Deciphering the functional nano‐anatomy of the tripartite synapse using s timulated emission depletion microscopy

Glia ◽  
2021 ◽  
Author(s):  
Misa Arizono ◽  
U. Valentin Nägerl
Keyword(s):  
Tripartite Synapse

Astroglial type-1 cannabinoid receptor (CB1): A new player in the tripartite synapse

Neuroscience ◽  
2016 ◽  
Vol 323 ◽  
pp. 35-42 ◽  
Author(s):  
J.F. Oliveira da Cruz ◽  
L.M. Robin ◽  
F. Drago ◽  
G. Marsicano ◽  
M. Metna-Laurent
Keyword(s):  
Cannabinoid Receptor ◽  
Tripartite Synapse ◽  
Type 1 Cannabinoid Receptor

scholarly journals Urokinase-type plasminogen activator (uPA) protects the tripartite synapse in the ischemic brain via ezrin-mediated formation of peripheral astrocytic processes

2018 ◽  
Vol 39 (11) ◽  
pp. 2157-2171 ◽  
Author(s):  
Ariel Diaz ◽  
Paola Merino ◽  
Luis G Manrique ◽  
Lihong Cheng ◽  
Manuel Yepes
Keyword(s):  
Ischemic Stroke ◽  
Plasminogen Activator ◽  
Harmful Effect ◽  
Ischemic Injury ◽  
Adult Brain ◽  
Subsequent Formation ◽  
Ischemic Brain ◽  
Tripartite Synapse ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator

Cerebral ischemia has a harmful effect on the synapse associated with neurological impairment. The “tripartite synapse” is assembled by the pre- and postsynaptic terminals, embraced by astrocytic elongations known as peripheral astrocytic processes (PAPs). Ischemic stroke induces the detachment of PAPs from the synapse, leading to synaptic dysfunction and neuronal death. Ezrin is a membrane-associated protein, required for the formation of PAPs, that links the cell surface to the actin cytoskeleton. Urokinase-type plasminogen activator (uPA) is a serine proteinase that upon binding to its receptor (uPAR) promotes neurite growth during development. In the adult brain, neurons release uPA and astrocytes recruit uPAR to the plasma membrane during the recovery phase from an ischemic stroke, and uPA/uPAR binding promotes functional improvement following an ischemic injury. We found that uPA induces the synthesis of ezrin in astrocytes, with the subsequent formation of PAPs that enter in direct contact with the synapse. Furthermore, either the release of neuronal uPA or intravenous treatment with recombinant uPA (ruPA) induces the formation of PAPs in the ischemic brain, and the interaction of these PAPs with the pre- and postsynaptic terminals protects the integrity of the “tripartite synapse” from the harmful effects of the ischemic injury.

scholarly journals Diverse Actions of Astrocytes in GABAergic Signaling

2019 ◽  
Vol 20 (12) ◽  
pp. 2964 ◽  
Author(s):  
Masaru Ishibashi ◽  
Kiyoshi Egawa ◽  
Atsuo Fukuda
Keyword(s):  
Synaptic Transmission ◽  
Crucial Role ◽  
Synaptic Cleft ◽  
Critical Component ◽  
Gaba Concentration ◽  
Tripartite Synapse ◽  
Inhibitory Synaptic Transmission ◽  
Inhibitory Neurotransmission

An imbalance of excitatory and inhibitory neurotransmission leading to over excitation plays a crucial role in generating seizures, while enhancing GABAergic mechanisms are critical in terminating seizures. In recent years, it has been reported in many studies that astrocytes are deeply involved in synaptic transmission. Astrocytes form a critical component of the “tripartite” synapses by wrapping around the pre- and post-synaptic elements. From this location, astrocytes are known to greatly influence the dynamics of ions and transmitters in the synaptic cleft. Despite recent extensive research on excitatory tripartite synapses, inhibitory tripartite synapses have received less attention, even though they influence inhibitory synaptic transmission by affecting chloride and GABA concentration dynamics. In this review, we will discuss the diverse actions of astrocytic chloride and GABA homeostasis at GABAergic tripartite synapses. We will then consider the pathophysiological impacts of disturbed GABA homeostasis at the tripartite synapse.

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