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L-theanine inhibits nicotine-induced dependence via regulation of the nicotine acetylcholine receptor-dopamine reward pathway
XiaoJing Di,JingQi Yan,Yan Zhao,YanZhong Chang,BaoLu Zhao
Science China Life Sciences , 2012, DOI: 10.1007/s11427-012-4401-0
Abstract: In this study, the inhibitory effect of L-theanine, an amino acid derivative of tea, on the rewarding effects of nicotine and its underlying mechanisms of action were studied. We found that L-theanine inhibited the rewarding effects of nicotine in a conditioned place preference (CPP) model of the mouse and reduced the excitatory status induced by nicotine in SH-SY5Y cells to the same extent as the nicotine receptor inhibitor dihydro-beta-erythroidine (DHβE). Further studies using high performance liquid chromatography, western blotting and immunofluorescence staining analyses showed that L-theanine significantly inhibited nicotine-induced tyrosine hydroxylase (TH) expression and dopamine production in the midbrain of mice. L-theanine treatment also reduced the upregulation of the α4, β2 and α7 nicotine acetylcholine receptor (nAChR) subunits induced by nicotine in mouse brain regions that related to the dopamine reward pathway, thus decreasing the number of cells that could react to nicotine. In addition, L-theanine treatment inhibited nicotine-induced c-Fos expression in the reward circuit related areas of the mouse brain. Knockdown of c-Fos by siRNA inhibited the excitatory status of cells but not the upregulation of TH induced by nicotine in SH-SY5Y cells. Overall, the present study showed that L-theanine reduced the nicotine-induced reward effects via inhibition of the nAChR-dopamine reward pathway. These results may offer new therapeutic strategies for treatment of tobacco addiction.
Nicotine-induced brain metabolism associated with anger provocation
Jean-G Gehricke, Steven G Potkin, Frances M Leslie, Sandra E Loughlin, Carol K Whalen, Larry D Jamner, James Mbogori, James H Fallon
Behavioral and Brain Functions , 2009, DOI: 10.1186/1744-9081-5-19
Abstract: Cigarette smoking is a major public health problem, and angry dispositions have been identified as an important risk factor for smoking initiation and subsequent nicotine dependence [1-4]. In particular, behavioral studies revealed a smoking-anger linkage [5-8], but little is known about the underlying brain circuitry subserving such linkage.Dysfunctional cortico-limbic brain activity associated with anger may be normalized by nicotine [4]. Functional imaging studies on regional brain activity in response to nicotine and smoking have documented the involvement of cortico-limbic structures such as the prefrontal cortex (including the dorsolateral prefrontal cortex, inferior frontal, medial frontal, and orbitofrontal gyri) [9-15], cingulate [12-16], thalamus [11,13,15,17-19], and amygdala [12,13,15,19]. Similarly, anger has been associated with activation of the medial prefrontal cortex, orbitofrontal cortex, and anterior cingulate cortex [20-22]. However, little is known about which brain areas are most responsive to the effects of nicotine during anger provocation. The elevated risk of dependence and the greater difficulty quitting may result, in part, from nicotine-associated normalization of activity of cortico-limbic circuitry [4].The cortico-limbic circuitry is part of the "prefrontal system", which was first described by Rosvold and Schwatzbart [23] (see also review by Divac [24]) and may be particularly sensitive to nicotine modulation. The objective of the present study was to identify the brain regions within the prefrontal system that are most reactive to the effects of nicotine and show the greatest association with anger task performance in nonsmokers. Nonsmokers were studied to determine the effects of a fixed low-dose of nicotine via patch without the confounding effects of smoking and nicotine withdrawal. It was hypothesized that nicotine-induced anger task performance is associated with nicotine-induced changes in the medial prefrontal cortex, orbitof
Intense Passionate Love Attenuates Cigarette Cue-Reactivity in Nicotine-Deprived Smokers: An fMRI Study  [PDF]
Xiaomeng Xu, Jin Wang, Arthur Aron, Wei Lei, J. Lee Westmaas, Xuchu Weng
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0042235
Abstract: Self-expanding experiences like falling in love or engaging in novel, exciting and interesting activities activate the same brain reward mechanism (mesolimbic dopamine pathway) that reinforces drug use and abuse, including tobacco smoking. This suggests the possibility that reward from smoking is substitutable by self-expansion (through competition with the same neural system), potentially aiding cessation efforts. Using a model of self-expansion in the context of romantic love, the present fMRI experiment examined whether, among nicotine-deprived smokers, relationship self-expansion is associated with deactivation of cigarette cue-reactivity regions. Results indicated that among participants who were experiencing moderate levels of craving, cigarette cue-reactivity regions (e.g., cuneus and posterior cingulate cortex) showed significantly less activation during self-expansion conditions compared with control conditions. These results provide evidence that rewards from one domain (self-expansion) can act as a substitute for reward from another domain (nicotine) to attenuate cigarette cue reactivity.
