Depletion type floating gate p-channel MOS transistor for recording action potentials generated by cultured neurons

2004 ◽  
Vol 19 (12) ◽  
pp. 1703-1709 ◽  
Author(s):  
Ariel Cohen ◽  
Micha E Spira ◽  
Shlomo Yitshaik ◽  
Gustaaf Borghs ◽  
Ofer Shwartzglass ◽  
...  
Keyword(s):  
Action Potentials ◽  
Floating Gate ◽  
Cultured Neurons ◽  
Mos Transistor

Inertial sensing MEMS device using a floating-gate MOS transistor as transducer by means of modifying the capacitance associated to the floating gate

2017 ◽  
Vol 24 (6) ◽  
pp. 2753-2764 ◽  
Author(s):  
G. S. Abarca-Jiménez ◽  
J. Mares-Carreño ◽  
M. A. Reyes-Barranca ◽  
B. Granados-Rojas ◽  
S. Mendoza-Acevedo ◽  
...  
Keyword(s):  
Floating Gate ◽  
Inertial Sensing ◽  
Mos Transistor ◽  
Mems Device

Effects of Ca ions on action potentials in immature cultured neurons from chick cerebral cortex

1982 ◽  
Vol 110 (3) ◽  
pp. 241-244 ◽  
Author(s):  
Junko Mori ◽  
Hiroshi Ashida ◽  
Eiichi Maru ◽  
Jiro Tatsuno
Keyword(s):  
Cerebral Cortex ◽  
Action Potentials ◽  
Cultured Neurons ◽  
Ca Ions ◽  
Chick Cerebral Cortex

scholarly journals Doc2b Ca2+ binding site mutants enhance synaptic release at rest at the expense of sustained synaptic strength

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Quentin Bourgeois-Jaarsma ◽  
Matthijs Verhage ◽  
Alexander J. Groffen
Keyword(s):  
Binding Site ◽  
Neurotransmitter Release ◽  
Action Potentials ◽  
Synaptic Strength ◽  
Cultured Neurons ◽  
Loss Of Function ◽  
Short Term ◽  
Synaptic Release ◽  
Activated State ◽  
Primary Cultured Neurons

Abstract Communication between neurons involves presynaptic neurotransmitter release which can be evoked by action potentials or occur spontaneously as a result of stochastic vesicle fusion. The Ca2+-binding double C2 proteins Doc2a and –b were implicated in spontaneous and asynchronous evoked release, but the mechanism remains unclear. Here, we compared wildtype Doc2b with two Ca2+ binding site mutants named DN and 6A, previously classified as gain- and loss-of-function mutants. They carry the substitutions D218,220N or D163,218,220,303,357,359A respectively. We found that both mutants bound phospholipids at low Ca2+ concentrations and were membrane-associated in resting neurons, thus mimicking a Ca2+-activated state. Their overexpression in hippocampal primary cultured neurons had similar effects on spontaneous and evoked release, inducing high mEPSC frequencies and increased short-term depression. Together, these data suggest that the DN and 6A mutants both act as gain-of-function mutants at resting conditions.

Some simulated properties of the pseudostructure of a floating gate MOS transistor

2009 ◽  
Author(s):  
Daniela Durackova ◽  
Mario Krajmer ◽  
Juraj Racko ◽  
Juraj Breza ◽  
Magdalena Kadlecikova
Keyword(s):  
Floating Gate ◽  
Mos Transistor

scholarly journals Large, stable spikes exhibit differential broadening in excitatory and inhibitory neocortical boutons

2020 ◽  
Author(s):  
Andreas Ritzau-Jost ◽  
Timur Tsintsadze ◽  
Martin Krueger ◽  
Jonas Ader ◽  
Ingo Bechmann ◽  
...  
Keyword(s):  
Patch Clamp ◽  
High Frequency ◽  
Neurotransmitter Release ◽  
Action Potentials ◽  
Pyramidal Neurons ◽  
Cultured Neurons ◽  
Presynaptic Action ◽  
Presynaptic Spike ◽  
Fast Spiking

SUMMARYPresynaptic action potential spikes control neurotransmitter release and thus interneuronal communication. However, the properties and the dynamics of presynaptic spikes in the neocortex remain enigmatic because boutons in the neocortex are small and direct patch-clamp recordings have not been performed. Here we report direct recordings from boutons of neocortical pyramidal neurons and interneurons. Our data reveal rapid and large presynaptic action potentials in layer 5 neurons and fast-spiking interneurons reliably propagating into axon collaterals. For in-depth analyses we validate boutons of mature cultured neurons as models for excitatory neocortical boutons, demonstrating that the presynaptic spike amplitude was unaffected by potassium channels, homeostatic long-term plasticity, and high-frequency firing. In contrast to the stable amplitude, presynaptic spikes profoundly broadened for example during high-frequency firing in layer 5 pyramidal neurons but not in fast-spiking interneurons. Thus, our data demonstrate large presynaptic spikes and fundamental differences between excitatory and inhibitory boutons in the neocortex.

Real-Time Measurements of Synaptic Autoinhibition Produced by Serotonin Release in Cultured Leech Neurons

2009 ◽  
Vol 102 (2) ◽  
pp. 1075-1085 ◽  
Author(s):  
Montserrat G. Cercós ◽  
Francisco F. De-Miguel ◽  
Citlali Trueta
Keyword(s):  
Action Potentials ◽  
Chloride Channels ◽  
Membrane Conductance ◽  
Serotonin Release ◽  
Cultured Neurons ◽  
Model Simulations ◽  
Pressure Sensitive ◽  
Iontophoretic Application ◽  
Intracellular Microelectrodes ◽  
Serotonergic Antagonist

We studied autoinhibition produced immediately after synaptic serotonin (5-HT) release in identified leech Retzius neurons, cultured singly or forming synapses onto pressure-sensitive neurons. Cultured Retzius neurons are isopotential, thus allowing accurate recordings of synaptic events using intracellular microelectrodes. The effects of autoinhibition on distant neuropilar presynaptic endings were predicted from model simulations. Following action potentials (APs), cultured neurons produced a slow hyperpolarization with a rise time of 85.4 ± 5.2 ms and a half-decay time of 252 ± 17.4 ms. These inhibitory postpotentials were reproduced by the iontophoretic application of 5-HT and became depolarizing after inverting the transmembranal chloride gradient by using microelectrodes filled with potassium chloride. The inhibitory postpotentials were reversibly abolished in the absence of extracellular calcium and absent in reserpine-treated neurons, suggesting an autoinhibition due to 5-HT acting on autoreceptors coupled to chloride channels. The autoinhibitory responses increased the membrane conductance and decreased subsequent excitability. Increasing 5-HT release by stimulating with trains of ten pulses at 10 or 30 Hz produced 23 ± 6 and 47 ± 2% of AP failures, respectively. These failures were reversibly abolished by the serotonergic antagonist methysergide (140 μM). Moreover, reserpine-treated neurons had only 5 ± 4% of failures during trains at 10 Hz. This percentage was increased to 35 ± 4% by iontophoretic application of 5-HT. Increases in AP failures correlated with smaller postsynaptic currents. Model simulations predicted that the autoinhibitory chloride conductance reduces the amplitude of APs arriving at neuropilar presynaptic endings. Altogether, our results suggest that 5-HT autoinhibits its subsequent release by decreasing the excitability of presynaptic endings within the same neuron.

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