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Literature DB >> 19252494

Thalamic activity that drives visual cortical plasticity.

Monica L Linden¹, Arnold J Heynen, Robert H Haslinger, Mark F Bear.

Abstract

Manipulations of activity in one retina can profoundly affect binocular connections in the visual cortex. Retinal activity is relayed to the cortex by the dorsal lateral geniculate nucleus (dLGN). We compared the qualities and amount of activity in the dLGN following monocular eyelid closure and monocular retinal inactivation in awake mice. Our findings substantially alter the interpretation of previous studies and define the afferent activity patterns that trigger cortical plasticity.

Entities: Chemical

Mesh：

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Year: 2009 PMID： 19252494 PMCID： PMC2669755 DOI： 10.1038/nn.2284

Source DB: PubMed Journal: Nat Neurosci ISSN： 1097-6256 Impact factor: 24.884

14 in total

1. Correlational structure of spontaneous neuronal activity in the developing lateral geniculate nucleus in vivo.

Authors: M Weliky; L C Katz
Journal: Science Date: 1999-07-23 Impact factor: 47.728

2. Critical periods for experience-dependent synaptic scaling in visual cortex.

Authors: Niraj S Desai; Robert H Cudmore; Sacha B Nelson; Gina G Turrigiano
Journal: Nat Neurosci Date: 2002-08 Impact factor: 24.884

3. Effects of membrane voltage on receptive field properties of lateral geniculate neurons in the cat: contributions of the low-threshold Ca2+ conductance.

Authors: S M Lu; W Guido; S M Sherman
Journal: J Neurophysiol Date: 1992-12 Impact factor: 2.714

Review 9. How the mechanisms of long-term synaptic potentiation and depression serve experience-dependent plasticity in primary visual cortex.

Authors: Sam F Cooke; Mark F Bear
Journal: Philos Trans R Soc Lond B Biol Sci Date: 2013-12-02 Impact factor: 6.237

10. Synaptic and intrinsic homeostatic mechanisms cooperate to increase L2/3 pyramidal neuron excitability during a late phase of critical period plasticity.

Authors: Mary E Lambo; Gina G Turrigiano
Journal: J Neurosci Date: 2013-05-15 Impact factor: 6.167

Thalamic activity that drives visual cortical plasticity.

1. Correlational structure of spontaneous neuronal activity in the developing lateral geniculate nucleus in vivo.

2. Critical periods for experience-dependent synaptic scaling in visual cortex.

3. Effects of membrane voltage on receptive field properties of lateral geniculate neurons in the cat: contributions of the low-threshold Ca2+ conductance.

4. How monocular deprivation shifts ocular dominance in visual cortex of young mice.

5. Population imaging of ongoing neuronal activity in the visual cortex of awake rats.

6. Effects of nerve growth factor on visual cortical plasticity require afferent electrical activity.

7. Experience-dependent plasticity of binocular responses in the primary visual cortex of the mouse.

8. Activity-dependent regulation of NMDAR1 immunoreactivity in the developing visual cortex.

9. Binocular impulse blockade prevents the formation of ocular dominance columns in cat visual cortex.

10. Monocular deprivation induces homosynaptic long-term depression in visual cortex.

1. Visual deprivation suppresses L5 pyramidal neuron excitability by preventing the induction of intrinsic plasticity.

2. Temporally coherent visual stimuli boost ocular dominance plasticity.

3. Neural heterogeneities determine response characteristics to second-, but not first-order stimulus features.

4. Thalamic Bursts and Single Spikes Evoke Distinct Inhibitory States in the Primary Sensory Cortex.

Review 5. The BCM theory of synapse modification at 30: interaction of theory with experiment.

6. A pilot randomized trial of contrast-rebalanced binocular treatment for deprivation amblyopia.

7. Maturation of GABAergic inhibition promotes strengthening of temporally coherent inputs among convergent pathways.

8. Synaptic plasticity controls sensory responses through frequency-dependent gamma oscillation resonance.

Review 9. How the mechanisms of long-term synaptic potentiation and depression serve experience-dependent plasticity in primary visual cortex.

10. Synaptic and intrinsic homeostatic mechanisms cooperate to increase L2/3 pyramidal neuron excitability during a late phase of critical period plasticity.