Developmental plasticity of NMDA receptor function in the retina and the influence of light

Guenther, Elke; Schmid, Susanne; Wheeler‐Schilling, Thomas H.; Albach, G.; Gründer, Tatiana; Fauser, Sascha; Köhler, Konrad

doi:10.1096/fj.03-0618fje

Cited by 24 publications

(48 citation statements)

References 46 publications

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“…Contemporary reports now show that visual deprivation during development interferes with the normal refinement of synaptic circuitry that occurs after exposure to light (Tootle, 1993;Copenhagen, 2001, 2003;Wang et al, 2001;Guenther et al, 2004). This synaptic refinement is reflected in changes of retinal ganglion-cell connectivity and synaptic activity.…”

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confidence: 99%

Choline acetyltransferase‐immunoreactive neurons in the retina of normal and dark‐reared turtle

Lee

Merwine

Padilla

et al. 2007

J of Comparative Neurology

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Visual deprivation alters retinal-ganglion-cell response properties through changes in spontaneous wave-like activity (Sernagor and Grzywacz [1996] Curr Biol 6:1503-1508). This activity depends on cholinergic synaptic transmission in the turtle retina (ibid; Sernagor and Mehta [ 2001] J Anat 199:375-383). We studied the expression of choline acetyltransferase (ChAT) by immunocytochemistry and Western blot in developing retinas of control and dark-reared turtles. At postnatal day 0 (P0), right after hatching, ChAT-immunoreactivity was present in the ganglion cell layer (GCL), in the inner nuclear layer (INL), and in two distinct bands of the inner plexiform layer (IPL). In P14- and P28-control, and P14- and P28-dark-reared retinas, ChAT-immunoreactivity showed similar patterns to those in P0. However, in P14- and P28-dark-reared retinas the density of ChAT-immunoreactive cells was higher in both the INL and GCL than in P14- and P28-control retinas, respectively. Moreover, Western blotting showed that ChAT protein levels were significantly increased in the dark-reared retina compared to those of the control. TUNEL studies indicated that the difference between normal and dark-reared conditions was not due to extra apoptosis in the former. In turn, proliferating-cell nuclear antigen immunocytochemistry showed no extra proliferating cells in the latter. Finally, nearest-neighbor analysis revealed that the denser population of cholinergic cells in dark-reared turtles formed a mosaic as regular as the normal ones in the GCL. Thus, light deprivation increases the expression of ChAT, increasing the apparent density of cholinergic neurons in the developing turtle retina.

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confidence: 99%

Choline acetyltransferase‐immunoreactive neurons in the retina of normal and dark‐reared turtle

Lee

Merwine

Padilla

et al. 2007

J of Comparative Neurology

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“…In the retina, a visual experience-dependent modulation of NMDAR currents in RGCs has been reported [41]. In the present study we examined the influence of visual experience on the postnatal developmental expression of the NR1 subunit splice variants.…”

Section: Introductionmentioning

confidence: 92%

“…Alterations in NMDAR function and composition have been known to occur during experience-dependent phases of circuitry maturation [36][37][38][39][40]. During retinal development, shortening of the NMDAR-mediated currents is observed in rat RGCs and this event is prevented by dark rearing the animals for 1 month [41]. Furthermore, modifications of retinal NMDAR subunit expression are observed during development and by dark rearing [28,[41][42][43].…”

Section: Introductionmentioning

confidence: 99%

“…During retinal development, shortening of the NMDAR-mediated currents is observed in rat RGCs and this event is prevented by dark rearing the animals for 1 month [41]. Furthermore, modifications of retinal NMDAR subunit expression are observed during development and by dark rearing [28,[41][42][43]. In addition, visual experience regulates the development of retinal circuitry itself.…”

Section: Introductionmentioning

confidence: 99%

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Age and Visual Experience-dependent Expression of NMDAR1 Splice Variants in Rat Retina

et al. 2011

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The N-methyl-D-aspartate receptor (NMDAR) is a key molecule mediating brain plasticity related processes. Knowing that alternative splicing of the NMDAR1 (NR1) subunit offers molecular diversity to NMDAR, controls the forward trafficking of the NR1 protein and is important for placing NMDA receptors at synapses, we investigated herein the postnatal developmental expression and the influence of visual deprivation on NR1 subunit splice variants in rat retina. Real-time PCR was performed using oligonucleotide primers specific for N- terminal (NR1a, NR1b) and C-terminal splice variants (NR1-1, NR1-2, NR1-3, NR1-4). The developmental profiles of mRNA expression levels of all NR1 isoforms peaked at the end of the third week. Dark rearing led to reductions in both N- and C-terminal NR1 variants in several developmental ages and a significant interaction between age and visual experience was observed for NR1a, NR1-2 and NR1-4 expression. Our results have demonstrated a developmental and visual experience-dependent regulation of NR1 splicing in rat retina.

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“…Oligodendrocytes are important and act as a negative regulatory activity, but are harmed by excessive Glu 149 . It is interesting to note that GluR activity is necessary for normal development of tectal cells 550,551 , probably through NMDA types of GluR 552 . Retinal photoreceptors, bipolar cells, and ganglion cells are can be visualized microscopically as they are Glu immunoreactive 68,71, [553][554][555][556][557][558][559] .…”

Section: Other Neurological Conditionsmentioning

confidence: 99%

A Review of Glutamate Receptors II: Pathophysiology and Pathology

Rousseaux

2008

J Toxicol Pathol

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Seventy years ago it was discovered that glutamate plays a central role in brain metabolism and is abundant in the brain. Glutamate was then found to be the principal excitatory neurotransmitter in the brain. As stated in the first article of this series, there are three families of ionotropic receptors with intrinsic cation permeable channels: Nmethyl-D-aspartate [NMDA], α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid [AMPA] and kainate [Ka].Among these there are three groups of metabotropic, G protein-coupled glutamate receptors [mGluR] that modify neuronal and glial excitability through G protein subunits acting on membrane ion channels and second messengers such as diacylglycerol and cAMP. There are also two glial glutamate transporters and three neuronal transporters in the brain. Although glutamate is the most abundant amino acid in the diet, there is no evidence for brain damage in humans resulting from dietary glutamate. However, a Ka analog, domoate, is sometimes ingested accidentally in blue mussels; this potent toxin causes limbic seizures, which can lead to hippocampal and related pathology and amnesia. Endogenous glutamate may contribute to the brain damage occurring acutely after status epilepticus, cerebral ischemia or traumatic brain injury by activating NMDA, AMPA or mGluR 1 receptors. Glutamate may also contribute to chronic neurodegeneration in such disorders as amyotrophic lateral sclerosis and Huntington's disease. In animal models of cerebral ischemia and traumatic brain injury, NMDA and AMPA receptor antagonists protect against acute brain damage and delayed behavioral deficits. Other clinical conditions that may respond to drugs acting on glutamatergic transmission include epilepsy, amnesia, anxiety, hyperalgesia and psychosis. In this second part of this review, we will explore those diseases in which the pathophysiology and pathology are associated, in part, with the glutamate system. (J Toxicol Pathol 2008; 21: 133-173)

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Developmental plasticity of NMDA receptor function in the retina and the influence of light

Cited by 24 publications

References 46 publications

Choline acetyltransferase‐immunoreactive neurons in the retina of normal and dark‐reared turtle

Choline acetyltransferase‐immunoreactive neurons in the retina of normal and dark‐reared turtle

Age and Visual Experience-dependent Expression of NMDAR1 Splice Variants in Rat Retina

A Review of Glutamate Receptors II: Pathophysiology and Pathology

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