NMDA receptors and L-type voltage-gated Ca2+ channels mediate the expression of bidirectional homeostatic intrinsic plasticity in cultured hippocampal neurons

Neuroscience ◽  
2014 ◽  
Vol 277 ◽  
pp. 610-623 ◽  
Author(s):  
K.Y. Lee ◽  
H.J. Chung
Keyword(s):  
Nmda Receptors ◽  
Hippocampal Neurons ◽  
Voltage Gated ◽  
Intrinsic Plasticity ◽  
Ca2 Channels ◽  
Cultured Hippocampal Neurons

Glycine regulation of synaptic NMDA receptors in hippocampal neurons

1996 ◽  
Vol 76 (5) ◽  
pp. 3415-3424 ◽  
Author(s):  
K. S. Wilcox ◽  
R. M. Fitzsimonds ◽  
B. Johnson ◽  
M. A. Dichter
Keyword(s):  
Nmda Receptor ◽  
Nmda Receptors ◽  
Hippocampal Neurons ◽  
Time Course ◽  
Hippocampal Slices ◽  
Maximal Effect ◽  
Patch Clamp Technique ◽  
Whole Cell Patch Clamp ◽  
Dissociated Cell Culture ◽  
Cultured Hippocampal Neurons

1. Although glycine has been identified as a required coagonist with glutamate at N-methyl-D-aspartate (NMDA) receptors, the understanding of glycine's role in excitatory synaptic neurotransmission is quite limited. In the present study, we used the whole cell patch-clamp technique to examine the ability of glycine to regulate current flow through synaptic NMDA receptors at excitatory synapses between cultured hippocampal neurons and in acutely isolated hippocampal slices. 2. These studies demonstrate that the glycine modulatory site on the synaptic NMDA receptor is not saturated under baseline conditions and that increased glycine concentrations can markedly increased NMDA-receptor-mediated excitatory postsynaptic currents (EPSCs) in hippocampal neurons in both dissociated cell culture and in slice. Saturation of the maximal effect of glycine takes place at different concentrations for different cells in culture, suggesting the presence of heterogenous NMDA receptor subunit compositions. 3. Bath-applied glycine had no effect on the time course of EPSCs in either brain slice or culture, indicating that desensitization of the NMDA receptor is not prevented by glycine over the time course of an EPSC. 4. When extracellular glycine concentration is high, all miniature EPSCs recorded in the cultured hippocampal neurons contained NMDA components, indicating that segregation of non-NMDA receptors at individual synaptic boutons does not occur.

Both NMDA and non-NMDA receptors mediate glutamate stimulation induced cofilin rod formation in cultured hippocampal neurons

2012 ◽  
Vol 1486 ◽  
pp. 1-13 ◽  
Author(s):  
Ben Chen ◽  
Min Jiang ◽  
Mi Zhou ◽  
Lulan Chen ◽  
Xu Liu ◽  
...  
Keyword(s):  
Nmda Receptors ◽  
Hippocampal Neurons ◽  
Cultured Hippocampal Neurons

scholarly journals Facilitation versus depression in cultured hippocampal neurons determined by targeting of Ca2+ channel Cavβ4 versus Cavβ2 subunits to synaptic terminals

2007 ◽  
Vol 178 (3) ◽  
pp. 489-502 ◽  
Author(s):  
Mian Xie ◽  
Xiang Li ◽  
Jing Han ◽  
Daniel L. Vogt ◽  
Silke Wittemann ◽  
...  
Keyword(s):  
Transmitter Release ◽  
Hippocampal Neurons ◽  
Presynaptic Terminal ◽  
Paired Pulse ◽  
Physiological Properties ◽  
Specific Manner ◽  
A Subunit ◽  
Synaptic Distribution ◽  
Ca2 Channels ◽  
Cultured Hippocampal Neurons

Ca2+ channel β subunits determine the transport and physiological properties of high voltage–activated Ca2+ channel complexes. Our analysis of the distribution of the Cavβ subunit family members in hippocampal neurons correlates their synaptic distribution with their involvement in transmitter release. We find that exogenously expressed Cavβ4b and Cavβ2a subunits distribute in clusters and localize to synapses, whereas Cavβ1b and Cavβ3 are homogenously distributed. According to their localization, Cavβ2a and Cavβ4b subunits modulate the synaptic plasticity of autaptic hippocampal neurons (i.e., Cavβ2a induces depression, whereas Cavβ4b induces paired-pulse facilitation [PPF] followed by synaptic depression during longer stimuli trains). The induction of PPF by Cavβ4b correlates with a reduction in the release probability and cooperativity of the transmitter release. These results suggest that Cavβ subunits determine the gating properties of the presynaptic Ca2+ channels within the presynaptic terminal in a subunit-specific manner and may be involved in organization of the Ca2+ channel relative to the release machinery.

scholarly journals L-type Ca2+ channel–mediated Ca2+ influx adjusts neuronal mitochondrial function to physiological and pathophysiological conditions

2020 ◽  
Vol 13 (618) ◽  
pp. eaaw6923 ◽  
Author(s):  
Matej Hotka ◽  
Michal Cagalinec ◽  
Karlheinz Hilber ◽  
Livia Hool ◽  
Stefan Boehm ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Atp Synthase ◽  
Mitochondrial Function ◽  
Hippocampal Neurons ◽  
Mitochondrial Depolarization ◽  
Voltage Gated ◽  
Beneficial Effects ◽  
Reverse Mode ◽  
Cultured Hippocampal Neurons

L-type voltage-gated Ca2+ channels (LTCCs) are implicated in neurodegenerative processes and cell death. Accordingly, LTCC antagonists have been proposed to be neuroprotective, although this view is disputed, because intentional LTCC activation can also have beneficial effects. LTCC-mediated Ca2+ influx influences mitochondrial function, which plays a crucial role in the regulation of cell viability. Hence, we investigated the effect of modulating LTCC-mediated Ca2+ influx on mitochondrial function in cultured hippocampal neurons. To activate LTCCs, neuronal activity was stimulated by increasing extracellular K+ or by application of the GABAA receptor antagonist bicuculline. The activity of LTCCs was altered by application of an agonistic (Bay K8644) or an antagonistic (isradipine) dihydropyridine. Our results demonstrated that activation of LTCC-mediated Ca2+ influx affected mitochondrial function in a bimodal manner. At moderate stimulation strength, ATP synthase activity was enhanced, an effect that involved Ca2+-induced Ca2+ release from intracellular stores. In contrast, high LTCC-mediated Ca2+ loads led to a switch in ATP synthase activity to reverse-mode operation. This effect, which required nitric oxide, helped to prevent mitochondrial depolarization and sustained increases in mitochondrial Ca2+. Our findings indicate a complex role of LTCC-mediated Ca2+ influx in the tuning and maintenance of mitochondrial function. Therefore, the use of LTCC inhibitors to protect neurons from neurodegeneration should be reconsidered carefully.

scholarly journals Novel glycine-dependent inactivation of NMDA receptors in cultured hippocampal neurons

2012 ◽  
Vol 28 (5) ◽  
pp. 550-560 ◽  
Author(s):  
Yun-Feng Zhang ◽  
Xia Li ◽  
Liang-Liang Peng ◽  
Guo-Hua Wang ◽  
Kai-Fu Ke ◽  
...  
Keyword(s):  
Nmda Receptors ◽  
Hippocampal Neurons ◽  
Dependent Inactivation ◽  
Cultured Hippocampal Neurons
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