scholarly journals Crucial Role of Postsynaptic Syntaxin 4 in Mediating Basal Neurotransmission and Synaptic Plasticity in Hippocampal CA1 Neurons

Cell Reports ◽  
2018 ◽  
Vol 23 (10) ◽  
pp. 2955-2966 ◽  
Author(s):  
Na-Ryum Bin ◽  
Ke Ma ◽  
Hidekiyo Harada ◽  
Chi-Wei Tien ◽  
Fiona Bergin ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Crucial Role ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1 ◽  
Syntaxin 4

scholarly journals Potential Role of PUMA in Delayed Death of Hippocampal CA1 Neurons After Transient Global Cerebral Ischemia

Stroke ◽  
2009 ◽  
Vol 40 (2) ◽  
pp. 618-625 ◽  
Author(s):  
Kuniyasu Niizuma ◽  
Hidenori Endo ◽  
Chikako Nito ◽  
D. Jeannie Myer ◽  
Pak H. Chan
Keyword(s):  
Cerebral Ischemia ◽  
Potential Role ◽  
Global Cerebral Ischemia ◽  
Ca1 Neurons ◽  
Transient Global Cerebral Ischemia ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1 ◽  
Delayed Death

scholarly journals Syntaxin-3 is dispensable for basal neurotransmission and synaptic plasticity in postsynaptic hippocampal CA1 neurons

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Shan Shi ◽  
Ke Ma ◽  
Na-Ryum Bin ◽  
Hidekiyo Harada ◽  
Xiaoyu Xie ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1 ◽  
Syntaxin 3

scholarly journals Inactivation of Presenilin in inhibitory neurons results in decreased GABAergic responses and enhanced synaptic plasticity

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Sang Hun Lee ◽  
Vadim Y. Bolshakov ◽  
Jie Shen
Keyword(s):  
Synaptic Plasticity ◽  
Calcium Homeostasis ◽  
Hippocampal Slices ◽  
Field Potential ◽  
Long Term Potentiation ◽  
Ca1 Neurons ◽  
Paired Pulse ◽  
Inhibitory Neurotransmission ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1

AbstractMutations in the Presenilin genes are the major genetic cause of Alzheimer's disease (AD). Presenilin (PS) is highly expressed in the hippocampus, which is particularly vulnerable in AD. Previous studies of PS function in the hippocampus, however, focused exclusively on excitatory neurons. Whether PS regulates inhibitory neuronal function remained unknown. In the current study, we investigate PS function in GABAergic neurons by performing whole-cell and field-potential electrophysiological recordings using acute hippocampal slices from inhibitory neuron-specific PS conditional double knockout (IN-PS cDKO) mice at 2 months of age, before the onset of age-dependent loss of interneurons. We found that the frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) is reduced in hippocampal CA1 neurons of IN-PS cDKO mice, whereas the amplitude of sIPSCs is normal. Moreover, the efficacy of inhibitory neurotransmission as assessed with synaptic input/output relations for evoked mono- and di-synaptic IPSCs is markedly lowered in hippocampal CA1 neurons of IN-PS cDKO mice. Consistent with these findings, IN-PS cDKO mice display enhanced paired-pulse facilitation, frequency facilitation and long-term potentiation in the Schaffer collateral-CA1 pathway. Interestingly, depletion of intracellular Ca2+ stores by inhibition of sarcoendoplasmic reticulum Ca2+ ATPase results in a reduction of IPSC amplitude in control hippocampal neurons but not in IN-PS cDKO neurons, suggesting that impaired intracellular calcium homeostasis in the absence of PS may contribute to the deficiencies in inhibitory neurotransmission. Furthermore, the amplitude of IPSCs induced by short trains of presynaptic stimulation and paired-pulse ratio are decreased in IN-PS cDKO mice. These findings show that inactivation of PS in interneurons results in decreased GABAergic responses and enhanced synaptic plasticity in the hippocampus, providing additional evidence for the importance of PS in the regulation of synaptic plasticity and calcium homeostasis.

Role of postsynaptic inositol 1, 4, 5-trisphosphate receptors in depotentiation in guinea pig hippocampal CA1 neurons

2016 ◽  
Vol 1642 ◽  
pp. 154-162 ◽  
Author(s):  
Makoto Sugita ◽  
Yoshihiko Yamazaki ◽  
Jun-Ichi Goto ◽  
Hiroki Fujiwara ◽  
Takeshi Aihara ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Ca1 Neurons ◽  
Inositol 1 ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1

Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway

2018 ◽  
Vol 96 (1) ◽  
pp. 80-87 ◽  
Author(s):  
Maedeh Arabian ◽  
Nahid Aboutaleb ◽  
Mansoureh Soleimani ◽  
Marjan Ajami ◽  
Rouhollah Habibey ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Mtor Pathway ◽  
Morphine Treatment ◽  
Chronic Morphine ◽  
Sod Activity ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1 ◽  
Chronic Morphine Treatment

The signaling pathway of chronic morphine treatment to prevent neuronal damage following transient cerebral ischemia is not clear. In this study, we examined the role of mammalian target of rapamycin (mTOR) to identify the neuroprotective effects of chronic morphine preconditioning on the hippocampus following ischemia–reperfusion (I/R) injury. Morphine was administered for 5 days, twice a day, before inducing I/R injury. The possible role of mTOR was evaluated by the injection of rapamycin (5 mg/kg body weight, by intraperitoneal injection) before I/R was induced. The passive avoidance test was used to evaluate memory performance. Neuronal density and apoptosis were measured in the CA1 region, 72 h after I/R injury. The expressions of mTOR and phosphorylated mTOR (p-mTOR), as well as superoxide dismutase (SOD) activity were determined 24 h after I/R injury. Chronic morphine treatment attenuated apoptosis and neuronal loss in the hippocampus after I/R injury, which led to improvement in memory (P < 0.05 vs. untreated I/R) and increase in the expression of p-mTOR (P < 0.05 vs. untreated I/R) and SOD activity (P < 0.05 vs. untreated I/R) in the hippocampus. Pretreatment with rapamycin abolished all the above-mentioned protective effects. These results describe novel findings whereby chronic morphine preconditioning in hippocampal CA1 neurons is mediated by the mTOR pathway, and through increased phosphorylation of mTOR can alleviate oxidative stress and apoptosis, and eventually protect the hippocampus from I/R injury.

Changes in [Ca2+]i during adenosine triphosphate-induced synaptic plasticity in hippocampal CA1 neurons of the guinea pig

2002 ◽  
Vol 324 (1) ◽  
pp. 65-68 ◽  
Author(s):  
Yoshihiko Yamazaki ◽  
Satoshi Fujii ◽  
Takeshi Nakamura ◽  
Hiroyoshi Miyakawa ◽  
Yoshihisa Kudo ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Guinea Pig ◽  
Adenosine Triphosphate ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1
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