Dark-rearing delays the loss of NMDA-receptor function in kitten visual cortex

Fox, Kevin; Daw, Nigel W.; Sato, Hiromichi; Czepita, Damian

doi:10.1038/350342a0

Cited by 103 publications

(39 citation statements)

References 19 publications

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“…Normally, the duration of the NMDA receptor-mediated EPSC shortens over development, but dark-rearing or TTX administration can prevent this shortening (Carmingnoto and Vicini, 1992). Similarly, the normal developmental decrease in the percentage of the visually driven response mediated by NMDA receptors is prevented when cats are raised in the dark and resumes when dark-reared animals are subsequently exposed to light (Fox et al, 1989(Fox et al, , 1991. Our results suggest that the physiological alterations that occur during darkrearing do not result from major changes in the amount of NMDAR1 protein.…”

Section: Regulation Of Nmdar1 Immunoreactivity By Vision and Activitysupporting

confidence: 47%

“…In cat visual cortex, the percentage of the visual response of individual neurons that is NMDAR-mediated decreases between 3 and 6 weeks of age; dark-rearing prevents this decrease (Fox et al, 1989(Fox et al, , 1991. One possible mechanism that might underlie the decrease in NMDA-mediated responses is a change in NMDA receptor kinetics.…”

Section: Abstract: Nmdar1; Activity-dependent; Visual Cortex; Develomentioning

confidence: 99%

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Activity-Dependent Regulation of NMDAR1 Immunoreactivity in the Developing Visual Cortex

1997

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NMDA receptors have been implicated in activity-dependent synaptic plasticity in the developing visual cortex. We examined the distribution of immunocytochemically detectable NMDAR1 in visual cortex of cats and ferrets from late embryonic ages to adulthood. Cortical neurons are initially highly immunostained. This level declines gradually over development, with the notable exception of cortical layers 2/3, where levels of NMDAR1 immunostaining remain high into adulthood. Within layer 4, the decline in NMDAR1 immunostaining to adult levels coincides with the completion of ocular dominance column formation and the end of the critical period for layer 4. To determine whether NMDAR1 immunoreactivity is regulated by retinal activity, animals were dark-reared or retinal activity was completely blocked in one eye with tetrodotoxin (TTX). Dark-rearing does not cause detectable changes in NMDAR1 immunoreactivity. However, 2 weeks of monocular TTX administration decreases NMDAR1 immunoreactivity in layer 4 of the columns of the blocked eye. Thus, high levels of NMDAR1 immunostaining within the visual cortex are temporally correlated with ocular dominance column formation and developmental plasticity; the persistence of staining in layers 2/3 also correlates with the physiological plasticity present in these layers in the adult. In addition, visual experience is not required for the developmental changes in the laminar pattern of NMDAR1 levels, but the presence of high levels of NMDAR1 in layer 4 during the critical period does require retinal activity. These observations are consistent with a central role for NMDA receptors in promoting and ultimately limiting synaptic rearrangements in the developing neocortex.

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Section: Regulation Of Nmdar1 Immunoreactivity By Vision and Activitysupporting

confidence: 47%

Section: Abstract: Nmdar1; Activity-dependent; Visual Cortex; Develomentioning

confidence: 99%

Activity-Dependent Regulation of NMDAR1 Immunoreactivity in the Developing Visual Cortex

1997

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“…NMDA receptors are ionotropic glutamate receptors that, when activated, mediate calcium influx. There is considerable evidence that NMDA receptors are critical mediators of activity-dependent synaptic changes (Kleinschmidt et al, 1987;Fox et al, 1991;Madison et al, 1991;Rabacchi et al, 1992). A well characterized example of this is NMDA-dependent long-term potentiation (LTP) in the neocortex (Kirkwood et al, 1993) and hippocampus (Jahr and Lester, 1992;Bliss and Collingridge, 1993;Malenka, 1994).…”

