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.

Activity-induced elevations of intracellular calcium concentration in pyramidal and nonpyramidal cells of the CA3 region of rat hippocampal slice cultures

1992 ◽  
Vol 68 (3) ◽  
pp. 961-963 ◽  
Author(s):  
T. Knopfel ◽  
B. H. Gahwiler
Keyword(s):  
Intracellular Calcium ◽  
Time Course ◽  
Calcium Concentration ◽  
Potassium Conductance ◽  
Pyramidal Cells ◽  
Calcium Transients ◽  
Intracellular Calcium Concentration ◽  
Calcium Signal ◽  
Cell Somata ◽  
Ca3 Region

1. Depolarization-induced elevations of intracellular calcium concentration ([Ca2+]i) were examined in slice-cultured hippocampal pyramidal and nonpyramidal cells of the CA3 region by combined intracellular and multisite fura-2 recording techniques. 2. In pyramidal cells, spiking activity induced by depolarizing current pulses (200–800 ms) induced transient elevations of somatic as well as of proximal dendritic [Ca2+]i. The calcium signals from the proximal dendrites were larger in amplitude and decayed much faster than those from the soma. Depolarization of presumed interneurons induced comparable somatic and dendritic calcium transients, which decayed faster than those observed in pyramidal cell somata. 3. The calcium transients of pyramidal cells, but not those of nonpyramidal cells, were associated with a slow afterhyperpolarization (sAHP), whose time course was correlated with that of the somatic calcium signal. We conclude that the lack of a sAHP in non-pyramidal cells cannot be explained by the absence of an efficient rise in [Ca2+]i but rather by the absence of the potassium conductance underlying the sAHP in pyramidal cells.

Presynaptic glutamate receptors depress inhibitory postsynaptic transmission in lobster neuromuscular synapse

1993 ◽  
Vol 70 (3) ◽  
pp. 1159-1167 ◽  
Author(s):  
A. Miwa ◽  
H. P. Robinson ◽  
N. Kawai
Keyword(s):  
Glutamate Receptors ◽  
Transmitter Release ◽  
Neuromuscular Synapse ◽  
Ibotenic Acid ◽  
Postsynaptic Potentials ◽  
Postsynaptic Currents ◽  
Effective Inhibition ◽  
The Mean ◽  
Gamma S

1. We examined the functional role of GTP-coupled glutamate receptor (GluB-R) in the presynaptic membrane of lobster neuromuscular synapse. 2. Injection of guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S), a hydrolysis-resistant analogue of GTP, into the excitatory axon mimicked the presynaptic glutamate response and effectively suppressed excitatory postsynaptic potentials or excitatory postsynaptic currents (EPSCs). 3. Statistical analysis revealed that the coefficient of variation (standard deviation divided by the mean of EPSC amplitude) was increased after injection of GTP gamma S into the excitatory axon, indicating a presynaptic inhibition of transmitter release. 4. The effect of glutamate on inhibitory postsynaptic potentials (IPSPs) or inhibitory postsynaptic currents (IPSCs) was studied when the postsynaptic glutamate receptors were blocked by the Joro spider toxin (JSTX). Glutamate depressed IPSPs or IPSCs in the JSTX-treated preparation. Furthermore, repetitive stimulation of the excitatory nerve produced effective inhibition of IPSCs. 5. Quisqualate and kainate suppressed IPSCs in a similar way to glutamate. In contrast, N-methyl-D-aspartate, ibotenic acid, trans-D,L-1-amino-1,3-cyclopentanedicarboxyloc acid, and 2-amino-4-phosphonobutanate had no effect on GluB-R. 6. Our results indicate that GluB-R, which exists in both excitatory and inhibitory nerve terminals, regulates transmitter release by a presynaptic inhibitory mechanism.

scholarly journals Correlation of Transmitter Release with Membrane Properties of the Presynaptic Fiber of the Squid Giant Synapse

1967 ◽  
Vol 50 (11) ◽  
pp. 2579-2601 ◽  
Author(s):  
Kiyoshi Kusano ◽  
David R. Livengood ◽  
Robert Werman
Keyword(s):  
Transmitter Release ◽  
Time Course ◽  
Membrane Properties ◽  
Ca Current ◽  
Permeability Changes ◽  
Postsynaptic Potential ◽  
Presynaptic Spike ◽  
Squid Giant Synapse ◽  
Giant Synapse ◽  
Tetraethylammonium Ions

