On the Mechanism of Increased Transmitter Release in LTP: Measurements of Calcium Concentration and Phosphatidylinositol Turnover in CA3 Synaptosomes

1988 ◽  
pp. 110-113 ◽  
Author(s):  
M. A. Lynch ◽  
M. P. Clements ◽  
M. L. Errington ◽  
T. V. P. Bliss
Keyword(s):  
Transmitter Release ◽  
Calcium Concentration ◽  
Phosphatidylinositol Turnover

Ca2+ cooperativity in neurosecretion measured using photolabile Ca2+ chelators

1994 ◽  
Vol 72 (2) ◽  
pp. 825-830 ◽  
Author(s):  
L. Lando ◽  
R. S. Zucker
Keyword(s):  
Motor Neuron ◽  
Intracellular Calcium ◽  
Transmitter Release ◽  
Time Course ◽  
Calcium Concentration ◽  
Postsynaptic Potentials ◽  
Postsynaptic Currents ◽  
Presynaptic Spike ◽  
Neuron Terminals ◽  
Light Flashes

1. The photolabile Ca2+ chelator DM-nitrophen was injected into crayfish motor neuron terminals and photolyzed with light flashes of different intensity to determine the cooperativity of Ca2+ action in releasing neurotransmitter. 2. Each flash elicited a phasic postsynaptic response resembling an excitatory junctional potential, apparently due to a presynaptic ”spike” in intracellular calcium concentration ([Ca2+]i). 3. When postsynaptic currents were measured under voltage clamp, a Ca2+ cooperativity of approximately 3–4 was inferred from a supralinear dependence of responses on changes in peak [Ca2+]i caused by flashes differing in intensity by 32–46%. 4. A similar Ca2+ cooperativity was inferred from postsynaptic potentials in response to flashes of varying intensity. 5. The time course of transmitter release indicated by flash responses had slightly slower rising and falling phases than excitatory postsynaptic potentials. There was also a slow tail of transmitter release lasting for approximately 200 ms after a flash. 6. This time course was explained quantitatively by simulations of DM-nitrophen photolysis and binding reactions and a model of Ca2+ activation of transmitter release.

scholarly journals Seasonal factors influence quantal transmitter release and calcium dependence at amphibian neuromuscular junctions

2017 ◽  
Vol 313 (3) ◽  
pp. R202-R210 ◽  
Author(s):  
Dengyun Ge ◽  
Nickolas Lavidis
Keyword(s):  
Transmitter Release ◽  
Calcium Concentration ◽  
Neuromuscular Junctions ◽  
Release Site ◽  
Extracellular Calcium ◽  
Fourth Power ◽  
Quantal Content ◽  
Wet Season ◽  
Quantal Release ◽  
Extracellular Calcium Concentration

Amphibian neuromuscular junctions (NMJs) are composed of hundreds of neurotransmitter release sites that exhibit nonuniform transmitter release probabilities and demonstrated seasonal modulation. We examined whether recruitment of release sites is variable when the extracellular calcium concentration ([Ca2+]o) is increased in the wet and dry seasons. The amount of transmitter released from the entire nerve terminal increases by approximately the fourth power as [Ca2+]o is increased. Toad ( Bufo marinus) NMJs were visualized using 3,3′-diethyloxardicarbocyanine iodide [DiOC2(5)] fluorescence, and focal loose patch extracellular recordings were used to record the end-plate currents (EPCs) from small groups of release sites. Quantal content ( m̄e), average probability of quantal release ( pe), and the number of active release sites ( ne) were determined for different [Ca2+]o. Our results indicated that the recruitment of quantal release sites with increasing [Ca2+]o differs spatially (between different groups of release sites) and also temporally (in different seasons). These differences were reflected by the nonuniform alterations in pe and ne. Most release site groups demonstrated an increase in both pe and ne when [Ca2+]o increased. In ~30% of release site groups examined, pe decreased while ne increased only during the active period (wet season). Although the dry season induced parallel right shift in the quantal release versus extracellular calcium concentration when compared with the wet season, the dependence of quantal content on [Ca2+]o was not changed. These results demonstrate the flexibility, reserve, and adaptive capacity of neuromuscular junctions in maintaining appropriate levels of neurotransmission.