Neurobiological Mechanism of Nicotine Dependence

Deng Linyuan,Fang Xiaoyi,

心理科学进展 , 2005,
Abstract: Nicotine dependence is the main cause of cigarette addiction, which is characterized by uncontrollable compulsion of nicotine-seeking, impulsive and continuous nicotine in-taking,in order to experience euphoria and happiness, and to avoid withdrawal symptoms without nicotine. This article reviewed some research findings of neurobiological mechanism of nicotine dependence from both animal model and human brain imaging study, which revealed that mesolimbic dopamine system is the important neurobiological basis of nicotine dependence. However, previous studies mostly took a static approach, but rarely considered the dynamic process of nicotine dependence; there are also lack of enough evidences of the differences between nicotine dependence and other drugs dependence, which will direct the future studies.
Chronic effect of olive oil on some neurotransmitter contents in different brain regions and physiological, histological structure of liver and kidney of male albino rats  [PDF]
A. E. Bawazir
World Journal of Neuroscience (WJNS) , 2011, DOI: 10.4236/wjns.2011.13005
Abstract: Olive oil is an important source of mono-unsaturated fat and a prime component of the Mediterranean diet. The beneficial health effects of olive oil are due to both its high content of mono-unsaturated fatty acids and its high content of anti-oxidative substances. The objective of this study was to investigate the basis for the epidemiological information relating to the health benefits associated with the consumption of ex-tra-virgin olive oil (EVOO). The effect of olive oil on norepinephrine (NE), dopamine (DA), serotonin (5-HT) and gamm-aminobutyric acid (GABA) con-tents in different brain regions and histological structure of liver and kindey of male albino rats was studied. The chronic administration of olive oil (7.5 mg/kg body wt.) caused a significant increase in norepinephrine (NE), dopamine (DA) , serotonin (5-HT) and gamm-aminobutyric acid (GABA) con-tent in different brain regions (Cerebellum, striatum, cerebral cortex, hypothalamus, brain steam and hip-pocampus) of male albino rats. The increase in NE, DA, 5-HT, and GABA content in the different CNS areas of male albino rat may be due to the inhibition of Ca2+/calmodulin binding which plays an important role in the release of these neurotransmitters. The results, also, revealed that urea and creatinne con-centrations in rats with oral administration with olive oil were decreased. Meanwhile, the activities of the enzymes AsT, AlT and ALP were elevated. The pre-sent results indicated that there is no change in tis-sues of kidney after treated with virgin olive oil. Olive oil may potentially be safe for use as a sedative drug. improvement also led to the reductions in risk of Alzheimer’s and Parkinson’s diseases.
Glutamatergic and GABAergic Metabolism in Mouse Brain under Chronic Nicotine Exposure: Implications for Addiction  [PDF]
Mohammad Shameem, Anant Bahadur Patel
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0041824
Abstract: Background and Purpose The effects of nicotine on cerebral metabolism and its influence on smoking behavior is poorly understood. An understanding of the chronic effects of nicotine on excitatory and inhibitory metabolic demand, and corresponding neurotransmission may provide clues for designing strategies for the optimal smoking cessation intervention. The objective of the current study was to investigate neuronal and astroglial metabolism in mice exposed to nicotine (0.5 and 2.0 mg/kg, sc) three times in a day for 4 weeks. Experimental Approach/Principal Findings Metabolic measurements were carried out by co-infusing [U-13C6]glucose and [2-13C]acetate, and monitoring 13C labeling of amino acids in brain tissue extract using 1H-[13C] and 13C-[1H]-NMR spectroscopy. Concentration of 13C-labeled glutamate-C4 was increased significantly from glucose and acetate with chronic nicotine treatment indicating an increase in glucose oxidation by glutamatergic neurons in all brain regions and glutamate-glutamine neurotransmitter cycle in cortical and subcortical regions. However, chronic nicotine treatment led to increased labeling of GABA-C2 from glucose only in the cortical region. Further, increased labeling of glutamine-C4 from [2-13C]acetate is suggestive of increased astroglial activity in subcortical and cerebellum regions of brain with chronic nicotine treatment. Conclusions and Significance Chronic nicotine exposure enhanced excitatory activity in the majority of brain regions while inhibitory and astroglial functions were enhanced only in selected brain regions.