Depolarization of the presynaptic terminal by current produced a postsynaptic potential (PSP) which increased with increasing presynaptic polarization and then reached a plateau. Iontophoretic injection of tetraethylammonium ions (TEA) into the presynaptic axon near the terminal produced a prolonged presynaptic spike. The resulting PSP is increased in size and its time course closely followed that of the presynaptic spike. The presynaptic fiber no longer exhibited rectification and strong depolarizations revealed that the PSP reached a maximum with about 110 mv depolarization. Further depolarization produced a decrease in PSP amplitude and finally transmission was blocked. However, a PSP then always appeared on withdrawal of the depolarizing current. Under the conditions of these experiments, the PSP could be considered a direct measure of transmitter release. Bathing the TEA-injected synapse with concentrations of tetrodotoxin (TTX) sufficient to block spike activity in both pre- and postsynaptic axons did not greatly modify postsynaptic electrogenesis. However, doubling TTX concentration reversibly blocked PSP. Thus the permeability changes to Na and K accompanying the spike do not appear necessary for transmitter release. Some other processes related to the level of presynaptic polarization must be involved to explain the data. The inhibition of transmitter release by strong depolarizations appears to be related to Ca action. A membrane Ca current may also be necessary for normal transmitter release.

Role of Mitochondrial Dysfunction in the Ca2+-Induced Decline of Transmitter Release at K+-Depolarized Motor Neuron Terminals

1999 ◽  
Vol 81 (2) ◽  
pp. 498-506 ◽  
Author(s):  
Michelle A. Calupca ◽  
Gregory M. Hendricks ◽  
Jean C. Hardwick ◽  
Rodney L. Parsons
Keyword(s):  
Motor Neuron ◽  
Mitochondrial Dysfunction ◽  
Transmitter Release ◽  
Synaptic Vesicles ◽  
Prolonged Exposure ◽  
Nerve Terminals ◽  
Atp Production ◽  
Neuron Terminals ◽  
Nerve Muscle

Role of mitochondrial dysfunction in the Ca2+-induced decline of transmitter release at K+-depolarized motor neuron terminals. The present study tested whether a Ca2+-induced disruption of mitochondrial function was responsible for the decline in miniature endplate current (MEPC) frequency that occurs with nerve-muscle preparations maintained in a 35 mM potassium propionate (35 mM KP) solution containing elevated calcium. When the 35 mM KP contained control Ca2+(1 mM), the MEPC frequency increased and remained elevated for many hours, and the mitochondria within twitch motor neuron terminals were similar in appearance to those in unstimulated terminals. All nerve terminals accumulated FM1–43 when the dye was present for the final 6 min of a 300-min exposure to 35 mM KP with control Ca2+. In contrast, when Ca2+ was increased to 3.6 mM in the 35 mM KP solution, the MEPC frequency initially reached frequencies >350 s− 1 but then gradually fell approaching frequencies <50 s−1. A progressive swelling and eventual distortion of mitochondria within the twitch motor neuron terminals occurred during prolonged exposure to 35 mM KP with elevated Ca2+. After ∼300 min in 35 mM KP with elevated Ca2+, only 58% of the twitch terminals accumulated FM1–43. The decline in MEPC frequency in 35 mM KP with elevated Ca2+ was less when 15 mM glucose was present or when preparations were pretreated with 10 μM oligomycin and then bathed in the 35 mM KP with glucose. When glucose was present, with or without oligomycin pretreatment, a greater percentage of twitch terminals accumulated FM1–43. However, the mitochondria in these preparations were still greatly swollen and distorted. We propose that prolonged depolarization of twitch motor neuron terminals by 35 mM KP with elevated Ca2+ produced a Ca2+-induced decrease in mitochondrial ATP production. Under these conditions, the cytosolic ATP/ADP ratio was decreased thereby compromising both transmitter release and refilling of recycled synaptic vesicles. The addition of glucose stimulated glycolysis which contributed to the maintenance of required ATP levels.

