共查询到20条相似文献,搜索用时 15 毫秒
1.
G. L. Collingridge P. A. Thompson† J. Davies J. Mellanby† 《Journal of neurochemistry》1981,37(4):1039-1041
Abstract Ca2+ -dependent K+ -stimulated γ-aminobutyric acid release from rat hippocampal slices was reduced about 30% by pre-incubation of the slices with 104 mouse LD50 /ml tetanus toxin for 3 h at 37°C. 相似文献
2.
Tomoyoshi Uchikawa Yuji Kiuchi Akihiko Yura Noriyuki Nakachi Yukako Yamazaki Chie Yokomizo Katsuji Oguchi 《Journal of neurochemistry》1995,65(5):2065-2071
Abstract: We studied effects of Ca2+ in the incubation medium on [3 H]dopamine ([3 H]DA) uptake by rat striatal synaptosomes. Both the duration of the preincubation period with Ca2+ (0–30 min) and Ca2+ concentration (0–10 m M ) in Krebs-Ringer medium affected [3 H]DA uptake by the synaptosomes. The increase was maximal at a concentration of 1 m M Ca2+ after a 10-min preincubation (2.4 times larger than the uptake measured without preincubation), which reflected an increase in V max of the [3 H]DA uptake process. On the other hand, [3 H]DA uptake decreased rapidly after addition of ionomycin in the presence of 1 m M Ca2+ . The Ca2+ -dependent enhancement of the uptake was still maintained after washing synaptosomes with Ca2+ -free medium following preincubation with 1 m M Ca2+ . Protein kinase C inhibitors did not affect apparently Ca2+ -dependent enhancement of the uptake, whereas 1-[ N,O -bis(1,5-isoquinolinesulfonyl)- N -methyl- l -tyrosyl]-4-phenylpiperazine (KN-62; a Ca2+ /calmodulin-dependent kinase II inhibitor) and wortmannin (a myosin light chain kinase inhibitor) significantly reduced it. Inhibitory effects of KN-62 and wortmannin appeared to be additive. N -(6-Aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride (W-7; a calmodulin antagonist) also remarkably inhibited the enhancement. These results suggest that Ca2+ -dependent enhancement of [3 H]DA uptake is mediated by activation of calmodulin-dependent protein kinases. 相似文献
3.
Microtubules and Microfilaments Participate in the Inhibition of Synaptosomal Noradrenaline Release by Tetanus Toxin 总被引:1,自引:1,他引:0
Abstract: Tetanus toxin (TeTX) has been demonstrated to inhibit transmitter release by two mechanisms: Zn2+ -dependent proteolytic cleavage of synaptobrevin and activation of a neuronal transglutaminase. Herein, attenuation of TeTX-induced blockade of noradrenaline release from synaptosomes was achieved by prior disassembly of microfilaments with cytochalasin D or breakdown of microtubules by colchicine or nocodazole. These drugs and monodansylcadaverine, a transglutaminase inhibitor, displayed some additivity in antagonizing the inhibitory effect of the toxin on synaptosomal transmitter release; as none of them reduced synaptobrevin cleavage, all appear to work independently of the toxin's proteolytic action. Prior stabilization of microtubules with taxol prevented the antagonism seen with colchicine, highlighting that this cytoskeletal component is the locus of the effect of colchicine. Replacement of Ca2+ with Ba2+ caused disappearance of the fraction of evoked secretion whose inhibition by TeTX is reliant on polymerized actin but did not alter the blockade by toxin that is dependent on microtubules. Two temporally distinguished phases of release were reduced by TeTX, and colchicine lessened its effects on both. Blockade of the fast phase (≤10 s) of secretion by TeTX was unaffected by cytochalasin D, but it clearly antagonized the toxin-induced inhibition of the slow (10-s to ≥5-min) component; it is notable that such antagonism was accentuated during a second bout of evoked release. These findings are consistent with sustained release requiring dissociation of synaptic vesicles from the microfilaments, a step that seems to be perturbed by TeTX. 相似文献
4.
Kazuhiro Takuma Toshio Matsuda Shoichi Asano Akemichi Baba 《Journal of neurochemistry》1995,64(4):1536-1540
Abstract: The effect of ascorbic acid on Ca2+ uptake in cultured rat astrocytes was examined in the presence of ouabain and monensin, which are considered to drive the Na+ -Ca2+ exchanger in the reverse mode. Ascorbic acid at 0.1–1 m M inhibited Na+ -dependent Ca2+ uptake significantly but not Na+ -dependent glutamate uptake in the cells, although the inhibition required pretreatment for more than 30 min. The effect of ascorbic acid on the Ca2+ uptake was blocked by simultaneous addition of ascorbate oxidase (10 U/ml). Na+ -dependent Ca2+ uptake was also inhibited by isoascorbate at 1 m M but not by ascorbate 2-sulfate, dehydroascorbate, and sulfhydryl-reducing reagents such as glutathione and 2-mercaptoethanol. The inhibitory effect of ascorbic acid was observed even in the presence of an inhibitor of lipid peroxidation, o -phenanthroline, or a radical scavenger, mannitol, and the degrading enzymes such as catalase and superoxide dismutase. On the other hand, the inhibitory effect was not observed under the Na+ -free conditions that inhibited the uptake of ascorbic acid in astrocytes. When astrocytes were cultured for 2 weeks in a medium containing ascorbic acid, the content of ascorbic acid in the cells was increased and conversely Na+ -dependent Ca2+ uptake was decreased. These results suggest that an increase in intracellular ascorbic acid results in a decrease of Na+ -Ca2+ exchange activity in cultured astrocytes and the mechanism is not related to lipid peroxidation. 相似文献
5.
