Effect of the endogenous ? opioid agonist dynorphin A(1?17) on cocaine-evoked increases in striatal dopamine levels and cocaine-induced place preference in C57BL/6J mice

Zhang, Yong; Butelman, Eduardo R.; Schlussman, Stefan D.; Ho, Ann; Kreek, Mary Jeanne

doi:10.1007/s00213-003-1688-3

Cited by 119 publications

(99 citation statements)

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“…S6). Pretreatment with Dyn A (1-17) is effective in decreasing striatal DA neurotransmission and attenuating cocaine-induced CPP in mice (34). Overexpression of CREB with resulting increases in ppDyn gene expression in the NAc has been shown to decrease the rewarding effects of cocaine (29).…”

Section: Discussionmentioning

confidence: 99%

Tissue plasminogen activator modulates the cellular and behavioral response to cocaine

Maiya

Zhou

Norris

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Cocaine exposure induces long-lasting molecular and structural adaptations in the brain. In this study, we show that tissue plasminogen activator (tPA), an extracellular protease involved in neuronal plasticity, modulates the biochemical and behavioral response to cocaine. When injected in the acute binge paradigm, cocaine enhanced tPA activity in the amygdala, which required activation of corticotropin-releasing factor type-1 (CRF-R1) receptors. Compared with WT mice, tPA؊/؊ mice injected with cocaine displayed attenuated phosphorylation of ERK, cAMP response element binding protein (CREB), and dopamine and cAMP-regulated phosphoprotein 32 kDa (DARPP-32) and blunted induction of immediate early genes (IEGs) c-Fos, Egr-1, and Homer 1a in the amygdala and the nucleus accumbens (NAc). tPA؊/؊ mice also displayed significantly higher basal preprodynorphin (ppDyn) mRNA levels in the NAc in comparison to WT mice, and cocaine decreased ppDyn mRNA levels in tPA؊/؊ mice only. Cocaineinduced locomotor sensitization and conditioned place preference (CPP) were attenuated in tPA؊/؊ mice. Cocaine exposure also had an anxiolytic effect in tPA؊/؊ but not WT mice. These results identify tPA as an important and novel component of the signaling pathway that modulates cocaine-induced changes in neuroadaptation and behavior.behavioral sensitization ͉ conditioned place preference ͉ corticotropin releasing factor ͉ neuronal signaling ͉ plasminogen activator inhibitor C ocaine is one of the most widely abused drugs in the United States, and there are currently no effective pharmacotherapies for cocaine addiction (1). The rewarding and reinforcing properties of cocaine correlate with its ability to inhibit reuptake and consequently increase synaptic concentrations of dopamine (DA). Cocaine induces complex molecular changes in discrete brain regions, leading to altered gene expression and changes in neuronal structure and function. Such drug-induced alterations in neuronal circuitry are associated with the development of addiction (1, 2). The mesolimbic DAergic system is thought to be the primary target for cocaine-induced molecular and behavioral adaptations in the brain (1). In addition, the dynorphin (Dyn)/ kappa opioid receptor (KOP-r) system, which is highly expressed in the nucleus accumbens (NAc), has been implicated in regulating the behavioral effects of cocaine by playing a homeostatic role that opposes alterations in brain function and behavior that result from cocaine exposure (3-5). Further, acute pretreatment with KOP-r agonists is effective in decreasing mesoaccumbal DA neurotransmission and cocaine reward (3, 4).The serine protease tissue plasminogen activator (tPA), which is released from neurons upon excitation and facilitates synaptic plasticity (6), is an attractive candidate for mediating some of cocaine's effects on neuronal plasticity. tPA is expressed in brain regions implicated in drug reward, including the NAc and amygdala, and is thought to regulate proteolytic events involved in neurite outgrowth and long-term...

