Synaptic Signaling by All-Trans Retinoic Acid in Homeostatic Synaptic Plasticity

Aoto, Jason; Nam, Christine I.; Poon, Michael M.; Ting, Pamela Y.; Chen, Lu

doi:10.1016/j.neuron.2008.08.012

Cited by 335 publications

(521 citation statements)

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“…Indeed, cortical neurons derived from TAp73 −/− mice show a reduction in the levels of the neurotransmitters glutamate and GABA. Because neuronal differentiation is a complex biological process that is regulated by intrinsic pathways [46][47][48][49][50][51] and extrinsic signals, 52,53 it will be of interest to see whether these other metabolic effects of TAp73 also affect this biological process.…”

Section: Discussionmentioning

confidence: 99%

GLS2 is transcriptionally regulated by p73 and contributes to neuronal differentiation

Velletri

Romeo²,

Tucci

et al. 2013

Cell Cycle

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The amino acid Glutamine is converted into Glutamate by a deamidation reaction catalyzed by the enzyme Glutaminase (GLS). Two isoforms of this enzyme have been described, and the GLS2 isoform is regulated by the tumor suppressor gene p53. Here, we show that the p53 family member TAp73 also drives the expression of GLS2. Specifically, we demonstrate that TAp73 regulates GLS2 during retinoic acid-induced terminal neuronal differentiation of neuroblastoma cells, and overexpression or inhibition of GLS2 modulates neuronal differentiation and intracellular levels of ATP. Moreover, inhibition of GLS activity, by removing Glutamine from the growth medium, impairs in vitro differentiation of cortical neurons. Finally, expression of GLS2 increases during mouse cerebellar development. Although, p73 is dispensable for the in vivo expression of GLS2, TAp73 loss affects GABA and Glutamate levels in cortical neurons. Together, these findings suggest a role for GLS2 acting, at least in part, downstream of p73 in neuronal differentiation and highlight a possible role of p73 in regulating neurotransmitter synthesis

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Section: Discussionmentioning

confidence: 99%

GLS2 is transcriptionally regulated by p73 and contributes to neuronal differentiation

Velletri

Romeo²,

Tucci

et al. 2013

Cell Cycle

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“…Molecular mechanisms controlling the level of βCaMKII are unclear, but could involve retinoic acid (11,32). Interestingly, changes in βCaMKII above or below its basal level both diminish αCaMKII protein.…”

Section: Discussionmentioning

confidence: 99%

“…This finding raises interesting questions about the mechanisms that link the very different modes of induction to their ultimate functional effects. Although α Ca 2+ /CaM-dependent kinase type II (αCaMKII) is generally accepted as a critical player in inducing LTP, a varied group of signaling molecules have been implicated in the response to chronic activity deprivation, including BDNF (4-7), Arc (8), TNF-α (9, 10), retinoic acid (11,12), and β3 integrin (13,14). The interrelationship between these putative signaling molecules and the overall organization of the signaling in response to prolonged activity block remain obscure.…”

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confidence: 99%

β Ca ²⁺ /CaM-dependent kinase type II triggers upregulation of GluA1 to coordinate adaptation to synaptic inactivity in hippocampal neurons

Groth

Lindskog

Thiagarajan

et al. 2010

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

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Prolonged AMPA-receptor blockade in hippocampal neuron cultures leads to both an increased expression of GluA1 postsynaptically and an increase in vesicle pool size and turnover rate presynaptically, adaptive changes that extend beyond simple synaptic scaling. As a molecular correlate, expression of the β Ca 2+ /CaM-dependent kinase type II (βCaMKII) is increased in response to synaptic inactivity. Here we set out to clarify the role of βCaMKII in the various manifestations of adaptation. Knockdown of βCaMKII by lentiviral-mediated expression of shRNA prevented the synaptic inactivity-induced increase in GluA1, as did treatment with the CaM kinase inhibitor KN-93, but not the inactive analog KN-92. These results demonstrate that, spurred by AMPA-receptor blockade, up-regulation of βCaMKII promotes increased GluA1 expression. Indeed, transfection of βCaMKII, but not a kinase-dead mutant, increased GluA1 expression on dendrites and elevated vesicle turnover (Syt-Ab uptake), mimicking the effect of synaptic inactivity on both sides of the synapse. In cells with elevated βCaMKII, relief of synaptic-activity blockade uncovered an increase in the frequency of miniature excitatory postsynaptic currents that could be rapidly and fully suppressed by PhTx blockade of GluA1 receptors. This increased mini frequency involved a genuine presynaptic enhancement, not merely an increased abundance of synapses. This finding suggests that Ca 2+ flux through GluA1 receptors may trigger the acute release of a retrograde messenger. Taken together, our results indicate that synaptic inactivity-induced increases in βCaMKII expression set in motion a series of events that culminate in coordinated pre-and postsynaptic adaptations in synaptic transmission.α Ca 2+ /CaM-dependent kinase type II | homeostasis | retrograde signaling | synaptic coordination

