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1 to manage several neurological disorders and nicotine addiction.
2 eceptors, processes thought to contribute to nicotine addiction.
3 promising new approach for the treatment of nicotine addiction.
4 ne and to the development of drugs to combat nicotine addiction.
5 d may have clinical implications in treating nicotine addiction.
6 icotine are probably critical for sustaining nicotine addiction.
7 ol processes are a primary characteristic of nicotine addiction.
8 be used in the treatment of lung cancer and nicotine addiction.
9 opment and progression of lung cancer and in nicotine addiction.
10 d up-regulation is believed to contribute to nicotine addiction.
11 ping compounds to selectively interfere with nicotine addiction.
12 g rewiring of glutamatergic circuitry during nicotine addiction.
13 immunotherapy may be effective in combating nicotine addiction.
14 en identified as a novel target for managing nicotine addiction.
15 ic stages, and identified new biomarkers for nicotine addiction.
16 k-1, and unc-30 to be potential effectors of nicotine addiction.
17 tors are critical for smoking initiation and nicotine addiction.
18 mice, mGluR5 is suggested to be involved in nicotine addiction.
19 subunit are associated with vulnerability to nicotine addiction.
20 unique target for therapeutic treatments for nicotine addiction.
21 f nicotine may contribute to the tenacity of nicotine addiction.
22 icated in pathological conditions, including nicotine addiction.
23 that has led to our present understanding of nicotine addiction.
24 olecular, cellular and systems mechanisms of nicotine addiction.
25 nal nAChR, the receptor most associated with nicotine addiction.
26 ebral cortex and white matter structure, and nicotine addiction.
27 other neurotensin receptor agonists to treat nicotine addiction.
28 ysiology and have been clearly implicated in nicotine addiction.
29 resent a new therapeutic target for treating nicotine addiction.
30 aptic transmission, synaptic plasticity, and nicotine addiction.
31 ribute to the development and maintenance of nicotine addiction.
32 It is also the likely receptor that mediates nicotine addiction.
33 numbers, which may underlie some aspects of nicotine addiction.
34 are logical candidates for vulnerability to nicotine addiction.
35 for understanding the mechanisms underlying nicotine addiction.
36 ation of dopaminergic pathways implicated in nicotine addiction.
37 ad of cigarettes does not reduce the risk of nicotine addiction; (3) as the number of cigars smoked a
38 everal neuropsychiatric disorders, including nicotine addiction, Alzheimer's, schizophrenia, and depr
46 1 and its analogues in preclinical models of nicotine addiction and perhaps other disorders involving
47 n and attention, which might be connected to nicotine addiction and probability of relapse in smokers
48 ough methods to help interrupt the spread of nicotine addiction and reduce the downstream morbidity.
50 her implicates the lateral PFC and insula in nicotine addiction and suggests the use of deep high-fre
51 ults offer new perspectives when considering nicotine addiction and the high prevalence of smoking in
56 lating neurotransmitter release, reinforcing nicotine addiction, and a role in neurological disorders
57 (nAChRs) is implicated in several aspects of nicotine addiction, and menthol cigarette smokers tend t
58 in the vertebrate nervous system, underlies nicotine addiction, and nicotinic receptor dysfunction l
59 y may serve as a circuit-level biomarker for nicotine addiction, and the development of new therapeut
60 ent, combination or novel drugs, and viewing nicotine addiction as a chronic disorder that might need
61 ciated with both a protective effect against nicotine addiction as a dichotomized trait (Z=-3.04, P<.
62 associated with a protective effect against nicotine addiction as either a dichotomized trait or a q
65 class of receptors, potentially important in nicotine addiction, binds alpha-conotoxin MII (alpha-Ctx
67 ribute to the vulnerability or resiliency to nicotine addiction by altering the rewarding effects of
68 examine the role of mGluR5 downregulation in nicotine addiction by investigating a group of long-term
69 the ultimate nicotine delivery device; that nicotine addiction can be perpetuated and even enhanced
71 ased genome scanning studies for ethanol and nicotine addictions failed to display much agreement.
72 Australian families who participated in the Nicotine Addiction Genetics Project, 423 autosomal marke
73 entifying genetic factors that contribute to nicotine addiction has revealed several single nucleotid
74 ecognized very early, the modern concepts of nicotine addiction have relied on knowledge of cholinerg
75 immunotherapeutic approaches for cocaine and nicotine addiction have stimulated interest in creating
76 gulin 3 (NRG3) and ErbB4 have been linked to nicotine addiction; however, the neuronal mechanisms and
80 cal role of mGluR2/3 in different aspects of nicotine addiction, including acquisition and maintenanc
89 a formidable challenge for the treatment of nicotine addiction is the high vulnerability to relapse
90 review representative documents relating to nicotine addiction, low-tar, low-nicotine cigarettes, an
91 ence elevates nicotine's reward magnitude or nicotine addiction may rely more importantly upon negati
92 ex, variables related to smoking history and nicotine addiction, medical history, family history of l
93 psychopharmacological factors contribute to nicotine addiction, midbrain dopaminergic systems have r
95 7 subtypes to treat such diverse diseases as nicotine addiction, neuropathic pain, and neurodegenerat
96 es may play a role in the increased risk for nicotine addiction observed in adolescent offspring of s
97 provide efficient drug discovery methods for nicotine addiction or for other disorders that result fr
98 Along with solving a chemical mystery in nicotine addiction, our results provide guidance for eff
99 activation of this pathway may contribute to nicotine addiction, particularly in individuals with gen
102 ne presented to the brain over the course of nicotine addiction-shapes brain circuits that, among oth
103 an R336C substitution, have greater risk of nicotine addiction than non-carriers as assessed by the
104 ha4beta2 brain receptors thought to underlie nicotine addiction, the high affinity for nicotine is th
105 es, the tobacco industry striving to sustain nicotine addictions, the pharmaceutical industry to end
106 ed ion channel in the brain and a target for nicotine addiction therapy, and the 19-residue conotoxin
108 sing numbers, Americans will seek to satisfy nicotine addictions through the use of novel nicotine-de
109 Understanding the mechanisms underlying nicotine addiction to develop more effective treatment i
110 re needed to clarify the role of dopamine in nicotine addiction to help develop smoking prevention an
111 s pathophysiological conditions ranging from nicotine addiction to the development and progression of
114 arly separated pathways that correlated with nicotine addiction vs nicotine's action were found.
116 stigations can elucidate the role of MORs in nicotine addiction, which may lead to development of nov
117 However, using nicotine replacement to treat nicotine addiction yields generally inconsistent results
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