Enduring vulnerability to reinstatement of methamphetamine‐seeking behavior in glial cell line‐derived neurotrophic factor mutant mice

Yan, Yijin; Yamada, Kiyofumi; Niwa, Minae; Nagai, Taku; Nitta, Atsumi; Nabeshima, Toshitaka

doi:10.1096/fj.06-7772com

Cited by 52 publications

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“…20,22) We have investigated a role for GDNF in the development and relapse of METH dependence by using intravenous selfadministration and the reinstatement of drug-seeking behavior in GDNF-(ϩ/Ϫ) mice, respectively. 31) The results indicated that GDNF potentiates METH self-administration, enhances motivation to take METH, increases vulnerability to drug-primed reinstatement, and prolongs the cue-induced reinstatement of extinguished METH-seeking behavior. In contrast, there is no significant difference in novelty responses, METH-induced hyperlocomotion and sensitization, food-reinforced operant behavior and motivation, or reinstatement of food-seeking behavior between GDNF-(ϩ/Ϫ) and wild-type littermates.…”

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confidence: 95%

“…Our findings suggest that GDNF is a potent antiaddictive factor involved in the development and relapse of METH dependence. 31) CONCLUSION AND REMARKS As reviewed in this article, various cytokines and proteinases are produced in the brain on treatment with drugs of abuse, and act as either pro-addictive or anti-addictive factors. Pro-addictive factors potentiate the rewarding effects of drugs of abuse, and thereby act to facilitate the development of drug dependence.…”

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confidence: 99%

“…[17][18][19] Chronic drug exposure induces the expression of various neurotrophins, cytokines, and proteinases in the brain, which plays a crucial role in the development and relapse of drug dependence. [20][21][22] These endogenous modulators of drug dependence are functionally classified into two groups, pro-addictive and anti-addictive factors.20) The former, including basic fibroblast growth factor (bFGF), 23,24) brain-derived neurotrophic factor (BDNF), 25) tissue plasminogen activator (tPA), 26,27) matrix metalloproteinase (MMP)-2 and MMP-9, 28) act to potentiate the rewarding effects of drugs, while the latter such as tumor necrosis factor-a (TNF-a) 29) and glial cell line-derived neurotrophic factor (GDNF) 30,31) reduce the reward (Table 1). The pathophysiological role of pro-addictive and anti-addictive factors in drug dependence is briefly described in this review article.…”

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Endogenous Modulators for Drug Dependence

Yamada

2008

Biological & Pharmaceutical Bulletin

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INTRODUCTIONDrugs of abuse are chemically divergent with distinct primary targets of action. Repeated intake of any drug of abuse, however, results in many common features of drug dependence. Activation of the mesocorticolimbic dopamine system has been implicated in the positive reinforcing (reward) effects of drugs of abuse, [1][2][3][4] although recent studies demonstrated a dopamine-independent rewarding effect of morphine. 5,6) The mesocorticolimbic dopamine reward system originates in the midbrain ventral tegmental area (VTA) and projects to the nucleus accumbens (NAc), prefrontal cortex and other limbic areas. The VTA-NAc dopamine system also plays a role in the discriminative stimulus effects of drugs. 7,8) Once drug dependence has developed, it can be a life-long condition under which individuals show compulsive drug taking, intense cravings, and vulnerability to relapse even after years of abstinence. This is a major clinical problem in treating patients suffering from drug dependence. Basic and clinical studies suggest that aberrant synaptic plasticity in the prefrontal glutamatergic system innervating the NAc is related to compulsive drug seeking. 9) Brain imaging studies in addicted subjects revealed that craving is associated with the activation of the prefrontal cortex.9,10) To study the molecular mechanism of relapse, an animal model for relapse of drugseeking behavior has been established in mice by using a reinstatement procedure involving the intravenous self-administration of drugs. 11,12) Regarding the long-lasting abnormalities in drug dependence, repeated exposure to amphetamine (AMPH) in rats produces a long-lasting increase in the length of dendrites, and the number of branched spines, 13) and interferes with the ability of experience in a complex environment to increase dendritic arborization and spine density in the NAc and prefrontal cortex.14) We have demonstrated that repeated methamphetamine (METH) treatment results in a long-lasting impairment of novelty-induced extracellular signal-regulated kinase 1/2 activation in the prefrontal cortex in mice. 15)These structural and functional abnormalities may contribute to long-term behavioral consequences of drug abuse including drug dependence, psychosis, and cognitive impairment. Changes in transcription factors may result in long-term changes in gene expression, thereby contributing to neuronal adaptations associated with drug dependence.16) For instance, a prolonged induction of DFosB, which can activate transcription at AP-1 sites, is a common response to many classes of addictive drugs. [17][18][19] Chronic drug exposure induces the expression of various neurotrophins, cytokines, and proteinases in the brain, which plays a crucial role in the development and relapse of drug dependence. [20][21][22] These endogenous modulators of drug dependence are functionally classified into two groups, pro-addictive and anti-addictive factors.20) The former, including basic fibroblast growth factor (bFGF), 23,24) brain-derived neurotrophic factor (...

