Experience-dependent plasticity without long-term depression by type 2 metabotropic glutamate receptors in developing visual cortex

Renger, John J.; Hartman, Kenichi N.; Tsuchimoto, Yoshiko; Yokoi, Mineto; Nakanishi, Shigetada; Hensch, Takao K.

doi:10.1073/pnas.022618799

Cited by 59 publications

(27 citation statements)

References 92 publications

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“…However, the role of type II mGluRs in visual cortical LTD remains unclear. In one study, the potent antagonist LY341495 was found ineffective in preventing LTD (Sawtell et al, 1999), whereas a complete block of LTD with the antagonist MCCG was reported recently (Renger et al, 2002). We examined the effects of 10 M MCCG (to selectively block type II mGluRs) and 100 M LY341495 (to block both, type I and type II mGluRs) on LTD under our experimental conditions.…”

Section: Resultsmentioning

confidence: 99%

Multiple Receptors Coupled to Phospholipase C Gate Long-Term Depression in Visual Cortex

Choi¹,

Chang²,

Jiang³

et al. 2005

J. Neurosci.

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Long-term depression (LTD) in sensory cortices depends on the activation of NMDA receptors. Here, we report that in visual cortical slices, the induction of LTD (but not long-term potentiation) also requires the activation of receptors coupled to the phospholipase C (PLC) pathway. Using immunolesions in combination with agonists and antagonists, we selectively manipulated the activation of ␣1 adrenergic, M1 muscarinic, and mGluR5 glutamatergic receptors. Inactivation of these PLC-coupled receptors prevents the induction of LTD, but only when the three receptors were inactivated together. LTD is fully restored by activating any one of them or by supplying intracellular D-myo-inositol-1,4,5-triphosphate (IP 3 ). LTD was also impaired by intracellular application of PLC or IP 3 receptor blockers, and it was absent in mice lacking PLC␤1, the predominant PLC isoform in the forebrain. We propose that visual cortical LTD requires a minimum of PLC activity that can be supplied independently by at least three neurotransmitter systems. This essential requirement places PLC-linked receptors in a unique position to control the induction of LTD and provides a mechanism for gating visual cortical plasticity via extra-retinal inputs in the intact organism.

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Section: Resultsmentioning

confidence: 99%

Multiple Receptors Coupled to Phospholipase C Gate Long-Term Depression in Visual Cortex

Choi¹,

Chang²,

Jiang³

et al. 2005

J. Neurosci.

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“…2 and 3A; ref. 15), suggesting that alternative mechanisms for disconnecting deprived eye input may be involved in a modest role, if at all (28).…”

Section: Discussionmentioning

confidence: 99%

Permissive proteolytic activity for visual cortical plasticity

Mataga

Nagai

Hensch

2002

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

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160

108

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The serine protease, tissue-type plasminogen activator (tPA) is a key regulator of extracellular proteolytic cascades. We demonstrate a requirement for tPA signaling in the experience-dependent plasticity of mouse visual cortex during the developmental critical period. Proteolytic activity by tPA in the binocular zone was typically increased within 2 days of monocular deprivation (MD). This regulation failed to occur in glutamic acid decarboxylase (GAD) 65 knockout mice, an animal model of impaired ocular dominance plasticity because of reduced ␥-aminobutyric acid (GABA)-mediated transmission described previously. Loss of responsiveness to the deprived eye consequent to MD was conversely suppressed in mice lacking tPA despite normal levels of neuronal activity. Plasticity was restored in a gene dose-dependent manner, or by direct tPA infusion. Permissive amounts of tPA may, thus, couple functional to structural changes downstream of the excitatory-inhibitory balance that triggers visual cortical plasticity. Our results not only support a molecular cascade leading to neurite outgrowth after sensory deprivation, but also identify a valuable tool for further proteomic and genomic dissection of experiencedependent plasticity downstream of electrical activity.

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“…As Daw et al (29) have pointed out, closer attention to laminar differences in LTD and ocular dominance plasticity may help resolve some of the lingering controversies in the field (see, e.g., ref. 30).…”

Section: Discussionmentioning

confidence: 99%

Deprivation-induced synaptic depression by distinct mechanisms in different layers of mouse visual cortex

Crozier

Wang

Liu

et al. 2007

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

145

183

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Long-term depression (LTD) induced by low-frequency synaptic stimulation (LFS) was originally introduced as a model to probe potential mechanisms of deprivation-induced synaptic depression in visual cortex. In hippocampus, LTD requires activation of postsynaptic NMDA receptors, PKA, and the clathrin-dependent endocytosis of ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. It has long been assumed that LTD induced in visual cortical layer 2/3 by LFS of layer 4 uses similar mechanisms. Here we show in mouse visual cortex that this conclusion requires revision. We find that LTD induced in layer 2/3 by LFS is unaffected by inhibitors of PKA or ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor endocytosis but is reliably blocked by an endocannabinoid CB1 receptor antagonist. Conversely, LFS applied to synapses on layer 4 neurons produces LTD that appears mechanistically identical to that in CA1 and is insensitive to CB1 blockers. Occlusion experiments suggest that both mechanisms contribute to the loss of visual responsiveness after monocular deprivation.endocannabinoid ͉ glutamate receptor ͉ long-term depression ͉ ocular dominance plasticity

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Experience-dependent plasticity without long-term depression by type 2 metabotropic glutamate receptors in developing visual cortex

Cited by 59 publications

References 92 publications

Multiple Receptors Coupled to Phospholipase C Gate Long-Term Depression in Visual Cortex

Multiple Receptors Coupled to Phospholipase C Gate Long-Term Depression in Visual Cortex

Permissive proteolytic activity for visual cortical plasticity

Deprivation-induced synaptic depression by distinct mechanisms in different layers of mouse visual cortex

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