Fast Calcium Signals in Drosophila Motor Neuron Terminals

2002 ◽  
Vol 88 (5) ◽  
pp. 2659-2663 ◽  
Author(s):  
G. T. Macleod ◽  
M. Hegström-Wojtowicz ◽  
M. P. Charlton ◽  
H. L. Atwood
Keyword(s):  
Motor Neuron ◽  
Intracellular Calcium ◽  
Signal To Noise Ratio ◽  
Physiological Solution ◽  
Calcium Signal ◽  
High Signal ◽  
Calcium Kinetics ◽  
Single Action ◽  
Calcium Dependent ◽  
Neuron Terminals

Drosophila is a powerful model for neuroscientists, but physiological techniques have not kept pace with advances in molecular genetics. We introduce a reliable assay for intracellular calcium dynamics in Drosophila larval motor neuron terminals, and a new physiological solution that improves the longevity of the larval preparation. By loading calcium indicators into motor neuron terminals through cut axons, we obtained a high signal-to-noise ratio with confocal microscopy, and good temporal resolution of calcium-dependent fluorescence changes. We provide an estimate for the resting intracellular calcium concentration, the first description of calcium kinetics for a single action potential (AP), and improved resolution of calcium kinetics during AP trains. The very rapid decay of the calcium signal following a single AP (τ ∼60 ms) indicates a previously unreported fast calcium extrusion mechanism in Drosophila motor neuron terminals well suited for sustaining physiological processes during the high rates of impulse activity which drive locomotor activity.

Effects of ethanol and other drugs on excitatory and inhibitory neurotransmission in the crayfish

1992 ◽  
Vol 67 (3) ◽  
pp. 576-587 ◽  
Author(s):  
J. A. Blundon ◽  
G. D. Bittner
Keyword(s):  
Presynaptic Inhibition ◽  
Time Course ◽  
Muscle Fibers ◽  
Gabab Receptors ◽  
Inhibitory Synapses ◽  
Gamma Aminobutyric Acid ◽  
Postsynaptic Potentials ◽  
Postsynaptic Currents ◽  
Gabaa Antagonist

1. Crayfish exposed to 434 mM ethanol (EtOH) showed signs of hyperactivity within 0.5-2 h, at which times crayfish hemolymph EtOH concentration had reached 60-90 mM. 2. A 10-min exposure to 60-90 mM EtOH reduced presynaptic inhibition of excitatory postsynaptic currents (EPSCs) at the crayfish opener neuromuscular junction (NMJ) in vitro but did not significantly alter excitatory neurotransmission. The same concentrations of EtOH did not alter other potentials or currents associated with inhibition at this synapse, such as presynaptic inhibitory potentials (PIPs), inhibitory postsynaptic potentials (IPSPs), and inhibitory postsynaptic currents (IPSCs). 3. Intermediate EtOH concentrations (120-180 mM) applied for 10 min in vitro reduced the amplitude of excitatory postsynaptic potentials (EPSPs) by decreasing the membrane resistance of opener muscle fibers and by reducing the amplitude of EPSCs. 4. High EtOH concentrations (434 mM) applied for 10 min in vitro had yet greater depressive effects on measures of postsynaptic properties described above. The time course of EPSCs was also significantly reduced. In addition, presynaptic properties such as action-potential (AP) amplitude and frequency of spontaneous release of neurotransmitter were reduced by 434 mM EtOH. 5. Presynaptic inhibition, gamma-aminobutyric acid (GABA; 250-500 microM), muscimol (50 microM), and baclofen (75 microM) all reduced the depolarizing afterpotential of APs in the excitor axon and reduced EPSPs in opener muscle fibers. GABA (500 microM) and baclofen (75 microM) significantly reduced presynaptic AP amplitudes, whereas presynaptic inhibition, GABA (250 microM), and muscimol (50 microM) had no effect on AP amplitude. Bicuculline (250-500 microM), a GABAA antagonist, did not entirely eliminate presynaptic inhibition, whereas picrotoxin (50 microM), another GABAA antagonist, completely removed presynaptic inhibition. Thus presynaptic inhibitory mechanisms may involve both GABAA and GABAB receptors on the opener excitor axon. 6. Our data suggest that the behavioral hyperactivity seen at hemolymph EtOH concentrations of 60-90 mM is not accompanied by a change in excitatory synaptic transmission observed at the opener NMJ. Rather, crayfish hyperactivity may be due to depressive effects of EtOH on inhibitory synapses in the CNS similar to the disinhibition evoked by EtOH at the opener NMJ.

cAMP does not regulate [Ca2+]i in human tracheal epithelial cells in primary culture

1994 ◽  
Vol 107 (10) ◽  
pp. 2899-2907
Author(s):  
P.B. Davis ◽  
C.L. Silski ◽  
A. Perez
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
Intracellular Calcium ◽  
Primary Culture ◽  
Time Course ◽  
Calcium Concentration ◽  
Second Messengers ◽  
Tracheal Epithelial Cells ◽  
Adrenergic Response ◽  
Tracheal Epithelial

