Interleukin 6 trans-signaling regulates basal synaptic transmission and sensitivity to pentylenetetrazole-induced seizures in mice

Synapse ◽  
2017 ◽  
Vol 71 (9) ◽  
pp. e21984 ◽  
Author(s):  
Roberto Cuevas-Olguin ◽  
Eric Esquivel-Rendon ◽  
Jorge Vargas-Mireles ◽  
Francisco Garcia-Oscos ◽  
Marcela Miranda-Morales ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Interleukin 6 ◽  
Basal Synaptic Transmission

scholarly journals Basal Synaptic Transmission: Astrocytes Rule!

Cell ◽  
2011 ◽  
Vol 146 (5) ◽  
pp. 675-677 ◽  
Author(s):  
Marta Navarrete ◽  
Alfonso Araque
Keyword(s):  
Synaptic Transmission ◽  
Basal Synaptic Transmission

scholarly journals σ2-Adaptin Facilitates Basal Synaptic Transmission and Is Required for Regenerating Endo-Exo Cycling Pool Under High-Frequency Nerve Stimulation in Drosophila

Genetics ◽  
2016 ◽  
Vol 203 (1) ◽  
pp. 369-385 ◽  
Author(s):  
Saumitra Dey Choudhury ◽  
Zeeshan Mushtaq ◽  
Suneel Reddy-Alla ◽  
Sruthi S. Balakrishnan ◽  
Rajan S. Thakur ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Nerve Stimulation ◽  
High Frequency ◽  
Basal Synaptic Transmission

scholarly journals The Kinase Function of MSK1 Regulates BDNF Signaling to CREB and Basal Synaptic Transmission, But Is Not Required for Hippocampal Long-Term Potentiation or Spatial Memory

eNeuro ◽  
2017 ◽  
Vol 4 (1) ◽  
pp. ENEURO.0212-16.2017 ◽  
Author(s):  
Stephanie Daumas ◽  
Christopher J. Hunter ◽  
Rajen B. Mistry ◽  
Lorenzo Morè ◽  
Lucia Privitera ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Spatial Memory ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Bdnf Signaling ◽  
Basal Synaptic Transmission

Lack of AMPA Receptor Desensitization During Basal Synaptic Transmission in the Hippocampal Slice

1999 ◽  
Vol 81 (6) ◽  
pp. 3096-3099 ◽  
Author(s):  
Gregory O. Hjelmstad ◽  
John T. R. Isaac ◽  
Roger A. Nicoll ◽  
Robert C. Malenka
Keyword(s):  
Synaptic Transmission ◽  
Ampa Receptor ◽  
Ampa Receptors ◽  
Hippocampal Slice ◽  
Hippocampal Slices ◽  
Release Site ◽  
Pyramidal Cells ◽  
Receptor Desensitization ◽  
Synaptic Receptors ◽  
Basal Synaptic Transmission

Lack of AMPA receptor desensitization during basal synaptic transmission in the hippocampal slice. Excitatory postsynaptic currents in the CA1 region of rat hippocampal slices are mediated primarily by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in response to synaptically released glutamate. Outside-out patches from pyramidal cells in this region have shown that AMPA receptors are desensitized by short (1 ms) pulses of glutamate. We have taken a number of approaches to ask whether synaptic receptors desensitize in response to synaptically released glutamate in the slice. Recordings with paired pulses and minimal stimulation conditions that are presumably activating only a single release site do not show evidence for desensitization. Furthermore, cyclothiazide, a drug that blocks desensitization, does not alter paired-pulse ratios even under conditions of high probability of release, which should maximize desensitization. These results suggest that synaptic receptors do not desensitize in response to synaptically released glutamate during basal synaptic transmission.

scholarly journals Basal Synaptic Transmission and Long-Term Plasticity at CA3-CA1 Synapses Are Unaffected in Young Adult PINK1-Deficient Rats