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Section: Discussionmentioning

confidence: 99%

Tissue plasminogen activator modulates the cellular and behavioral response to cocaine

Maiya

Zhou

Norris

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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“…Central infusion of dynorphin A(1-17) prevents the development of cocaine-induced CPP (Zhang et al, 2004), and kappa opioid receptor (KOP-r) agonists elevate the ICSS threshold in the LH (Todtenkopf et al, 2004). The ppDyn gene is co-expressed in most LH orexin neurons (Chou et al, 2001) and dynorphin A (1-13) has regulatory effects on the orexin system (Li and van den Pol, 2006).…”

Section: Discussionmentioning

confidence: 99%

Effects of cocaine place conditioning, chronic escalating-dose “binge” pattern cocaine administration and acute withdrawal on orexin/hypocretin and preprodynorphin gene expressions in lateral hypothalamus of Fischer and Sprague–Dawley rats

et al. 2008

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Recent evidence suggests an important role for hypothalamic orexins/hypocretins in modulation of drug reward and addiction-like behaviors in rodents. Our recent study has shown that the aversive state of arousal during acute morphine withdrawal is associated with increased orexin gene expression in lateral hypothalamus (LH) of Fischer 344 (F344) inbred rats, with no change in the expression of preprodynorphin (ppDyn), a gene co-expressed with LH orexin. Therefore, we determined whether orexin and ppDyn mRNA levels in LH or medial hypothalamus (including perifornical and dorsomedial areas) of F344 or Sprague-Dawley (SD) outbred rats, are altered following: 1) cocaine (10 mg/kg, i.p.) conditioned place preference (CPP); 2) chronic (14 days) cocaine exposure using both "binge" pattern administration in steady-dose (45 mg/kg/day) and escalating-dose (45 to 90 mg/kg/day) regimens; and 3) acute (1 day) and chronic (14 days) withdrawal from cocaine with opioid receptor antagonist naloxone treatment (1 mg/kg). We found that orexin mRNA levels were decreased after cocaine place conditioning in the LH of SD rats. A decreased LH orexin mRNA level was also observed after chronic escalating-dose cocaine (but not CPP pattern regimen without conditioning, or steady-dose regimen) in both strains. In F344 rats only, acute withdrawal from chronic escalating-dose cocaine administration resulted in increases in both LH orexin and ppDyn mRNA levels, which were unaltered by naloxone or after chronic withdrawal. Our results suggest that (1) alteration of LH orexin gene expression is region specific after cocaine place conditioning in SD rats and dose-dependent after chronic exposure in both strains; and (2) increased LH orexin and ppDyn gene expressions in F344 rats may contribute to negative affective states in cocaine withdrawal.

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“…Whereas TRPM8 activation by cold as well as by exogenous substances such as menthol have been the matter of extensive studies (Almaraz et al, 2014), endogenous activators or inhibitors of TRPM8 have more rarely been identified. Interestingly, it was shown previously that androgens increase TRPM8 expression in non-neural cells (L. Zhang and Barritt, 2004;Thebault et al, 2005). In addition to this genomic regulation by androgens, testosterone acts directly on the TRPM8 channel at subphysiological concentrations (Asuthkar et al, 2015), and recent unpublished work also shows that, in the presence of the androgen receptor, physiological concentration of testosterone specifically inhibits TRPM8 activity in transfected cells and primary sensory neurons through direct interaction of the channel with the androgen receptor at the plasma membrane.…”

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confidence: 90%

New Insight in Cold Pain: Role of Ion Channels, Modulation, and Clinical Perspectives

et al. 2016

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Cold temperature detection involves the process of sensory transduction in cutaneous primary sensory nerve terminals, which converts thermal stimuli into depolarizations of the membrane. This transformation into electrical signals is followed by the subsequent propagation of action potentials in cold-sensitive afferent nerve fibers. A large array of ion channels shapes this process; however, the precise contribution of specific ion channel subtypes to cold perception and cold pain remains elusive. This review aims at giving an update on our current understanding of the role played by TRPs, leak K ϩ and voltage-gated Na ϩ and K ϩ channels in the transduction of cold by nociceptors and in cold-induced pain.

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Effect of the endogenous ? opioid agonist dynorphin A(1?17) on cocaine-evoked increases in striatal dopamine levels and cocaine-induced place preference in C57BL/6J mice

Abstract: The blockade of the cocaine-induced rise in striatal dopamine may contribute to both dynorphin's ability to prevent the development of cocaine-induced conditioned place preference and to attenuate the increase in locomotor activity.

Cited by 119 publications

References 37 publications

Tissue plasminogen activator modulates the cellular and behavioral response to cocaine

Tissue plasminogen activator modulates the cellular and behavioral response to cocaine

Effects of cocaine place conditioning, chronic escalating-dose “binge” pattern cocaine administration and acute withdrawal on orexin/hypocretin and preprodynorphin gene expressions in lateral hypothalamus of Fischer and Sprague–Dawley rats

New Insight in Cold Pain: Role of Ion Channels, Modulation, and Clinical Perspectives

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