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“…Suppression of synaptic activity increases synaptic AMPARs by homeostatic synaptic scaling 59 . The initial phases of scaling are mediated by CP-AMPARs since more GluA1 than GluA2 is recruited to synapses 60,61 . Furthermore, CP-AMPAR selective inhibitors block the increase in synaptic current and suppression of synaptic activity is associated with local dendritic translation of GluA1, providing a rapid source of AMPARs, and suggesting the inserted CP-AMPARs are likely GluA1 homomers 62 .…”

Section: Cp-ampars In Synaptic Plasticitymentioning

confidence: 99%

Synaptic AMPA receptor composition in development, plasticity and disease

2016

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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. PrefaceAMPARs are assemblies of four core subunits, GluA1-4, that mediate most fast excitatory neurotransmission. The component subunits determine the functional properties of AMPARs and the prevailing view is that the subunit composition also determines AMPAR trafficking, which is dynamically regulated during development, synaptic plasticity, and in response to neuronal stress in disease. Recently, the subunit-dependence of AMPAR trafficking has been questioned leading to a reappraisal of the field. Here we review what is known, uncertain, conjectured and unknown about the roles of individual subunits and how they impact on AMPAR assembly, trafficking and function under normal and pathological conditions. IntroductionAMPA receptors (AMPARs) are a subtype of ionotropic glutamate receptors that are the 'work-horses' of fast excitatory neurotransmission in the CNS. Developmentallyand activity-regulated changes in the numbers and properties of AMPARs localized at the postsynaptic membrane are essential for excitatory synapse formation, stabilization, synaptic plasticity and neural circuit formation. Consequently, the logistics of the delivery, retention and removal of individual AMPARs with defined subunit compositions at specific synapses is highly complex. A typical cortical or hippocampal pyramidal neuron contains on the order of 10,000 synapses and the AMPARs at each synapse are independently and dynamically regulated in response to developmental cues, synaptic activity and environmental stresses. Furthermore, defects in the processes that control AMPAR assembly, trafficking and synaptic expression are intimately linked to psychiatric and neurological conditions, and also with cognitive decline in neurodegenerative diseases. Remarkable progress has been achieved in understanding how AMPAR trafficking, is orchestrated by a large array of AMPAR interacting proteins. These studies have established a set of hierarchical subunit-specific rules that control AMPAR trafficking under basal and activity-dependent conditions. Furthermore, there has been a growing appreciation that subunit composition can tune the properties of AMPARs to specific conditions. Nonetheless, how AMPARs comprising different subunits are differentially trafficked to control synaptic development, stabilisation and plasticity is a key unanswered question. Here, we provide an overview of the current state of knowledge of subunit-specific AMPAR trafficking and outline what we believe to be the key unresolved questions in the field. 2 Subunit-specific traffickingMost AMPARs are heterotetrameric assemblies of combinations of the subunits GluA1, GluA2, GluA3 and GluA4. AMPARs are expressed in both neurons and glia throughout the CNS 1 and have a turnover time of between 10 hours and 2 days depending on the type of neuron and developmental stage 2,3 . Each subunit has an identical membrane topology and c...

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Synaptic Signaling by All-Trans Retinoic Acid in Homeostatic Synaptic Plasticity

Cited by 335 publications

References 62 publications

GLS2 is transcriptionally regulated by p73 and contributes to neuronal differentiation

GLS2 is transcriptionally regulated by p73 and contributes to neuronal differentiation

β Ca ²⁺ /CaM-dependent kinase type II triggers upregulation of GluA1 to coordinate adaptation to synaptic inactivity in hippocampal neurons

Synaptic AMPA receptor composition in development, plasticity and disease

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Synaptic Signaling by All-Trans Retinoic Acid in Homeostatic Synaptic Plasticity

Cited by 335 publications

References 62 publications

GLS2 is transcriptionally regulated by p73 and contributes to neuronal differentiation

GLS2 is transcriptionally regulated by p73 and contributes to neuronal differentiation

β Ca 2+ /CaM-dependent kinase type II triggers upregulation of GluA1 to coordinate adaptation to synaptic inactivity in hippocampal neurons

Synaptic AMPA receptor composition in development, plasticity and disease

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β Ca ²⁺ /CaM-dependent kinase type II triggers upregulation of GluA1 to coordinate adaptation to synaptic inactivity in hippocampal neurons