2021 ◽  
Vol 15 ◽  
Author(s):  
Adeel A. Memon ◽  
Micah E. Bagley ◽  
Rose B. Creed ◽  
Amy W. Amara ◽  
Matthew S. Goldberg ◽  
...  
Keyword(s):  
Young Adult ◽  
Synaptic Transmission ◽  
Projection Neurons ◽  
Excitatory Postsynaptic Potential ◽  
Excitatory Synapses ◽  
Motor Symptoms ◽  
Excitatory Transmission ◽  
The Impact ◽  
Basal Synaptic Transmission

Loss of function mutations in PARK6, the gene that encodes the protein PTEN-induced kinase 1 (PINK1), cause autosomal recessive familial Parkinson’s disease (PD). While PD is clinically diagnosed by its motor symptoms, recent studies point to the impact of non-motor symptoms, including cognitive dysfunction in the early pre-motor stages of the disease (Aarsland et al., 2004; Chaudhuri and Schapira, 2009). As the hippocampus is a key structure for learning and memory, this study aimed to determine whether synaptic transmission is affected at CA3-CA1 excitatory synapses in PINK1 knockout rats at an age when we recently reported a gain of function at excitatory synapses onto spiny projection neurons in the dorsal striatum (Creed et al., 2020) and when motor symptoms are beginning to appear (Dave et al., 2014). Using extracellular dendritic field excitatory postsynaptic potential recordings at CA3-CA1 synapses in dorsal hippocampus 4-to 5- month old PINK1 KO rats and wild-type littermate controls, we observed no detectable differences in the strength of basal synaptic transmission, paired-pulse facilitation, or long-term potentiation. Our results suggest that loss of PINK1 protein does not cause a general dysfunction of excitatory transmission throughout the brain at this young adult age when excitatory transmission is abnormal in the striatum.

Activation of Postsynaptic Ca2+ Stores Modulates Glutamate Receptor Cycling in Hippocampal Neurons

2005 ◽  
Vol 93 (1) ◽  
pp. 178-188 ◽  
Author(s):  
Brady J. Maher ◽  
Roger L. MacKinnon ◽  
Jihong Bai ◽  
Edwin R. Chapman ◽  
Paul T. Kelly
Keyword(s):  
Synaptic Transmission ◽  
Glutamate Receptor ◽  
Hippocampal Neurons ◽  
Pdz Domain ◽  
Interacting Protein ◽  
Hippocampal Ca1 ◽  
Adenophostin A ◽  
Vesicle Exocytosis ◽  
Ampar Trafficking ◽  
Basal Synaptic Transmission

We show that activation of postsynaptic inositol 1,4,5-tris-phosphate receptors (IP3Rs) with the IP3R agonist adenophostin A (AdA) produces large increases in AMPA receptor (AMPAR) excitatory postsynaptic current (EPSC) amplitudes at hippocampal CA1 synapses. Co-perfusion of the Ca2+ chelator bis-( o-aminophenoxy)- N,N,N′,N′-tetraacetic acid strongly inhibited AdA-enhanced increases in EPSC amplitudes. We examined the role of AMPAR insertion/anchoring in basal synaptic transmission. Perfusion of an inhibitor of synaptotagmin-soluble n-ethylmaleimide-sensitive factor attachment protein (SNAP) receptor SNARE-mediated exocytosis depressed basal EPSC amplitudes, whereas a peptide that inhibits GluR2/3 interactions with postsynaptic density-95 (PDZ) domain proteins glutamate receptor interacting protein (GRIP)/protein interacting with C-kinase-1 (PICK1) enhanced basal synaptic transmission. These results suggest that constitutive trafficking and anchoring of AMPARs help maintain basal synaptic transmission. The regulation of postsynaptic AMPAR trafficking involves synaptotagmin-SNARE-mediated vesicle exocytosis and interactions between AMPARs and the PDZ domains in GRIP/PICK1. We show that inhibitors of synaptotagmin-SNARE-mediated exocytosis, or interactions between AMPARs and GRIP/PICK1, attenuated AdA-enhanced increases in EPSC amplitudes. These results suggest that IP3R-mediated Ca2+ release can enhance AMPAR EPSC amplitudes through mechanisms that involve AMPAR-PDZ interactions and/or synaptotagmin-SNARE-mediated receptor trafficking.

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