Structural and functional plasticity of astrocyte processes and dendritic spine interactions
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Structural and functional plasticity of astrocyte processes and dendritic spine interactions. / Perez-Alvarez, Alberto; Navarrete, Marta; Covelo, Ana; Martin, Eduardo D; Araque, Alfonso.
In: J NEUROSCI, Vol. 34, No. 38, 17.09.2014, p. 12738-44.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Structural and functional plasticity of astrocyte processes and dendritic spine interactions
AU - Perez-Alvarez, Alberto
AU - Navarrete, Marta
AU - Covelo, Ana
AU - Martin, Eduardo D
AU - Araque, Alfonso
N1 - alle EXTERNE sind INTERNE
PY - 2014/9/17
Y1 - 2014/9/17
N2 - Experience-dependent plasticity of synaptic transmission, which represents the cellular basis of learning, is accompanied by morphological changes in dendritic spines. Astrocytic processes are intimately associated with synapses, structurally enwrapping and functionally interacting with dendritic spines and synaptic terminals by responding to neurotransmitters and by releasing gliotransmitters that regulate synaptic function. While studies on structural synaptic plasticity have focused on neuronal elements, the structural-functional plasticity of astrocyte-neuron relationships remains poorly known. Here we show that stimuli inducing hippocampal synaptic LTP enhance the motility of synapse-associated astrocytic processes. This motility increase is relatively rapid, starting <5 min after the stimulus, and reaching a maximum in 20-30 min (t(1/2) = 10.7 min). It depends on presynaptic activity and requires G-protein-mediated Ca(2+) elevations in astrocytes. The structural remodeling is accompanied by changes in the ability of astrocytes to regulate synaptic transmission. Sensory stimuli that increase astrocyte Ca(2+) also induce similar plasticity in mouse somatosensory cortex in vivo. Therefore, structural relationships between astrocytic processes and dendritic spines undergo activity-dependent changes with metaplasticity consequences on synaptic regulation. These results reveal novel forms of synaptic plasticity based on structural-functional changes of astrocyte-neuron interactions.
AB - Experience-dependent plasticity of synaptic transmission, which represents the cellular basis of learning, is accompanied by morphological changes in dendritic spines. Astrocytic processes are intimately associated with synapses, structurally enwrapping and functionally interacting with dendritic spines and synaptic terminals by responding to neurotransmitters and by releasing gliotransmitters that regulate synaptic function. While studies on structural synaptic plasticity have focused on neuronal elements, the structural-functional plasticity of astrocyte-neuron relationships remains poorly known. Here we show that stimuli inducing hippocampal synaptic LTP enhance the motility of synapse-associated astrocytic processes. This motility increase is relatively rapid, starting <5 min after the stimulus, and reaching a maximum in 20-30 min (t(1/2) = 10.7 min). It depends on presynaptic activity and requires G-protein-mediated Ca(2+) elevations in astrocytes. The structural remodeling is accompanied by changes in the ability of astrocytes to regulate synaptic transmission. Sensory stimuli that increase astrocyte Ca(2+) also induce similar plasticity in mouse somatosensory cortex in vivo. Therefore, structural relationships between astrocytic processes and dendritic spines undergo activity-dependent changes with metaplasticity consequences on synaptic regulation. These results reveal novel forms of synaptic plasticity based on structural-functional changes of astrocyte-neuron interactions.
KW - Action Potentials
KW - Animals
KW - Astrocytes
KW - Calcium
KW - Dendritic Spines
KW - Female
KW - Hippocampus
KW - Long-Term Potentiation
KW - Male
KW - Mice
KW - Neuronal Plasticity
KW - Somatosensory Cortex
KW - Synaptic Transmission
U2 - 10.1523/JNEUROSCI.2401-14.2014
DO - 10.1523/JNEUROSCI.2401-14.2014
M3 - SCORING: Journal article
C2 - 25232111
VL - 34
SP - 12738
EP - 12744
JO - J NEUROSCI
JF - J NEUROSCI
SN - 0270-6474
IS - 38
ER -