AMPA Receptor Trafficking and Synaptic Plasticity

Malinow, Roberto; Malenka, Robert C.

doi:10.1146/annurev.neuro.25.112701.142758

Cited by 2,306 publications

(2,027 citation statements)

References 137 publications

(167 reference statements)

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“…Our observations are consistent with those reported recently for amphetamine and several other drugs of abuse (Ungless et al, 2001;Saal et al, 2003). In the hippocampus, an increase in the AMPAR component of the excitatory postsynaptic response occurs at synapses that have undergone LTP (Kauer et al, 1988;Isaac et al, 1995;Liao et al, 1995;Malinow and Malenka, 2002). By extension, the increased AMPAR/NMDAR ratios in the VTA suggest that excitatory VTA synapses in animals exposed to drugs of abuse are potentiated 24 h later.…”

Section: A Single Dose Of Amphetamine Alters Glutamatergic Synapses Isupporting

confidence: 92%

Rapid Synaptic Plasticity of Glutamatergic Synapses on Dopamine Neurons in the Ventral Tegmental Area in Response to Acute Amphetamine Injection

Faleiro

Jones

Kauer

2004

Neuropsychopharmacol

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Drugs of abuse activate the reward circuitry of the mesocorticolimbic system, and it has been hypothesized that drug exposure triggers synaptic plasticity of glutamatergic synapses onto dopamine (DA) neurons of the ventral tegmental area. Here, we show that just a 2 h in vivo exposure to amphetamine is sufficient to potentiate these synapses, measured as an increase in the synaptic AMPAR/NMDAR ratio. We tested the prediction that an increase in GluR1-containing AMPA receptors would result in an increase in GluR1 homomeric receptors at synapses, but were unable to observe any evidence of the predicted rectification in DA neurons from animals treated with amphetamine. We also examined the possibility of increased AMPA receptor insertion in the membrane, but did not detect a significant increase in biotinylated surface GluR1. We conclude that amphetamine induces rapid changes in synaptic AMPAR/NMDAR ratios, suggesting that potentiation of glutamatergic synapses is a relatively early event in the series of neuroadaptations in response to drugs of abuse.

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Section: A Single Dose Of Amphetamine Alters Glutamatergic Synapses Isupporting

confidence: 92%

Rapid Synaptic Plasticity of Glutamatergic Synapses on Dopamine Neurons in the Ventral Tegmental Area in Response to Acute Amphetamine Injection

Faleiro

Jones

Kauer

2004

Neuropsychopharmacol

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“…No functional role for the extreme C-terminal region of GluA4 has yet been proposed. This region is similar to the PDZ binding motif critically involved in GluA1 trafficking but blocked with an extra proline residue Malinow and Malenka, 2002;Coleman et al, 2010). However, the extreme C-terminal sequence alone was not sufficient to regulate GluA4 trafficking, as GST-A4(870-902) had no effect.…”

Section: Molecular Mechanism Underlying Pka-driven Synaptic Insertionmentioning

confidence: 98%

“…Hayashi et al, 2000;Malinow and Malenka, 2002;Anggono and Huganir, 2012). In GluA4, this PDZ binding motif is masked by an extreme C-terminal proline residue, and so far no proteins have been identified to bind this region in vivo (Coleman et al, 2010).…”

Section: Extreme C-terminal Sequences Of Glua4 Are Involved In Pka-dementioning

confidence: 99%

Molecular mechanisms controlling synaptic recruitment of GluA4 subunit-containing AMPA-receptors critical for functional maturation of CA1 glutamatergic synapses

et al. 2017

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Synaptic recruitment of AMPA receptors (AMPARs) represents a key postsynaptic mechanism driving functional development and maturation of glutamatergic synapses. At immature hippocampal synapses, PKA-driven synaptic insertion of GluA4 is the predominant mechanism for synaptic reinforcement. However, the physiological significance and molecular determinants of this developmentally restricted form of plasticity are not known. Here we show that PKA activation leads to insertion of GluA4 to synaptic sites with initially weak or silent AMPAR-mediated transmission. This effect depends on a novel mechanism involving the extreme C-terminal end of GluA4, which interacts with the membrane proximal region of the C-terminal domain to control GluA4 trafficking. In the absence of GluA4, strengthening of AMPAR-mediated transmission during postnatal development was significantly delayed. These data suggest that the GluA4-mediated activation of silent synapses is a critical mechanism facilitating the functional maturation of glutamatergic circuitry during the critical period of experience-dependent fine-tuning.

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“…These dynamic changes are determined by the architecture of its actin cytoskeleton [94]. Significantly, increasing evidence indicates that proper regulation of spine shape and size is crucial for processing of information [13,44,52,55,89]. For instance, spine morphology and/or dynamics have been associated with long-term potentiation (LTP) and long term-depression (LTD), which are two well studied forms of learning and memory [55].…”

Section: Introductionmentioning

confidence: 99%

“…Significantly, increasing evidence indicates that proper regulation of spine shape and size is crucial for processing of information [13,44,52,55,89]. For instance, spine morphology and/or dynamics have been associated with long-term potentiation (LTP) and long term-depression (LTD), which are two well studied forms of learning and memory [55]. One particular mechanism proposed for some forms of LTP is the addition of new α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) at the postsynaptic site, which has been correlated with an increase in spine size, whereas internalization of AMPARs during LTD has been associated with smaller spines [49].…”

Section: Introductionmentioning

confidence: 99%

Rho-linked genes and neurological disorders

Kasri

Aelst

2007

Pflugers Arch - Eur J Physiol

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Mental retardation (MR) is a common cause of intellectual disability and affects approximately 2 to 3 % of children and young adults. MR has been consistently associated with changes in dendrites and dendritic spine structure. Given that dendritic spine morphology has been tightly linked to synaptic activity, altered spine morphology has been suggested to be the underlying cause of cognitive disabilities observed in MR. The structure and dynamics of dendritic spines is determined by its underlying actin cytoskeleton. Signaling molecules and cascades important for cytoskeletal regulation have therefore naturally attracted a great deal of attention. As key regulators of both the actin and microtubule cytoskeletons, it is not surprising that the Rho GTPases have emerged as important regulators of dendrite and spine structural plasticity. In support of this, mutations in regulators and effectors of Rho GTPases have been associated with diseases affecting the nervous system, including MR and amyotropic lateral sclerosis (ALS). Here we will discuss Rho GTPase related genes and their signaling pathways involved in MR and ALS.

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AMPA Receptor Trafficking and Synaptic Plasticity

Cited by 2,306 publications

References 137 publications

Rapid Synaptic Plasticity of Glutamatergic Synapses on Dopamine Neurons in the Ventral Tegmental Area in Response to Acute Amphetamine Injection

Rapid Synaptic Plasticity of Glutamatergic Synapses on Dopamine Neurons in the Ventral Tegmental Area in Response to Acute Amphetamine Injection

Molecular mechanisms controlling synaptic recruitment of GluA4 subunit-containing AMPA-receptors critical for functional maturation of CA1 glutamatergic synapses

Rho-linked genes and neurological disorders

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