GABAA transmission is a critical step in the process of triggering homeostatic increases in quantal amplitude
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Mechanisms of GABAergic homeostatic plasticityHomeostatic synaptic plasticity in developing spinal networks driven by excitatory GABAergic currentsThe effect of repetitive transcranial magnetic stimulation on gamma oscillatory activity in schizophreniaNormal hearing is required for the emergence of long-lasting inhibitory potentiation in cortex.Pharmacological manipulation of GABA-driven activity in ovo disrupts the development of dendritic morphology but not the maturation of spinal cord network activity.Decreased spinal synaptic inputs to phrenic motor neurons elicit localized inactivity-induced phrenic motor facilitation.Mechanisms underlying spontaneous patterned activity in developing neural circuitsGABAergic synaptic scaling in embryonic motoneurons is mediated by a shift in the chloride reversal potential.Activity-dependent regulation of the binomial parameters p and n at the mouse neuromuscular junction in vivo.Activity blockade and GABAA receptor blockade produce synaptic scaling through chloride accumulation in embryonic spinal motoneurons and interneuronsRefuting the challenges of the developmental shift of polarity of GABA actions: GABA more exciting than ever!In vivo synaptic scaling is mediated by GluA2-lacking AMPA receptors in the embryonic spinal cord.Spontaneous Release Regulates Synaptic Scaling in the Embryonic Spinal Network In Vivo.Compensatory changes in cellular excitability, not synaptic scaling, contribute to homeostatic recovery of embryonic network activity.Timing of developmental sequences in different brain structures: physiological and pathological implications.The effects of endocannabinoid signaling on network activity in developing and motor circuits.GABAA receptor-mediated tonic depolarization in developing neural circuits.Model calcium sensors for network homeostasis: sensor and readout parameter analysis from a database of model neuronal networks.Compensation for variable intrinsic neuronal excitability by circuit-synaptic interactions.Regulation of synaptic scaling by action potential-independent miniature neurotransmission.Glucose is an adequate energy substrate for the depolarizing action of GABA and glycine in the neonatal rat spinal cord in vitro.Manipulations of spinal cord excitability evoke developmentally-dependent compensatory changes in the lamprey spinal cord.
P2860
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P2860
GABAA transmission is a critical step in the process of triggering homeostatic increases in quantal amplitude
description
2008 nî lūn-bûn
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2008年の論文
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2008年論文
@yue
2008年論文
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2008年論文
@zh-hk
2008年論文
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2008年論文
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2008年论文
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2008年论文
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2008年论文
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name
GABAA transmission is a critic ...... increases in quantal amplitude
@en
type
label
GABAA transmission is a critic ...... increases in quantal amplitude
@en
prefLabel
GABAA transmission is a critic ...... increases in quantal amplitude
@en
P2860
P356
P1476
GABAA transmission is a critic ...... increases in quantal amplitude
@en
P2093
Jennifer C Wilhelm
P2860
P304
11412-11417
P356
10.1073/PNAS.0806037105
P407
P50
P577
2008-08-04T00:00:00Z