Modulation of Tyrosine Hydroxylase, Neuropeptide Y, Glutamate, and Substance P in Ganglia and Brain Areas Involved in Cardiovascular Control after Chronic Exposure to Nicotine  [PDF]
Merari F. R. Ferrari,Emerson F. Coelho,Karen L. G. Farizatto,Gerson Chadi,Debora R. Fior-Chadi
International Journal of Hypertension , 2011, DOI: 10.4061/2011/216464
Abstract: Considering that nicotine instantly interacts with central and peripheral nervous systems promoting cardiovascular effects after tobacco smoking, we evaluated the modulation of glutamate, tyrosine hydroxylase (TH), neuropeptide Y (NPY), and substance P (SP) in nodose/petrosal and superior cervical ganglia, as well as TH and NPY in nucleus tractus solitarii (NTS) and hypothalamic paraventricular nucleus (PVN) of normotensive Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR) after 8 weeks of nicotine exposure. Immunohistochemical and in situ hybridization data demonstrated increased expression of TH in brain and ganglia related to blood pressure control, preferentially in SHR, after nicotine exposure. The alkaloid also increased NPY immunoreactivity in ganglia, NTS, and PVN of SHR, in spite of decreasing its receptor (NPY1R) binding in NTS of both strains. Nicotine increased SP and glutamate in ganglia. In summary, nicotine positively modulated the studied variables in ganglia while its central effects were mainly constrained to SHR. 1. Introduction Cardiovascular effects of tobacco smoking are primarily attributed to the presence of nicotine in cigarettes. This alkaloid may promote decrease in baroreflex sensitivity, increase in heart rate and blood pressure, atherosclerosis, coronary heart disease, and myocardial infarction [1]. Nicotine potentiates sympathetic nervous system leading to increase in plasma and brain catecholamine levels [2, 3]. In addition, we have previously demonstrated the acceleration of onset and the exacerbation of hypertension in genetic hypertension predisposed rats after nicotine exposure [4]. The activation of sympathetic neurotransmission by nicotine may be based on its direct effect on the central nervous system, on sympathetic ganglia to increase the efferent nerve activity, and/or on peripheral sympathetic nerve endings and adrenal medulla stimulating catecholamine release [5]. Nevertheless, the activated sympathetic system might promote the reflex parasympathetic response composing an elaborated physiological effect after nicotine administration. The alkaloid instantly interacts with the central nervous system binding to nicotinic acetylcholine receptors in the hypothalamus, hippocampus, midbrain, and medulla oblongata [6, 7] modulating norepinephrine, dopamine, vasopressin, glutamate, neuropeptide Y (NPY), and other neurotransmitter systems [8]. Nicotine acts also on chemoreceptors afferents [9], enteric nervous system [10], and visceral sensory afferents (for a review about nicotinic mechanisms in the
Effect of madecassoside on depression behavior of mice and activities of MAO in different brain regions of rats  [cached]
LIU Mu-Rong,QIN Lu-Ping
Zhong Xi Yi Jie He Xue Bao , 2004,
Abstract: Objective: To evaluate the effects of madecassoside (MC) on the depression behavior of mice and the activities of monoamine oxidase (MAO) in different rat brain regions. Methods: Imipramine as the positive contrast medicine, effects of MC on the depression behavior of mice were observed by forced swimming test and reserpine antagonist test. Moclobemide and pargyline as the positive controlled medicines, the activities of monoamine oxidase-A (MAO-A) and monoamine oxidase-B (MAO-B) in different rat brain regions were determined after intragastric administration of MC in 3 different dosages for 3 days or 21 days. Results: (1) The low, middle and high dosages of MC (i.g.) significantly reduced the immobility time of mice in forced swimming test (P<0.05). (2) MC in dosages of 10 mg/kg and 20 mg/kg prevented the lowering of temperature induced by reserpine (P<0.05), while 40 mg/kg had no significant effects on it (P>0.05). (3) With acute administration (3 days), the low, middle and high dosagey of MC (i.g.) significantly inhibited the activity of MAO-A in hippocampus (P<0.01), and the high dosage significantly inhibited the activity of MAO-A in hypothalamus (P<0.01), while the 3 dosages had no significant effects on the activity of MAO-A in cortex (P>0.05). With chronic administration (21 days), MC in 3 dosages had no significant effects on the activities of MAO-A in cortex and hypothalamus (P>0.05), and the high dosage (40 mg/kg) significantly enhanced the activity of MAO-A in hippocampus (P<0.01). (4) With acute administration, MC in dosages of 10 mg/kg and 20 mg/kg significantly inhibited the activity of MAO-B in cortex (P<0.05), and MC in dosage of 10 mg/kg significantly inhibited the activity of MAO-B in hypothalamus (P<0.05), and MC in dosage of 20 mg/kg significantly enhanced the activity of MAO-B in hippocampus (P<0.01). With chronic administration, MC of 3 dosages produced no significant effects on the activities of MAO-B in 3 different rat brain regions (P>0.05).Conclusion: These results support the idea that MC produces antidepressant effects through MAO inhibition in rat brain, which seems stronger with acute administration than chronic administration, while its mechanism remains to be further studied.
