In vitro exposure to nicotine induces endocytosis of presynaptic AMPA receptors modulating dopamine release in rat nucleus accumbens nerve terminals

Grilli, Massimo; Summa, Maria; Salamone, Alessia; Olivero, Guendalina; Zappettini, Stefania; Prisco, Silvia Di; Feligioni, Marco; Usai, Cesare; Pittaluga, Anna; Marchi, Mario

doi:10.1016/j.neuropharm.2012.06.049

Cited by 37 publications

(36 citation statements)

References 76 publications

(94 reference statements)

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“…However, we and others have previously suggested that presynaptic AMPARs may function as autoreceptors, regulating neurotransmitter release (Patel and Croucher, 1997;Schenk et al, 2003;Feligioni et al, 2006;Pittaluga et al, 2006;Haglerød et al, 2009;Summa et al, 2011;Grilli et al, 2012). Intriguingly, we have also demonstrated that presynaptic AMPARs appear to be regulated in an opposite direction to the postsynaptic receptors by AMPA and NMDA stimulation .…”

Section: Introductionsupporting

confidence: 62%

“…Several others have reported the presence of presynaptic AMPARs in other CNS synapses (Satake et al, 2000;Schenk et al, 2003;Takago et al, 2005;Chavez et al, 2006;Pittaluga et al, 2006;Summa et al, 2011;Grilli et al, 2012). However, this is the first quantitative analysis of the intrasynaptic distribution of this AMPAR subunit.…”

Section: Discussionmentioning

confidence: 88%

“…Moreover, in the nucleus accumbens, presynaptic AMPARs have been reported to modulate nerve terminal dopamine release (Grilli et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

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Presynaptic PICK1 facilitates trafficking of AMPA-receptors between active zone and synaptic vesicle pool

et al. 2017

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General rightsThis document is made available in accordance with publisher policies. Please cite only the published version using the reference above. AbstractPrevious studies have indicated that presynaptic -amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors (AMPARs) contribute to the regulation of neurotransmitter release. In hippocampal synapses, the presynaptic surface expression of several AMPAR subunits, including GluA2, is regulated in a ligand dependent manner. However, the molecular mechanisms underlying the presynaptic trafficking of AMPARs are still unknown. Here, using bright-field immunocytochemistry, western blots, and quantitative immunogold electron microscopy of the hippocampal CA1 area from intact adult rat brain, we demonstrate the association of AMPA receptors with the presynaptic active zone and with small presynaptic vesicles, in Schaffer collateral synapses in CA1 of the hippocampus. Furthermore, we show that GluA2 and protein interacting with C kinase 1 (PICK1) are colocalized at presynaptic vesicles. Similar to postsynaptic mechanisms, overexpression of either PICK1 or pep2m, which inhibit the N-ethylmaleimide sensitive fusion protein (NSF)-GluA2 interaction, decreases the concentration of GluA2 in the presynaptic active zone membrane. These data suggest that the interacting proteins PICK1 and NSF act as regulators of presynaptic GluA2-containing AMPAR trafficking between the active zone and a vesicle pool that may provide the basis of presynaptic components of synaptic plasticity.

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Section: Introductionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 88%

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Presynaptic PICK1 facilitates trafficking of AMPA-receptors between active zone and synaptic vesicle pool

et al. 2017

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“…This decoupling of the dopaminergic and glutamatergic systems in the accumbens has also been suggested by animal models of cocaine relapse [209]. Animal models of addiction have also demonstrated the importance of accumbal glutamate in response reinforcement learning [210], which may play a role in nicotine reward [211], and dissociable differences in drug-seeking behavior mediated by core and shell glutamate neurons [212]. …”

Section: Pharmacologymentioning

confidence: 81%

The Nucleus Accumbens: A Comprehensive Review

Salgado

Kaplitt²

2015

Stereotact Funct Neurosurg

379

289

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There is increasing interest among functional neurosurgeons in the potential for novel therapies to impact upon diseases beyond movement disorders and pain. A target of increasing interest is the nucleus accumbens (NAc), which has long been studied as a key brain region mediating a variety of behaviors, including reward and satisfaction. As such, focal modulation of the biology of the NAc with deep brain stimulation or novel biological therapies such as gene therapy or cell transplantation could have a major impact upon disorders such as depression and drug addiction. In order to both develop appropriate therapies and then deliver them in an effective fashion, a thorough understanding of the biology, physiology, and anatomy of the NAc is critical. Here, we review the existing literature regarding several areas critical to the development of new therapies, including the known pharmacology, physiology, and connectivity of the NAc, as well as evidence supporting the potential for various NAc surgical therapies in animal models. We then review the relevant anatomy of the NAc, with particular attention to the surgical anatomy, imaging, and targeting necessary to facilitate a proper localization and delivery of new agents to this region. The NAc is a fascinating and potentially rich target for stereotactic neurosurgical intervention, and analysis of existing information regarding all aspects of this structure should help potentiate therapeutic advances and reduce complications from future studies of neurosurgical intervention in this region for a variety of disorders.

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“…These receptors are widely distributed in the central nervous system (CNS) and, although they are preferentially located postsynaptically, they are also involved in neurotransmitter release from presynaptic compartments in different neuronal systems8. However, existence of glutamate receptors at presynaptic terminals has been suggested by immunochemical localization experiments910, functional studies1112 and receptor subunit trafficking analyses913. Physiological NMDA receptor (NMDAR) activity underlies normal synaptic plasticity, whereas its excessive activation leads to apoptosis and excitotoxicity.…”

mentioning

confidence: 99%

Presynaptic c-Jun N-terminal Kinase 2 regulates NMDA receptor-dependent glutamate release

Nisticò

Florenzano

Mango

et al. 2015

Sci Rep

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Activation of c-Jun N-terminal kinase (JNK) signaling pathway is a critical step for neuronal death occurring in several neurological conditions. JNKs can be activated via receptor tyrosine kinases, cytokine receptors, G-protein coupled receptors and ligand-gated ion channels, including the NMDA glutamate receptors. While JNK has been generally associated with postsynaptic NMDA receptors, its presynaptic role remains largely unexplored. Here, by means of biochemical, morphological and functional approaches, we demonstrate that JNK and its scaffold protein JIP1 are also expressed at the presynaptic level and that the NMDA-evoked glutamate release is controlled by presynaptic JNK-JIP1 interaction. Moreover, using knockout mice for single JNK isoforms, we proved that JNK2 is the essential isoform in mediating this presynaptic event. Overall the present findings unveil a novel JNK2 localization and function, which is likely to play a role in different physiological and pathological conditions.

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In vitro exposure to nicotine induces endocytosis of presynaptic AMPA receptors modulating dopamine release in rat nucleus accumbens nerve terminals

Cited by 37 publications

References 76 publications

Presynaptic PICK1 facilitates trafficking of AMPA-receptors between active zone and synaptic vesicle pool

Presynaptic PICK1 facilitates trafficking of AMPA-receptors between active zone and synaptic vesicle pool

The Nucleus Accumbens: A Comprehensive Review

Presynaptic c-Jun N-terminal Kinase 2 regulates NMDA receptor-dependent glutamate release

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