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Endogenous Modulators for Drug Dependence

Yamada

2008

Biological & Pharmaceutical Bulletin

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“…GDNF +/À mice have lower levels of GDNF and exhibit greater MA conditioned place preference . GDNF +/À mice acquire stable MA self-administration behavior more quickly than wild-type mice, exhibit greater motivation to self-administer MA (increased dose-response curve for MA self-administration and higher break point on progressive ratio schedule), and display greater reinstatement of prime-and cue-induced drug seeking following extinction, an effect that remained even 6 months after extinction training (Yan et al, 2007). In humans, polymorphisms in the GDNF gene have been associated with age of onset of MA dependence and addiction severity in Japanese MA users (Yoshimura et al, 2011).…”

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Opportunities for the Development of Neuroimmune Therapies in Addiction

Ray

Roche

Heinzerling

et al. 2014

International Review of Neurobiology

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“…METH dependence and craving can be modeled by a self-administration paradigm in mice. A recent study demonstrated that glial-derived neurotrophic factor (GDNF) plays an important role in the craving for METH after long-term abstinence using GDNF-deficient mice (3).…”

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Tissue Plasminogen Activator Is Not Involved in Methamphetamine-Induced Neurotoxicity

et al. 2008

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Abstract. To investigate the role of tissue plasminogen activator (tPA) in methamphetamine (METH)-induced dopaminergic neurotoxicity, we compared the changes in tyrosine hydroxylase (TH) and dopamine transporter (DAT) levels in the striatum after repetitive treatment of METH at 4 mg/ kg among wild-type, tPA-deficient (tPA−/ −), and protease activated receptor-1-deficient (PAR-1−/ −) mice. METH treatment caused a marked decrease in TH and DAT levels in the striatum of those mice with a similar magnitude. No difference in METH-induced abnormal behavior and hyperthermia was observed among the three types of mice. These results suggest that neither tPA nor PAR-1 is involved in METH-induced dopaminergic neurotoxicity in vivo.Keywords: methamphetamine, neurotoxicity, tissue plasminogen activator Methamphetamine (METH) is an abused drug. It has a strong rewarding effect that is related to the stimulating effect of dopamine release in the brain (1, 2). Repeated treatment with METH in rodents leads to the development of behavioral sensitization, which may be associated with METH psychosis or a strong craving in METH abusers. METH dependence and craving can be modeled by a self-administration paradigm in mice. A recent study demonstrated that glial-derived neurotrophic factor (GDNF) plays an important role in the craving for METH after long-term abstinence using GDNF-deficient mice (3).We have previously demonstrated that endogenous tumor necrosis factor-α (TNF-α) is induced in the brain after repeated administration of METH, and this cytokine acts to suppress METH dependence and its dopaminergic neurotoxicity (1, 2, 4). Thus, METHinduced conditioned place preference (CPP), behavioral sensitization, and loss of tyrosine hydroxylase (TH) in the striatum are potentiated in TNF-α-deficient (TNF-α−/ −) mice compared with wild-type mice, whereas systemic administration of TNF-α in mice suppresses METH-induced hyperlocomotion, behavioral sensitization, conditioned place preference, and the loss of TH in the striatum (2).On the other hand, our recent studies demonstrated that tissue plasminogen activator (tPA) acts as a proaddictive substance to enhance the reward of and behavioral sensitization to METH (4, 5); thus, METHinduced CPP and behavioral sensitization are reduced in tPA-deficient (tPA−/ −) mice compared to wild-type mice. It remains to be determined, however, whether tPA is also involved in the dopaminergic neurotoxicity of METH.In the present study, to investigate the role of tPA in METH-induced dopaminergic neurotoxicity, we compared TH and dopamine transporter (DAT) levels in

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Enduring vulnerability to reinstatement of methamphetamine‐seeking behavior in glial cell line‐derived neurotrophic factor mutant mice

Cited by 52 publications

References 51 publications

Endogenous Modulators for Drug Dependence

Endogenous Modulators for Drug Dependence

Opportunities for the Development of Neuroimmune Therapies in Addiction

Tissue Plasminogen Activator Is Not Involved in Methamphetamine-Induced Neurotoxicity

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