Effect of prolonged exposure to diesel engine exhaust on proinflammatory markers in different regions of the rat brain
Miriam E Gerlofs-Nijland, Damien van Berlo, Flemming R Cassee, Roel PF Schins, Kate Wang, Arezoo Campbell
Particle and Fibre Toxicology , 2010, DOI: 10.1186/1743-8977-7-12
Abstract: Baseline levels of the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-α) and interleukin-1 alpha (IL-1α) were dependent on the region analyzed and increased in the striatum after exposure to DEE. In addition, baseline level of activation of the transcription factors (NF-κB) and (AP-1) was also region dependent but the levels were not significantly altered after exposure to DEE. A similar, though not significant, trend was seen with the mRNA expression levels of TNF-α and TNF Receptor-subtype I (TNF-RI).Our results indicate that different brain regions may be uniquely responsive to changes induced by exposure to DEE. This study once more underscores the role of neuroinflammation in response to ambient air pollution, however, it is valuable to assess if and to what extent the observed changes may impact the normal function and cellular integrity of unique brain regions.There is an association between chronic exposure to combustion-related fine particles (present in air pollution) and an increased risk of mortality attributed to lung cancer and cardiopulmonary causes [1]. One of the major contributors to particulate air pollution is diesel engine exhaust. As diesel fuel undergoes combustion in automobile engines, it produces particles of different sizes, chemical composition, and physical characteristics [2]. Because of the substantial number of epidemiological studies showing a link between exposure to air pollution and adverse cardiovascular changes, the need for air quality controls and suggestions for future research has been addressed [3]. Recent studies show that the cardiopulmonary system may not be the only vulnerable target adversely affected by air pollution. The brain may be another potential target [4,5].In a prospective birth cohort study, the association between exposure to black carbon, which is a surrogate for traffic-related particles, and cognition among children was assessed. The authors discovered that higher exposure to black carbon wa
Administration of the GABAA receptor antagonist picrotoxin into rat supramammillary nucleus induces c-Fos in reward-related brain structures. Supramammillary picrotoxin and c-Fos expression
Rick Shin, Satoshi Ikemoto
BMC Neuroscience , 2010, DOI: 10.1186/1471-2202-11-101
Abstract: Picrotoxin administration into the SuM markedly facilitated locomotion and rearing. Further, it increased c-Fos expression in this region, suggesting blockade of tonic inhibition and thus the disinhibition of local neurons. This manipulation also increased c-Fos expression in structures including the ventral tegmental area, medial shell of the nucleus accumbens, medial prefrontal cortex, septal area, preoptic area, lateral hypothalamic area and dorsal raphe nucleus.Picrotoxin administration into the SuM appears to disinhibit local neurons and recruits activation of brain structures associated with motivational processes, including the mesolimbic dopamine system, prefrontal cortex, septal area, preoptic area, lateral hypothalamic area and dorsal raphe nucleus. These regions may be involved in mediating positive motivational effects triggered by intra-SuM picrotoxin.Recent intracranial self-administration studies have helped to define key brain structures involved in positive motivational processes involved in approach/seeking [1]. One such structure is the supramammillary nucleus (SuM), located in the posterior hypothalamic area, just dorsal to the mammillary body and anterior to the ventral tegmental area (VTA). The SuM was initially implicated in reward-related processes by the finding that rats learn instrumental responses to obtain brief electrical stimulation in the vicinity of the SuM [2]. We recently found that rats readily learn to lever-press for infusions of GABAA receptor antagonists, picrotoxin or bicuculline [3], the excitatory amino acid AMPA [4], or nicotine [5] into the SuM, suggesting that activation of supramammillary neurons recruits approach-related motivational processes [1].We have also shown low systemic doses of dopamine receptor antagonists decrease rats' self-administration of picrotoxin or AMPA into the SuM [3,4]. These findings suggest that motivational effects of supramammillary manipulations depend on intact dopamine transmission. In add
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