scholarly journals Transmitter release modulation by intracellular Ca 2+ buffers in facilitating and depressing nerve terminals of pyramidal cells in layer 2/3 of the rat neocortex indicates a target cell‐specific difference in presynaptic calcium dynamics

2001 ◽  
Vol 531 (3) ◽  
pp. 807-826 ◽  
Author(s):  
A. Rozov ◽  
N. Burnashev ◽  
B. Sakmann ◽  
E. Neher
Keyword(s):  
Target Cell ◽  
Transmitter Release ◽  
Pyramidal Cells ◽  
Nerve Terminals ◽  
Calcium Dynamics ◽  
Specific Difference ◽  
Layer 2 ◽  
Rat Neocortex ◽  
Intracellular Ca ◽  
Presynaptic Calcium

scholarly journals Gain of Function in FHM-1 Cav2.1 Knock-In Mice Is Related to the Shape of the Action Potential

2010 ◽  
Vol 104 (1) ◽  
pp. 291-299 ◽  
Author(s):  
Carlota González Inchauspe ◽  
Francisco J. Urbano ◽  
Mariano N. Di Guilmi ◽  
Ian D. Forsythe ◽  
Michel D. Ferrari ◽  
...  
Keyword(s):  
Pyramidal Cells ◽  
Familial Hemiplegic Migraine ◽  
Cortical Layer ◽  
Calcium Currents ◽  
Inhibitory Neurons ◽  
Missense Mutations ◽  
Calyx Of Held ◽  
Gain Of Function ◽  
Layer 2 ◽  
Presynaptic Calcium

Familial hemiplegic migraine type-1 FHM-1 is caused by missense mutations in the CACNA1A gene that encodes the α1A pore-forming subunit of CaV2.1 Ca2+ channels. We used knock-in (KI) transgenic mice harboring the pathogenic FHM-1 mutation R192Q to study neurotransmission at the calyx of Held synapse and cortical layer 2/3 pyramidal cells (PCs). Using whole cell patch-clamp recordings in brain stem slices, we confirmed that KI CaV2.1 Ca2+ channels activated at more hyperpolarizing potentials. However, calyceal presynaptic calcium currents ( IpCa) evoked by presynaptic action potentials (APs) were similar in amplitude, kinetic parameters, and neurotransmitter release. CaV2.1 Ca2+ channels in cortical layer 2/3 PCs from KI mice also showed a negative shift in their activation voltage. PCs had APs with longer durations and smaller amplitudes than the calyx of Held. AP-evoked Ca2+ currents ( ICa) from PCs were larger in KI compared with wild-type (WT) mice. In contrast, when ICawas evoked in PCs by calyx of Held AP waveforms, we observed no amplitude differences between WT and KI mice. In the same way, Ca2+ currents evoked at the presynaptic terminals ( IpCa)of the calyx of Held by the AP waveforms of the PCs had larger amplitudes in R192Q KI mice that in WT. These results suggest that longer time courses of pyramidal APs were a key factor for the expression of a synaptic gain of function in the KI mice. In addition, our results indicate that consequences of FHM-1 mutations might vary according to the shape of APs in charge of triggering synaptic transmission (neurons in the calyx of Held vs. excitatory/inhibitory neurons in the cortex), adding to the complexity of the pathophysiology of migraine.

scholarly journals Depolarization-Induced Calcium-Independent Synaptic Vesicle Exo- and Endocytosis at Frog Motor Nerve Terminals

Acta Naturae ◽  
2013 ◽  
Vol 5 (4) ◽  
pp. 77-82 ◽  
Author(s):  
M. M. Abdrakhmanov ◽  
A. M. Petrov ◽  
P. N. Grigoryev ◽  
A. L. Zefirov
Keyword(s):  
Synaptic Vesicle ◽  
Transmitter Release ◽  
Synaptic Vesicles ◽  
Fluorescent Microscopy ◽  
Constant Current ◽  
Nerve Terminals ◽  
Ca Channels ◽  
Cooperative Action ◽  
Intracellular Ca ◽  
Vesicle Exocytosis

The transmitter release and synaptic vesicle exo- and endocytosis induced by constant current depolarization of nerve terminals were studied by microelectode extracellular recording of miniature endplate currents and fluorescent microscopy (FM 1-43 styryl dye). Depolarization of the plasma membrane of nerve terminals in the control specimen was shown to significantly increase the MEPC frequency (quantal transmitter release) and exocytotic rate (FM 1-43 unloading from the synaptic vesicles preliminarily stained with the dye), which was caused by a rise in the intracellular Ca 2+ concentration due to opening of voltage-gated Ca channels. A slight increase in the MEPC frequency and in the rate of synaptic vesicle exocytosis was observed under depolarization in case of blockade of Ca channels and chelating of intracellular Ca 2+ ions (cooperative action of Cd 2+ and EGTA-AM). The processes of synaptic vesicle endocytosis (FM 1-43 loading) were proportional to the number of synaptic vesicles that had undergone exocytosis both in the control and in case of cooperative action of Cd 2+ and EGTA-AM. A hypothesis has been put forward that Ca-independent synaptic vesicle exo- and endocytosis that can be induced directly by depolarization of the membrane exists in the frog motor terminal in addition to the conventional Ca-dependent process.

