N-methyl-D-aspartate receptor antagonists disrupt the formation of a mammalian neural map.

Simon, David K.; Prusky, Glen T.; O’Leary, Dennis D.M.; Constantine‐Paton, Martha

doi:10.1073/pnas.89.22.10593

Cited by 291 publications

(163 citation statements)

References 45 publications

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“…In the rodent superior colliculus, chronic NMDAR blockade disrupts retinocollicular topography (Simon et al, 1992) and increases the sprouting of RGC axons and the density of retinocollicular synapses during the period of map refinement (Colonnese and Constantine-Paton, 2006). This supports the hypothesis that synaptic competition stabilizes developing axons and eliminates inappropriate connections in mammals as well.…”

Section: Model Of Synaptic-competition-based Retinotopic Map Refinementsupporting

confidence: 72%

Retinocollicular Synapse Maturation and Plasticity Are Regulated by Correlated Retinal Waves

Shah¹,

Crair²

2008

J. Neurosci.

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During development, spontaneous retinal waves are thought to provide an instructive signal for retinotopic map formation in the superior colliculus. In mice lacking the ␤2 subunit of nicotinic ACh receptors (␤2 Ϫ/Ϫ ), correlated retinal waves are absent during the first postnatal week, but return during the second postnatal week. In control retinocollicular synapses, in vitro analysis reveals that AMPA/ NMDA ratios and AMPA quantal amplitudes increase during the first postnatal week while the prevalence of silent synapses decreases. In age-matched ␤2 Ϫ/Ϫ mice, however, these parameters remain unchanged through the first postnatal week in the absence of retinal waves, but quickly mature to control levels by the end of the second week, suggesting that the delayed onset of correlated waves is able to drive synapse maturation. To examine whether such a mechanistic relationship exists, we applied a "burst-based" plasticity protocol that mimics coincident activity during retinal waves. We find that this pattern of activation is indeed capable of inducing synaptic strengthening [long-term potentiation (LTP)] on average across genotypes early in the first postnatal week [postnatal day 3 (P3) to P4] and, interestingly, that the capacity for LTP at the end of the first week (P6 -P7) is significantly greater in immature ␤2 Ϫ/Ϫ synapses than in mature control synapses. Together, our results suggest that retinal waves drive retinocollicular synapse maturation through a learning rule that is physiologically relevant to natural wave statistics and that these synaptic changes may serve an instructive role during retinotopic map refinement.

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Section: Model Of Synaptic-competition-based Retinotopic Map Refinementsupporting

confidence: 72%

Retinocollicular Synapse Maturation and Plasticity Are Regulated by Correlated Retinal Waves

Shah¹,

Crair²

2008

J. Neurosci.

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“…Thus, as has been described for many sensory systems (Knudsen, 1985;Singer, 1990;Simon et al, 1992;Schlaggar, 1993;Benedetti and Ferro, 1995), this spinal nociceptive motor system seems to attain its adult organization at least partially through experience-dependent mechanisms. The eventual formation of an "imprint" of the movement pattern on the reflex pathway may indicate a special form of somatosensory "imprinting" mechanisms during development (see below).…”

Section: Discussionmentioning

confidence: 99%

“…In the latter case, numerous studies indicate a crucial role of Hebbian mechanisms, perhaps involving NMDA receptor-mediated detection of temporally correlated synaptic activity (Singer, 1990;Simon et al, 1992;Schlaggar et al, 1993;Scheetz and Constantine-Paton, 1994). Hebb (1949) postulated that the connections between a pre-and postsynaptic neuron may in some cases be strengthened if the probability is high that impulses in the presynaptic neuron are followed by postsynaptic action potentials.…”

Section: Mechanisms Underlying the Postnatal Tuning Of Withdrawal Refmentioning

confidence: 99%

Developmental Adaptation of Rat Nociceptive Withdrawal Reflexes after Neonatal Tendon Transfer

Holmberg

Schouenborg

et al. 1997

J. Neurosci.

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Nociceptive withdrawal reflexes (NWRs) were studied in adult rats in which the movement patterns produced by single muscles had been altered by neonatal tendon transfer. NWRs evoked by cutaneous noxious mechanical and thermal (CO 2 -laser) stimulation were recorded using electromyography in a decerebrate spinal preparation. The sensitivity distribution within the receptive fields of the NWRs of the extensor digitorum longus and the peronei muscles exhibited changes corresponding to the altered movement patterns. No detectable change of NWRs was found in normal muscles whose receptive fields overlapped that of the modified muscle. Furthermore, NWRs of muscles that regained an essentially normal function after neonatal tendon transfer did not differ from normal. It is proposed that a developmental experience-dependent mechanism, which takes into account the hindlimb movement pattern caused by contraction of single muscles, underlies the functionally adapted organization of adult NWRs.

