor for alcohol drinking and a new target in addiction therapy.
31 ent with mifepristone also blocked escalated alcohol drinking and compulsive responding during protra
32 ationship between plasma aldosterone levels, alcohol drinking and craving was investigated in alcohol
37 ronal ensemble in the CeA reversed excessive alcohol drinking and somatic signs of alcohol dependence
38 T We examined the relationship between binge alcohol drinking and spike timing-dependent plasticity i
39 ts selectively block emotionality, excessive alcohol drinking and stress-induced reinstatement of alc
41 which neuroimmune pathways mediate excessive alcohol drinking and these findings will help to priorit
42 animal models were used to examine excessive alcohol drinking and to discover genes that may contribu
43 NAc and CeA is a major contributor to binge alcohol drinking and to the genetic propensity to consum
45 ut not in the BLA, are crucial in regulating alcohol-drinking and anxiety-like behaviors in rats.
46 on and participates in mechanisms underlying alcohol-drinking and reconsolidation of alcohol-related
47 literature showing CRF knockout (KO) induces alcohol drinking, and central administrations of CRF red
48 of sexual partners, use of hormonal creams, alcohol drinking, and condom use by a sexual partner.
49 for age, body mass index, cigarette smoking, alcohol drinking, and dietary nutrient intake, the diffe
52 , the manner by which STDP responds to binge alcohol drinking, and its sensitivity to dopamine recept
53 DAR modulators can reduce aversion-resistant alcohol drinking, and support testing of D-serine and D-
54 autophosphorylation in the establishment of alcohol drinking as an addiction-related behavior in mic
55 Nicotine produced an early escalation of alcohol drinking associated with compulsive alcohol drin
58 ted the association of maternal and paternal alcohol drinking before and early in pregnancy with infa
59 dings indicate that the hPer1 gene regulates alcohol drinking behavior during stressful conditions an
60 s) in hPer1 were tested for association with alcohol drinking behavior in 273 adolescents and an adul
63 cilitating mechanism in the establishment of alcohol drinking behavior with changing the DA-5-HT bala
72 ere is substantial individual variability in alcohol drinking behaviors in the population, the neural
81 EB) in genetic predisposition to anxiety and alcohol-drinking behaviors using alcohol-preferring (P)
94 ytes isolated from healthy subjects after an alcohol drinking binge showed enhanced apoptosis (before
95 Y1R) activation in the BNST suppressed binge alcohol drinking by enhancing inhibitory synaptic transm
99 for age, race, sex, study center, education, alcohol drinking, current smoking, prevalent coronary he
100 memory impairments associated with excessive alcohol drinking during acute (24-72 h) but not protract
102 of the glucocorticoid receptor in excessive alcohol drinking during protracted alcohol abstinence.
103 ody mass index, district, cigarette smoking, alcohol drinking, education, occupation, use of vitamin
105 6-April 2002) using Medical Subject Headings alcohol drinking, ethanol, cerebrovascular accident, cer
106 However, Nf1(+/-) mice failed to escalate alcohol drinking following chronic intermittent ethanol
109 ed according to age, sex, race, smoking, and alcohol drinking) for the presence of mutant p53 protein
111 ctedly, VTA dopamine neuron activity in high alcohol drinking (HAD) mice does not differ from alcohol
114 x, study center, education, tobacco smoking, alcohol drinking, hepatitis B surface antigen, and/or an
116 FTI-276, produced a robust decrease of rats' alcohol drinking; however, sucrose consumption was unalt
117 rom alcohol is causally related to excessive alcohol drinking in alcohol-dependent rats, whereas a si
122 alcohol drinking associated with compulsive alcohol drinking in dependent, but not in nondependent r
123 tic strategy for the treatment of compulsive alcohol drinking in humans carrying the Met66BDNF allele
124 ifically, a mouse paradigm that mimics binge alcohol drinking in humans produced a robust reduction i
125 ped a method to assess long-term patterns of alcohol drinking in mice housed in groups using the Inte
128 during abstinence is required for excessive alcohol drinking in nondependent rats that binge drink a
129 tudies have shown that nicotine can increase alcohol drinking in nondependent rats, yet it is unknown
130 nic nicotine will speed up the escalation of alcohol drinking in rats and that this effect will be ac
132 because increased CRF system activity drives alcohol drinking in rodents, we examined whether it pred
138 ality was seen for frequency of non-beverage alcohol drinking independent of volume of beverage ethan
142 stulate that a genetic predisposition toward alcohol drinking is accompanied by increased responsiven
145 rophysiological techniques, we find that low alcohol drinking (LAD) mice have dramatically higher ven
148 d H&N cancer patients, especially those with alcohol drinking, lower BMI, and advanced stage of prima
149 past smoking (pack-years <5), no or moderate alcohol drinking (</=1 drink/d for women, </=2 drinks/d
153 the amygdala proteome in mice after moderate alcohol drinking (n = 12/group) followed by behavioral s
154 l, we determined the impact of preconception alcohol drinking of the mother on offspring stress respo
157 f dopamine in mediating the effects of binge alcohol drinking on synaptic plasticity of NAc MSNs diff
158 in the CeA is causally related to excessive alcohol drinking or if it represents a consequence of ex
159 ), smoking (p < 0.0001), evidence of harmful alcohol drinking (p = 0.0001), and ART non-adherence (p
162 human Met66BDNF allele (Met68BDNF) and used alcohol-drinking paradigms in combination with viral-med
165 bottle choice paradigm that models excessive alcohol drinking produces a mobilization of DLS p75 neur
166 stores dopaminergic dysfunction in long-term alcohol-drinking rats and shows promise as a novel treat
167 etic stimulation of mPFC-NAcore terminals in alcohol-drinking rats, similar to reported effects of th
168 -preferring, alcohol-nonpreferring, and high-alcohol-drinking replicate 1 line of rats (Indiana Unive
169 ogether, our results indicate that the first alcohol drinking session induces synaptic plasticity in
170 hibition of mTORC1 activity during the first alcohol drinking session reduced alcohol consumption and
171 t FGF2 in the DMS is a positive regulator of alcohol drinking.SIGNIFICANCE STATEMENT Long-term alcoho
173 ion in the mPFC increased aversion-resistant alcohol drinking, supporting a mechanistic role of Syt2
174 isk of developing uncontrolled and excessive alcohol drinking that can be reversed by directly activa
175 ice were tested in two models of free-choice alcohol drinking: the continuous and intermittent access
176 inking in the dark (DID) as a model of binge alcohol drinking to assess its effects on spike timing-d
177 titis B virus, cirrhosis, diabetes, obesity, alcohol drinking, tobacco smoking, and host genetic poly
178 on of diabetes, diabetes treatment, smoking, alcohol drinking, total energy intake, and physical acti
180 ogic characteristics, cigarette smoking, and alcohol drinking was abstracted from hospital charts.
183 serum LPS, sCD14, sCD163 and the quantity of alcohol drinking was observed after adjusting for covari
185 ng continuous or intermittent access or when alcohol drinking was tested in the context of aversive o
188 ) are critical for promoting compulsion-like alcohol drinking, where rats consume alcohol despite pai
189 r binding exhibited a 50% reduction in binge alcohol drinking, which was related to reduced NAC basal
190 deprivation effect (ADE) model in long-term alcohol drinking Wistar rats, two behavioral models for
191 Systemic D-serine reduced aversion-resistant alcohol drinking, without altering consumption of quinin
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