The role of posthypoxic reoxygenation in destruction of cultured hippocampal neurons

1993 ◽  
Vol 115 (2) ◽  
pp. 120-122
Author(s):  
L. G. Khaspekov ◽  
A. A. Lyzhin ◽  
I. V. Viktorov
Keyword(s):  
Hippocampal Neurons ◽  
Cultured Hippocampal Neurons

Role of GluN2A and GluN2B subunits in the formation of filopodia and secondary dendrites in cultured hippocampal neurons

2011 ◽  
Vol 385 (2) ◽  
pp. 171-180 ◽  
Author(s):  
Frank Henle ◽  
Martina Dehmel ◽  
Jost Leemhuis ◽  
Catharina Fischer ◽  
Dieter K. Meyer
Keyword(s):  
Hippocampal Neurons ◽  
Cultured Hippocampal Neurons

Role of Presynaptic L-Type Ca2+ Channels in GABAergic Synaptic Transmission in Cultured Hippocampal Neurons

1999 ◽  
Vol 81 (3) ◽  
pp. 1225-1230 ◽  
Author(s):  
Kimmo Jensen ◽  
Morten Skovgaard Jensen ◽  
John D. C. Lambert
Keyword(s):  
Synaptic Transmission ◽  
Transmitter Release ◽  
Hippocampal Neurons ◽  
Low Frequency ◽  
Tetanic Stimulation ◽  
Vesicle Release ◽  
Gabaergic Synaptic Transmission ◽  
Cultured Hippocampal Neurons ◽  
40 Hz

Role of presynaptic L-type Ca2+ channels in GABAergic synaptic transmission in cultured hippocampal neurons. Using dual whole cell patch-clamp recordings of monosynaptic GABAergic inhibitory postsynaptic currents (IPSCs) in cultured rat hippocampal neurons, we have previously demonstrated posttetanic potentiation (PTP) of IPSCs. Tetanic stimulation of the GABAergic neuron leads to accumulation of Ca2+ in the presynaptic terminals. This enhances the probability of GABA-vesicle release for up to 1 min, which underlies PTP. In the present study, we have examined the effect of altering the probability of release on PTP of IPSCs. Baclofen (10 μM), which depresses presynaptic Ca2+ entry through N- and P/Q-type voltage-dependent Ca2+ channels (VDCCs), caused a threefold greater enhancement of PTP than did reducing [Ca2+]o to 1.2 mM, which causes a nonspecific reduction in Ca2+ entry. This finding prompted us to investigate whether presynaptic L-type VDCCs contribute to the Ca2+ accumulation in the boutons during spike activity. The L-type VDCC antagonist, nifedipine (10 μM), had no effect on single IPSCs evoked at 0.2 Hz but reduced the PTP evoked by a train of 40 Hz for 2 s by 60%. Another L-type VDCC antagonist, isradipine (5 μM), similarly inhibited PTP by 65%. Both L-type VDCC blockers also depressed IPSCs during the stimulation (i.e., they increased tetanic depression). The L-type VDCC “agonist” (−)BayK 8644 (4 μM) had no effect on PTP evoked by a train of 40 Hz for 2 s, which probably saturated the PTP process, but enhanced PTP evoked by a train of 1 s by 91%. In conclusion, the results indicate that L-type VDCCs do not participate in low-frequency synchronous transmitter release, but contribute to presynaptic Ca2+ accumulation during high-frequency activity. This helps maintain vesicle release during tetanic stimulation and also enhances the probability of transmitter release during the posttetanic period, which is manifest as PTP. Involvement of L-type channels in these processes represents a novel presynaptic regulatory mechanism at fast CNS synapses.

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.

Role of glutamatergic receptors and associated signaling in arsenic induced neurotoxicity and protective efficacy of curcumin in rat primary cultured hippocampal neurons

2015 ◽  
Vol 49 ◽  
pp. 115
Author(s):  
Pranay Srivastava ◽  
Vivek Kumar ◽  
Rajendra Shukla ◽  
Yogesh Dhuriya ◽  
Richa Gupta ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Protective Efficacy ◽  
Cultured Hippocampal Neurons

scholarly journals Overexpression of Tropomyosin Isoform Tpm3.1 Does Not Alter Synaptic Function in Hippocampal Neurons

2021 ◽  
Vol 22 (17) ◽  
pp. 9303
Author(s):  
Chanchanok Chaichim ◽  
Tamara Tomanic ◽  
Holly Stefen ◽  
Esmeralda Paric ◽  
Lucy Gamaroff ◽  
...  
Keyword(s):  
Dendritic Spines ◽  
Hippocampal Neurons ◽  
Brain Slices ◽  
Structure And Function ◽  
Spine Morphology ◽  
Dendritic Spine Morphology ◽  
And Function ◽  
Cultured Hippocampal Neurons

Tropomyosin (Tpm) has been regarded as the master regulator of actin dynamics. Tpms regulate the binding of the various proteins involved in restructuring actin. The actin cytoskeleton is the predominant cytoskeletal structure in dendritic spines. Its regulation is critical for spine formation and long-term activity-dependent changes in synaptic strength. The Tpm isoform Tpm3.1 is enriched in dendritic spines, but its role in regulating the synapse structure and function is not known. To determine the role of Tpm3.1, we studied the synapse structure and function of cultured hippocampal neurons from transgenic mice overexpressing Tpm3.1. We recorded hippocampal field excitatory postsynaptic potentials (fEPSPs) from brain slices to examine if Tpm3.1 overexpression alters long-term synaptic plasticity. Tpm3.1-overexpressing cultured neurons did not show a significantly altered dendritic spine morphology or synaptic activity. Similarly, we did not observe altered synaptic transmission or plasticity in brain slices. Furthermore, expression of Tpm3.1 at the postsynaptic compartment does not increase the local F-actin levels. The results suggest that although Tpm3.1 localises to dendritic spines in cultured hippocampal neurons, it does not have any apparent impact on dendritic spine morphology or function. This is contrary to the functional role of Tpm3.1 previously observed at the tip of growing neurites, where it increases the F-actin levels and impacts growth cone dynamics.

The role of G protein in muscarinic depolarization near resting potential in cultured hippocampal neurons

1993 ◽  
Vol 612 (1-2) ◽  
pp. 200-209 ◽  
Author(s):  
Leslee D. Brown ◽  
Kyeong-Man Kim ◽  
Yasuko Nakajima ◽  
Shigehiro Nakajima
Keyword(s):  
G Protein ◽  
Hippocampal Neurons ◽  
Resting Potential ◽  
Cultured Hippocampal Neurons
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