Modification of transmitter release by electrical interference with motor nerve endings

1967 ◽  
Vol 167 (1006) ◽  
pp. 1-7 ◽  
Keyword(s):  
Action Potential ◽  
Nerve Terminal ◽  
Transmitter Release ◽  
Calcium Concentration ◽  
Motor Nerve ◽  
Nerve Impulse ◽  
Nerve Endings ◽  
External Calcium ◽  
Electrical Interference

1. A hyperpolarizing pulse applied through an external microelectrode to a nerve terminal during the falling phase of its action potential can suppress transmitter release; a depolarizing pulse applied during the same period can potentiate the release. 2. The facilitating action of calcium on transmitter release was studied by synchronizing the arrival of the nerve impulse with a rapid increment of the external calcium concentration. Using ionophoretic pulses of calcium, an effect could be produced with very little delay; sometimes the calcium pulse was effective when it preceded the arrival of the nerve impulse by only 1 to 2 ms.

scholarly journals Post-tetanic decay of evoked and spontaneous transmitter release and a residual-calcium model of synaptic facilitation at crayfish neuromuscular junctions.

1983 ◽  
Vol 81 (3) ◽  
pp. 355-372 ◽  
Author(s):  
R S Zucker ◽  
L O Lara-Estrella
Keyword(s):  
Transmitter Release ◽  
Calcium Concentration ◽  
Neuromuscular Junctions ◽  
Slow Component ◽  
Nonlinear Relationship ◽  
Time Constants ◽  
Excitatory Junction Potential ◽  
Excitatory Junction Potentials ◽  
Presynaptic Calcium ◽  
Junction Potential

The post-tetanic decay in miniature excitatory junction potential (MEJP) frequency and in facilitation of excitatory junction potentials (EJPs) was measured at crayfish neuromuscular junctions. A 2-s tetanus at 20 Hz caused the MEJP frequency to increase an average of 40 times and the EJP amplitude to increase an average of 13 times. Both MEJP frequency and EJP facilitation decayed with two time constants. The fast component of MEJP frequency decay was 47 ms, and that of EJP facilitation was 130 ms. The slow component of MEJP frequency decay was 0.57 s, and that of EJP facilitation was approximately 1 s. These results were consistent with the predictions of a residual calcium model, with a nonlinear relationship between presynaptic calcium concentration and transmitter release.

The effect of ionophore A23178 on the α-actinin crosslinks in the z-band of frog skeletal muscle: An EM study

1986 ◽  
Vol 44 ◽  
pp. 154-155
Author(s):  
F.T. Llados ◽  
V. Krlho ◽  
G.D. Pappas
Keyword(s):  
Muscle Damage ◽  
Transmitter Release ◽  
Skeletal Muscles ◽  
Calcium Uptake ◽  
Muscle Membrane ◽  
Frog Skeletal Muscle ◽  
Ach Release ◽  
Sustained Action ◽  
Calcium Deposits ◽  
Intense Stimulation

It Is known that Ca++ enters the muscle fiber at the junctional area during the action of the neurotransmitter, acetylcholine (ACh). Pappas and Rose demonstrated that following Intense stimulation, calcium deposits are found In the postsynaptic muscle membrane, Indicating the existence of calcium uptake In the postsynaptic area following ACh release. In addition to this calcium uptake, when mammal Ian skeletal muscles are exposed to a sustained action of the neurotransmitter, muscle damage develops. These same effects, l.e., Increased transmitter release, calcium uptake and finally muscle damage, can be obtained by Incubating the muscle with lonophore A23178.

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