Place-Cell Impairment in Glutamate Receptor 2 Mutant Mice

Yan, Jun; Zhang, Yunfeng; Jia, Zhenping; Taverna, Franco A.; McDonald, Robert J.; Muller, Robert U.; Roder, John

doi:10.1523/jneurosci.22-03-j0002.2002

Cited by 31 publications

(22 citation statements)

References 36 publications

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“…The addition of this second form of plasticity to excitatory neurons may undermine the specificity imparted by Hebbian plasticity. Consistent with this idea, several studies have shown that the presence of GluR2-lacking AMPARs can reduce the specificity and stability of plastic changes mediated by NMDARs [28], [57]. The current study extends these results by demonstrating that the selective addition of AMPAR-mediated plasticity to CA1 pyramidal cells impairs NMDAR-dependent learning.…”

Section: Discussionsupporting

confidence: 88%

A Role for Calcium-Permeable AMPA Receptors in Synaptic Plasticity and Learning

et al. 2010

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A central concept in the field of learning and memory is that NMDARs are essential for synaptic plasticity and memory formation. Surprisingly then, multiple studies have found that behavioral experience can reduce or eliminate the contribution of these receptors to learning. The cellular mechanisms that mediate learning in the absence of NMDAR activation are currently unknown. To address this issue, we examined the contribution of Ca2+-permeable AMPARs to learning and plasticity in the hippocampus. Mutant mice were engineered with a conditional genetic deletion of GluR2 in the CA1 region of the hippocampus (GluR2-cKO mice). Electrophysiology experiments in these animals revealed a novel form of long-term potentiation (LTP) that was independent of NMDARs and mediated by GluR2-lacking Ca2+-permeable AMPARs. Behavioral analyses found that GluR2-cKO mice were impaired on multiple hippocampus-dependent learning tasks that required NMDAR activation. This suggests that AMPAR-mediated LTP interferes with NMDAR-dependent plasticity. In contrast, NMDAR-independent learning was normal in knockout mice and required the activation of Ca2+-permeable AMPARs. These results suggest that GluR2-lacking AMPARs play a functional and previously unidentified role in learning; they appear to mediate changes in synaptic strength that occur after plasticity has been established by NMDARs.

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Section: Discussionsupporting

confidence: 88%

A Role for Calcium-Permeable AMPA Receptors in Synaptic Plasticity and Learning

et al. 2010

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“…This supports the idea that impaired LTP mechanisms are responsible for the deficient stabilization of hippocampal place cell representations, resulting in spatial memory deficits, and is consistent with studies in which manipulations of specific components of intracellular signaling pathways underlying LTP induction or maintenance were found to affect location-specific place cell firing and spatial memory. Pharmacologic or genetic inactivation of NMDA receptors (15,17), the GluR2 AMPA receptor subunit (19), or mutations affecting plasticity-related proteins, such as the kinase CaMKII or CREB, in transgenic mice (16,20,21), all result in degraded and unstable place fields. In addition, both the reduction of forebrain protein kinase A activity in transgenic R(AB) mice (22) and pharmacologic inhibition of protein synthesis using anisomycin in rats (23) were found to affect place cell maps in a manner resembling the effects seen with zif268 inactivation in the present study.…”

Section: Discussionmentioning

confidence: 99%

Impaired long-term stability of CA1 place cell representation in mice lacking the transcription factor zif268 / egr1

Renaudineau

Poucet

Laroche

et al. 2009

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

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Zif268 is a transcriptional regulator that plays a crucial role in maintenance of the late phases of hippocampal long-term potentiation (LTP) and consolidation of spatial memories. Because the hippocampal place cell system is essential for long-term spatial memory, we tested the hypothesis that zif268 is required for long-term stability of hippocampal place cell representations by recording CA1 place cells in mice lacking zif268. We found that zif268 gene deletion destabilized the representation of a familiar environment after exposure to a novel environment and impaired the long-term (24 h), but not short-term (1 h), stability of newly formed representations. These impairments could be rescued by repeated exposure to the novel environment, however. These results indicate that zif268 contributes to the long-term stability of spatial representations in CA1 and support the notion that the long-term stability of place cell representations requires transcriptiondependent mechanisms similar to those observed in LTP.hippocampus ͉ spatial memory

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“…Single‐unit activities were sorted out by cluster cutting based on eight parameters of the action potential waveform including peak, valley, peak duration, valley duration, peak time, valley time and peak height (Yan & Ehret, 2002; Yan et al. , 2002, 2003).…”

Section: Methodsmentioning

confidence: 99%

Corticofugal feedback for auditory midbrain plasticity elicited by tones and electrical stimulation of basal forebrain in mice

Zhang

Hakes

Bonfield

et al. 2005

Eur J of Neuroscience

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The auditory cortex (AC) is the major origin of descending auditory projections and is one of the targets of the cholinergic basal forebrain, nucleus basalis (NB). In the big brown bat, cortical activation evokes frequency-specific plasticity in the inferior colliculus and the NB augments this collicular plasticity. To examine whether cortical descending function and NB contributions to collicular plasticity are different between the bat and mouse and to extend the findings in the bat, we induced plasticity in the central nucleus of the mouse inferior colliculus by a tone paired with electrical stimulation of the NB (hereafter referred to as tone-ES(NB)). We show here that tone-ES(NB) shifted collicular best frequencies (BFs) towards the frequency of the tone paired with ES(NB) when collicular BFs were different from tone frequency. The shift in collicular BF was linearly correlated to the difference between collicular BFs and tone frequencies. The changes in collicular BFs after tone-ES(NB) were similar to those found in the big brown bat. Compared with cortical plasticity evoked by tone-ES(NB), the pattern of collicular BF shifts was identical but the shifting range of collicular BFs was narrower. A GABA(A) agonist (muscimol) or a muscarinic acetylcholine receptor antagonist (atropine) applied to the AC completely abolished the collicular plasticity evoked by tone-ES(NB). Therefore, our findings strongly suggest that the AC plays a critical role in experience-dependent auditory plasticity through descending projections.

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Place-Cell Impairment in Glutamate Receptor 2 Mutant Mice

Cited by 31 publications

References 36 publications

A Role for Calcium-Permeable AMPA Receptors in Synaptic Plasticity and Learning

A Role for Calcium-Permeable AMPA Receptors in Synaptic Plasticity and Learning

Impaired long-term stability of CA1 place cell representation in mice lacking the transcription factor zif268 / egr1

Corticofugal feedback for auditory midbrain plasticity elicited by tones and electrical stimulation of basal forebrain in mice

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