Human tracheal epithelial cells in primary culture respond to different receptor agonists with different peak intracellular calcium concentrations. From resting concentration 138 +/- 13 nM, bradykinin (0.1 microM) produces an increase to a maximum of 835 +/- 195 nM, histamine (10 microM) to 352 +/- 51 nM, and ATP (5-500 microM) to more than 1500 nM. Nine of 14 cultures also responded to isoproterenol (10 microM), though with a smaller increase, to 210 +/- 29 nM. A response was observed with isoproterenol, and epinephrine, but not norepinephrine, phenylephrine or methoxamine, was inhibited by propranolol but not phentolamine, and so this appeared to be a beta-adrenergic response. However, no response could be detected to adenosine, prostaglandin E2 or forskolin, agents that activate adenylate cyclase, or to permeant analogs of cAMP (CPT-cAMP or db-cAMP). The intracellular calcium response to isoproterenol did not follow either the time-course or the desensitization pattern of the cAMP response. Thus, this response to isoproterenol is not mediated by cAMP. No relation was demonstrated between cAMP production by other agonists and the response of intracellular calcium. Pretreatment with agents that increase cAMP did not affect the calcium responses to ATP or bradykinin. Thus, cAMP does not regulate intracellular calcium concentration in human tracheal epithelial cells. The variation in peak intracellular calcium responses to various agonists may be explained by the presence of multiple second messengers (other than cAMP), multiple intracellular pools of calcium, or cell heterogeneity. The agonists tested had the same relative potency in cells from patients with cystic fibrosis as in non-cystic fibrosis cells.

scholarly journals Presynaptic calcium currents and facilitation of serotonin release at synapses between cultured leech neurones

1989 ◽  
Vol 144 (1) ◽  
pp. 1-12
Author(s):  
R. R. Stewart ◽  
W. B. Adams ◽  
J. G. Nicholls
Keyword(s):  
Transmitter Release ◽  
Time Course ◽  
Divalent Cations ◽  
Serotonin Release ◽  
Calcium Currents ◽  
Postsynaptic Potentials ◽  
The Central Nervous System ◽  
Presynaptic Calcium ◽  
Retzius Cells

1. The role of presynaptic Ca2+ entry in facilitation of transmitter release has been analysed by voltage-clamp measurements at synapses formed in culture by Retzius and P neurones isolated from the central nervous system (CNS) of the leech. The transmitter released by Retzius cells is serotonin. 2. Synaptic transmission persisted in solutions containing raised concentrations of divalent cations, reduced concentrations of Na+, and tetraethylammonium (TEA+) and 4-AP (to block K+ currents). Ca2+ and Sr2+ were more effective in promoting transmitter release than Ba2+, as assessed by the postsynaptic potentials in P cells. The degree and time course of facilitation in Ca2+- and Sr2+-containing solutions were similar to those observed for synapses bathed in normal L-15 medium. 3. Transmitter release depended upon the amplitude and the duration of presynaptic depolarization and inward Ca2+ current. Peak Ca2+ currents and postsynaptic potentials occurred with depolarizing steps to +15 mV. Frequent or prolonged pulses depressed the postsynaptic potentials. 4. Pairs of depolarizing pulses that caused facilitation were accompanied by identical inward Ca2+ currents. These results indicate that the mechanism responsible for facilitated serotonin release must occur following Ca2+ entry and that residual Ca2+ plays a role.

scholarly journals Orientia tsutsugamushi Inhibits Apoptosis of Macrophages by Retarding Intracellular Calcium Release

2002 ◽  
Vol 70 (8) ◽  
pp. 4692-4696 ◽  
Author(s):  
Mee-Kyung Kim ◽  
Seung-Yong Seong ◽  
Ju-Young Seoh ◽  
Tae-Hee Han ◽  
Hyeon-Je Song ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Calcium Release ◽  
Cytosolic Calcium ◽  
Orientia Tsutsugamushi ◽  
Cytosolic Calcium Concentration ◽  
Infected Cells ◽  
Intracellular Calcium Release ◽  
Calcium Redistribution ◽  
In Cells

ABSTRACT Orientia tsutsugamushi shows both pro- and antiapoptotic activities in infected vertebrate cells. Apoptosis of THP-1 cells induced by beauvericin was inhibited by O. tsutsugamushi infection. Beauvericin-induced calcium redistribution was significantly reduced and retarded in cells infected with O. tsutsugamushi. Antiapoptotic activities of O. tsutsugamushi in infected cells are most probably due to inhibition of the increase in the cytosolic calcium concentration.

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