A SIMPLE MODEL FOR INTERACTION OF VOLTAGE AND CALCIUM DYNAMICS IN VIRTUAL VENTRICULAR TISSUE

2003 ◽  
Vol 13 (12) ◽  
pp. 3873-3886
Author(s):  
O. V. ASLANIDI ◽  
A. V. HOLDEN
Keyword(s):  
Intracellular Calcium ◽  
Calcium Release ◽  
Cell Model ◽  
Excitation Threshold ◽  
Calcium Dynamics ◽  
Variable Model ◽  
Ventricular Cell ◽  
Calcium Dependent ◽  
Intracellular Ca ◽  
A Site

A simple two-variable model is used to replace the formulation of calcium dynamics in the Luo–Rudy ventricular cell model. Virtual ventricular cell and tissue are developed and validated to reproduce restitution properties and calcium-dependent voltage patterns present in the original model. Basic interactions between the membrane potential and Ca 2+ dynamics in the virtual cell and a strand of the virtual tissue are studied. Intracellular calcium waves can be linked to both action potentials (APs) and delayed afterdepolarizations (DADs). An intracellular calcium wave propagating from the cell interior can induce an AP upon reaching the cell membrane. The voltage and the intracellular Ca 2+ patterns within the same cell can be highly desynchronized. In a one-dimensional strand of the virtual tissue calcium motion is driven by the AP propagation. However, calcium release can be induced upon certain conditions (e.g. Na + overload of the cells), which results in DADs propagating in the wake of AP. Such propagating DADs can reach the excitation threshold, generating a pair of extrasystolic APs. Collision of a propagating AP with a site of elevated intracellular Ca 2+ concentration does not affect the propagation under the normal conditions. Under Na + overload local elevation of the intracellular Ca 2+ leads to generation of an extrasystolic AP, which destroys the original propagating AP.

Characterization of postsynaptic Ca2+ signals at the Drosophila larval NMJ

2011 ◽  
Vol 106 (2) ◽  
pp. 710-721 ◽  
Author(s):  
Sunil A. Desai ◽  
Gregory A. Lnenicka
Keyword(s):  
Transmitter Release ◽  
Postsynaptic Membrane ◽  
Synaptic Activity ◽  
Synaptic Efficacy ◽  
Single Action ◽  
Synaptic Homeostasis ◽  
Multiple Transcripts ◽  
Quantal Size ◽  
Intracellular Ca ◽  
Larval Neuromuscular Junction

Postsynaptic intracellular Ca2+ concentration ([Ca2+]i) has been proposed to play an important role in both synaptic plasticity and synaptic homeostasis. In particular, postsynaptic Ca2+ signals can alter synaptic efficacy by influencing transmitter release, receptor sensitivity, and protein synthesis. We examined the postsynaptic Ca2+ transients at the Drosophila larval neuromuscular junction (NMJ) by injecting the muscle fibers with Ca2+ indicators rhod-2 and Oregon Green BAPTA-1 (OGB-1) and then monitoring their increased fluorescence during synaptic activity. We observed discrete postsynaptic Ca2+ transients along the NMJ during single action potentials (APs) and quantal Ca2+ transients produced by spontaneous transmitter release. Most of the evoked Ca2+ transients resulted from the release of one or two quanta of transmitter and occurred largely at synaptic boutons. The magnitude of the Ca2+ signals was correlated with synaptic efficacy; the Is terminals, which produce larger excitatory postsynaptic potentials (EPSPs) and have a greater quantal size than Ib terminals, produced a larger Ca2+ signal per terminal length and larger quantal Ca2+ signals than the Ib terminals. During a train of APs, the postsynaptic Ca2+ signal increased but remained localized to the postsynaptic membrane. In addition, we showed that the plasma membrane Ca2+-ATPase (PMCA) played a role in extruding Ca2+ from the postsynaptic region of the muscle. Drosophila melanogaster has a single PMCA gene, predicted to give rise to various isoforms by alternative splicing. Using RT-PCR, we detected the expression of multiple transcripts in muscle and nervous tissues; the physiological significance of the same is yet to be determined.

Transmitter release induced by a ‘factor’ in rabbit serum

1974 ◽  
Vol 187 (1087) ◽  
pp. 235-241 ◽  
Keyword(s):  
Complement System ◽  
Transmitter Release ◽  
Motor Nerve ◽  
Nerve Endings ◽  
Rabbit Serum ◽  
Nerve Terminals ◽  
The Complement System ◽  
The Way

Non-heated rabbit serum causes massive transmitter release from motor nerve endings. The effect is not observed after heating the serum, in the way usually done to destroy complement. It seems that serum may be acting on the nerve terminals by a mechanism involving the complement system in the absence of antibody.

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