Section: Abstract: Transfection; Neurons; Transcription C-fos; Glutmentioning

confidence: 99%

Calcium Influx via the NMDA Receptor Induces Immediate Early Gene Transcription by a MAP Kinase/ERK-Dependent Mechanism

et al. 1996

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The regulation of gene expression by neurotransmitters is likely to play a key role in neuroplasticity both during development and in the adult animal. Therefore, it is important to determine the mechanisms of neuronal gene regulation to understand fully the mechanisms of learning, memory, and other long-term adaptive changes in neurons. The neurotransmitter glutamate stimulates rapid and transient induction of many genes, including the c-fos proto-oncogene. The c-fos promoter contains several critical regulatory elements, including the serum response element (SRE), that mediate glutamate-induced transcription in neurons; however, the mechanism by which the SRE functions in neurons has not been defined. In this study, we sought to identify transcription factors that mediate glutamate induction of transcription through the SRE in cortical neurons and to elucidate the mechanism(s) of transcriptional activation by these factors. To facilitate this analysis, we developed an improved calcium phosphate coprecipitation procedure to transiently introduce DNA into primary neurons, both efficiently and consistently. Using this protocol, we demonstrate that the transcription factors serum response factor (SRF) and Elk-1 can mediate glutamate induction of transcription through the SRE in cortical neurons. There are at least two distinct pathways by which glutamate signals through the SRE: an SRF-dependent pathway that can operate in the absence of Elk and an Elk-dependent pathway. Activation of the Elkdependent pathway of transcription seems to require phosphorylation of Elk-1 by extracellular signal-regulated kinases (ERKs), providing evidence for a physiological function of ERKs in glutamate signaling in neurons. Taken together, these findings suggest that SRF, Elk, and ERKs may have important roles in neuroplasticity.

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“…The classic example is the necessity of visual stimulation on the development of ocular dominance columns [97], which has provided a body of information about how synaptic activity sculpts brain morphology by its influence on neuronal survival. Three crucial components for activity-dependent plasticity exist: (1) a critical period for neuroanatomical rearrangements [66,96,97]; (2) 'use it or lose it', in which the remaining inputs expand into enucleated projection sites [76,173,198]; and (3) the necessity of a number of factors, including the n-methyl-D-aspartate (NMDA) receptor system [65], the neurotrophin BDNF [89], GABA [61], class I major histocompatability (I MHC) genes [41], and modulatory neurotransmitter systems, especially serotonin [218]. Disruption of any of these components during key periods demonstrates their involvement in an experienceexpectant manner.…”

Section: Experience-expectant Developmentmentioning

confidence: 99%

Trajectories of brain development: point of vulnerability or window of opportunity?

Andersen

2003

Neuroscience & Biobehavioral Reviews

1,325

1,006

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Brain development is a remarkable process. Progenitor cells are born, differentiate, and migrate to their final locations. Axons and dendrites branch and form important synaptic connections that set the stage for encoding information potentially for the rest of life. In the mammalian brain, synapses and receptors within most regions are overproduced and eliminated by as much as 50% during two phases of life: immediately before birth and during the transitions from childhood, adolescence, to adulthood. This process results in different critical and sensitive periods of brain development. Since Hebb (1949) first postulated that the strengthening of synaptic elements occurs through functional validation, researchers have applied this approach to understanding the sculpting of the immature brain. In this manner, the brain becomes wired to match the needs of the environment. Extensions of this hypothesis posit that exposure to both positive and negative elements before adolescence can imprint on the final adult topography in a manner that differs from exposure to the same elements after adolescence. This review endeavors to provide an overview of key components of mammalian brain development while simultaneously providing a framework for how perturbations during these changes uniquely impinge on the final outcome. q

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Dark-rearing delays the loss of NMDA-receptor function in kitten visual cortex

Cited by 103 publications

References 19 publications

Activity-Dependent Regulation of NMDAR1 Immunoreactivity in the Developing Visual Cortex

Activity-Dependent Regulation of NMDAR1 Immunoreactivity in the Developing Visual Cortex

Calcium Influx via the NMDA Receptor Induces Immediate Early Gene Transcription by a MAP Kinase/ERK-Dependent Mechanism

Trajectories of brain development: point of vulnerability or window of opportunity?

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