NR2A-containing NMDA receptors are required for LTP induction in rat dorsolateral striatum in vitro

Li, Ping; Li, Yanhai; Han, Tao

doi:10.1016/j.brainres.2009.04.016

Cited by 23 publications

(22 citation statements)

References 45 publications

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“…High frequency stimulation (HFS) trains, in accord with previous reports (Partridge et al, 2000; Fino et al, 2005; Marrone et al, 2006; Li et al, 2009), did not trigger lasting potentiation of striatal EPSPs when administered in the presence of APV (Fig 2A), indicating that NMDARs are necessary for induction but by themselves do not express LTP. As noted, APV substantially reduced pre-HFS baseline responses.…”

Section: Resultssupporting

confidence: 86%

“…Neurons were also filled with Neurobiotin or AlexaFluor 488 for subsequent morphological confirmation (Fig 1B). EPSPs, recorded in the presence of the GABA-A receptor antagonist picrotoxin, were comparable to those described in the literature (Rohrbacher et al, 1994; Moriguchi et al, 2002; Li et al, 2009) and were notable for having a slow decay constant. Previous studies have described a significant NMDAR-mediated component to EPSPs recorded from MSNs (Li et al, 2009) and, in agreement with this, we found that the AMPAR antagonist CNQX reduced the amplitude of cortically evoked responses by almost half; the remainder of the fast response was eliminated by the NMDAR antagonist APV (Fig 1C).…”

Section: Resultssupporting

confidence: 82%

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Presynaptic BDNF Promotes Postsynaptic Long-Term Potentiation in the Dorsal Striatum

Jia¹,

Gall²,

Lynch³

2010

J. Neurosci.

103

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Brain-derived neurotrophic factor (BDNF) facilitates the formation of long-term potentiation (LTP) in hippocampus, but whether this involves release from presynaptic versus postsynaptic pools is unclear. We therefore tested whether BDNF is essential for LTP in dorsal striatum, a structure in which the neurotrophin is present only in afferent terminals. Whole-cell recordings were collected from medium spiny neurons in striatal slices prepared from adult mice. High-frequency stimulation (HFS) of neocortical afferents produced a rapid and stable NMDA receptor-dependent potentiation. The ratio of AMPA to NMDA receptor-mediated components of the EPSPs was substantially increased after inducing potentiation, suggesting that the response enhancement involved postsynaptic changes. In accord with this, paired-pulse response ratios, a measure of transmitter release kinetics, were reduced by elevated calcium but not by LTP. Infusion of the BDNF scavenger TrkB-Fc blocked the formation of potentiation, beginning with the second minute after HFS, without reducing responses to HFS. These results suggest that presynaptic pools of BDNF can act within 2 min of HFS to support the formation of a postsynaptic form of LTP in striatum.

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Section: Resultssupporting

confidence: 86%

Section: Resultssupporting

confidence: 82%

Presynaptic BDNF Promotes Postsynaptic Long-Term Potentiation in the Dorsal Striatum

Jia¹,

Gall²,

Lynch³

2010

J. Neurosci.

103

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“…This difference between wide and narrow timing intervals is significant for the Ifenprodil condition (p<0.05; Figure 4D). These results demonstrate that GluN2 subunits not only control whether potentiation occurs, as previous studies have shown [26]–[28], but also that they hone plasticity, making it sensitive to wider or narrower time intervals between pre-synaptic neurotransmitter release and post-synaptic firing.…”

Section: Resultssupporting

confidence: 73%

“…In addition, GluN2A, because of its fast decay time, results in a narrowing of the STDP curve (compared to GluN2B) by decreasing the Δt that permits sufficient calcium influx. While previous studies have focused on whether a particular GluN2 subunit is necessary for plasticity [26]–[28], we have shown that the relationship between GluN2 subunit and plasticity is more complex than simply allowing or preventing LTP.…”

Section: Discussionmentioning

confidence: 65%

The Effects of NMDA Subunit Composition on Calcium Influx and Spike Timing-Dependent Plasticity in Striatal Medium Spiny Neurons

et al. 2012

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Calcium through NMDA receptors (NMDARs) is necessary for the long-term potentiation (LTP) of synaptic strength; however, NMDARs differ in several properties that can influence the amount of calcium influx into the spine. These properties, such as sensitivity to magnesium block and conductance decay kinetics, change the receptor's response to spike timing dependent plasticity (STDP) protocols, and thereby shape synaptic integration and information processing. This study investigates the role of GluN2 subunit differences on spine calcium concentration during several STDP protocols in a model of a striatal medium spiny projection neuron (MSPN). The multi-compartment, multi-channel model exhibits firing frequency, spike width, and latency to first spike similar to current clamp data from mouse dorsal striatum MSPN. We find that NMDAR-mediated calcium is dependent on GluN2 subunit type, action potential timing, duration of somatic depolarization, and number of action potentials. Furthermore, the model demonstrates that in MSPNs, GluN2A and GluN2B control which STDP intervals allow for substantial calcium elevation in spines. The model predicts that blocking GluN2B subunits would modulate the range of intervals that cause long term potentiation. We confirmed this prediction experimentally, demonstrating that blocking GluN2B in the striatum, narrows the range of STDP intervals that cause long term potentiation. This ability of the GluN2 subunit to modulate the shape of the STDP curve could underlie the role that GluN2 subunits play in learning and development.

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“…In the striatum, long‐term potentiation (LTP) and long‐term depression (LTD) are believed to underlie motor learning. NMDARs, in particular those containing GluN2A, are involved in LTP, but not LTD, induction in the striatum . Several studies have shown that LTP and LTD are lost in the striatum of animal models of PD and that aberrant synaptic plasticity occurs in models of L‐DOPA‐induced dyskinesia .…”

Section: Introductionmentioning

confidence: 99%

CIQ, a positive allosteric modulator of GluN2C/D‐containing N‐methyl‐d‐aspartate receptors, rescues striatal synaptic plasticity deficit in a mouse model of Parkinson's disease

et al. 2017

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NR2A-containing NMDA receptors are required for LTP induction in rat dorsolateral striatum in vitro

Cited by 23 publications

References 45 publications

Presynaptic BDNF Promotes Postsynaptic Long-Term Potentiation in the Dorsal Striatum

Presynaptic BDNF Promotes Postsynaptic Long-Term Potentiation in the Dorsal Striatum

The Effects of NMDA Subunit Composition on Calcium Influx and Spike Timing-Dependent Plasticity in Striatal Medium Spiny Neurons

CIQ, a positive allosteric modulator of GluN2C/D‐containing N‐methyl‐d‐aspartate receptors, rescues striatal synaptic plasticity deficit in a mouse model of Parkinson's disease

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