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“…Alternatively, the kinetics Ca 2ϩ flux mediated by NR2A-rich versus NR2B-rich receptors may have important implications for the type of signal generated (42). It will be important to determine whether subunit dependent changes in receptor binding affinities and kinetics, or synaptic versus periand extrasynaptic positions are differentially involved in the various developmental processes, activity-dependent gene activation (43), map refinement (14,44), synapse elimination (45), receptive field development (46), and ocular dominance plasticity (28) in which NMDARs are thought to be involved.…”

Section: Discussionmentioning

confidence: 99%

Developmental loss of miniature N -methyl- d -aspartate receptor currents in NR2A knockout mice

Townsend

Yoshii

Mishina

et al. 2003

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

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The N-methyl-D-aspartate (NMDA) glutamate receptor (NMDAR), long implicated in developmental plasticity, shows decay time kinetics that shorten postnatally as NR2A subunits are added to the receptor. Neither the mechanism nor immediate effect of this change is known. We studied developing NMDAR currents by using visual neurons in slices from NR2A knockout (NR2AKO) and WT mice. Both strains show increased dendritic levels of synaptic density scaffolding protein PSD-95 with age. Dendritic levels of NR2A increased at the same time in WT and immunoprecipitated with PSD-95. PSD-95͞NMDAR binding was significantly decreased in the NR2AKO. Moreover, NMDAR miniature currents (minis) were lost and rise times of NMDAR evoked currents increased in mutant mice. Age-matched WT cells showed NR2A-rich receptors predominating in minis, yet slow NR2B mediated currents persisted in evoked currents. Disrupting photoreceptor activation of retinal ganglion cells eliminated increases in PSD-95 and NR2A in superior collicular dendrites of WT mice and slowed the loss of miniature NMDAR currents in NR2AKOs. These data demonstrate that NMDARs that respond to single quantal events mature faster during development by expressing the NR2A subunit earlier than NMDARs that respond to evoked release. We hypothesize that NR2A-rich NMDARs may be localized to the center of developing synapses by an activity-dependent process that involves the targeting of PSD-95 to the postsynaptic density. Neonatal receptors become restricted to perisynpatic or extrasynaptic sites, where they participate primarily in evoked currents. I n visual pathways, N-methyl-D-aspartate (NMDA) receptors(NMDARs) contain NR1 (GluR 1) plus varying proportions of NR2A (GluR 1) and NR2B (GluR 2) subunits (1, 2). The decay times of evoked NMDAR currents (NMDARcs) become faster during development as NR2A is incorporated (3-6). Reducing visual activity, delays synaptic refinement in the visual cortex (VC) (7,8), delays the shortening of NMDRc decay time (9) and up-regulation of NR2A (10). Furthermore dark-reared rats rapidly up-regulate NR2A at cortical synapses upon light exposure, whereas rats placed in darkness down-regulate NR2A in dendrites over several days (11,12). The mechanism of this rapid activity-dependent trafficking is unknown, but related work in our laboratory suggests that scaffolding of the NMDAR by PSD-95 may be involved. MethodsAnimals. All surgical procedures were compliant with the Massachusetts Institute of Technology Committee on Animal Care (CAC) animal protocol review. WT C57BL͞6 mice and NR2AKO mice (13) with a C57BL͞6 background were used in all experiments. All animals were killed before eye opening on postnatal day 13 (P13).Surgery. Preparation of Elvax plastic (DuPont) for drug delivery in the eye was carried out as in ref. 14. Glutamate antagonists were dissolved in DMSO and Elvax [MK801 final concentration ϭ 6 mM, estimated active concentration in eye ϭ 200 M and 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo[f]quinoxaline (NBQX) final concentration ϭ 600 M, ...

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N-methyl-D-aspartate receptor antagonists disrupt the formation of a mammalian neural map.

Cited by 291 publications

References 45 publications

Retinocollicular Synapse Maturation and Plasticity Are Regulated by Correlated Retinal Waves

Retinocollicular Synapse Maturation and Plasticity Are Regulated by Correlated Retinal Waves

Developmental Adaptation of Rat Nociceptive Withdrawal Reflexes after Neonatal Tendon Transfer

Developmental loss of miniature N -methyl- d -aspartate receptor currents in NR2A knockout mice

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