Alcohol Inhibits the Depolarization-Induced Stimulation of Oxidative Phosphorylation in Synaptosomes
Abstract: The effects of alcohol and Ca2+ transport inhibitors on depolarization-induced stimulation of oxidative phosphorylation and free-Ca2+ concentrations in rat synaptosomes were investigated. Glucose oxidation was stimulated by depolarization with K+ or veratridine and by the Ca2+ ionophore ionomycin. The stimulation by K+ , veratridine, and ionomycin was correlated with elevation of synaptosomal free Ca2+ . Depolarization-stimulated respiration was inhibited by verapamil, Cd2+ , and ruthenium red but not by diltiazem. Synaptosomal Ca2+ elevation was inhibited by verapamil but not by ruthenium red. These results indicate that the stimulation depends on elevation of mitochondrial free Ca2+ . Ethanol, at pharmacological concentrations (50–200 m M ), inhibited the Ca2+ -dependent stimulation of oxidative phosphorylation. This inhibition resulted, in part, from the inhibition of voltage-gated Ca2+ channels, which inhibited the elevation of synaptosomal free Ca2+ , and, in part, from the stimulation of the mitochondrial Ca2+ /Na+ antiporter, which inhibited the elevation of the mitochondrial matrix free Ca2+ . The inhibition by ethanol of the excitation-induced stimulation of oxidative phosphorylation in the synapse may contribute to the depressant and narcotic effects of alcohol and enhance excitotoxicity. 相似文献
6.
V. Niggli D. E. Knight P. F. Baker A. Vigny† J.-P. Henry† 《Journal of neurochemistry》1984,43(3):646-658
Abstract: The systems responsible for phosphorylating tyrosine hydroxylase, the rate-limiting enzyme of catecholamine biosynthesis, were investigated in situ in adrenal medullary cells made permeable to solutes of up to 1,000 dalton by exposure to brief intense electric fields. Two different phosphorylation systems were found. One is dependent on Ca2+ , the other on cyclic AMP. The Ca2+ -dependent system is half-maximally activated by 1-2 μ M Ca2+ and 0.5 m M ATP, and follows a time course similar to that of secretion of catecholamines. Trifluoperazine (0.1 m M ) does not inhibit significantly Ca2+ -dependent phosphorylation of tyrosine hydroxylase in situ. The cyclic AMP-dependent system is half-maximally activated by addition of 0.5 μ M cyclic AMP and about 0.3 m M ATP. Ca2+ -dependent and cyclic AMP-dependent phosphorylations of tyrosine hydroxylase have roughly the same time course and are additive under conditions where one system is already saturated. Peptide maps of immunoprecipitated tyrosine hydroxylase, after in situ phosphorylation of the enzyme either in the presence of 10−8 M Ca2+ plus 2 × 10−5 M cyclic AMP or of 10−5 M Ca2+ , show a marked difference indicating that the enzyme contains several phosphorylation sites. At least one of these sites is phosphorylated only by the Ca2+ -dependent system, whereas the other site(s) are phosphorylated by both the Ca2+ - and cyclic AMP-dependent systems. The effect of in situ phosphorylation of tyrosine hydroxylase on its enzymatic activity was also investigated. 相似文献
7.
Abstract: Histamine is a known chromaffin cell secretagogue that induces Ca2+ -dependent release of catecholamines. However, conflicting evidence exists as to the source of Ca2+ utilized in histamine-evoked secretion. Here we report that histamine-H1 receptor activation induces redistribution of scinderin, a Ca2+ -dependent F-actin severing protein, cortical F-actin disassembly, and catecholamine release. Histamine evoked similar patterns of distribution of scinderin and filamentous actin. The rapid responses to histamine occurred in the absence of extracellular Ca2+ and were triggered by release of Ca2+ from intracellular stores. The trigger for the release of Ca2+ was inositol 1,4,5-trisphosphate because U-73122, a phospholipase C inhibitor, but not its inactive isomer (U-73343), inhibited the increases in IP3 and intracellular Ca2+ levels, scinderin redistribution, cortical F-actin disassembly, and catecholamine release in response to histamine. Thapsigargin, an agent known to mobilize intracellular Ca2+ , blocked the rise in intracellular Ca2+ concentration, scinderin redistribution, F-actin disassembly, and catecholamine secretion in response to histamine. Calphostin C and chelerythrine, two inhibitors of protein kinase C, blocked all responses to histamine with the exception of the release of Ca2+ from intracellular stores. This suggests that protein kinase C is involved in histamine-induced responses. The results also show that in the absence of F-actin disassembly, rises in intracellular Ca2+ concentration are not by themselves capable of triggering catecholamine release. 相似文献
8.
Fumi Katoh Kazuo Kitamura Hiromi Niina Ryuichi Yamamoto Hisanori Washimine †Kenji Kangawa Yoshitaka Yamamoto Hideyuki Kobayashi Tanenao Eto Akihiko Wada 《Journal of neurochemistry》1995,64(1):459-461
Abstract: In cultured bovine adrenal medullary cells, stimulation of nicotinic receptors by carbachol evoked the Ca2+ -dependent exocytotic cosecretion of proadrenomedullin N-terminal 20 peptide (PAMP) (EC50 = 50.1 µ M ) and catecholamines (EC50 = 63.0 µ M ), with the molar ratio of PAMP/catecholamines secreted being equal to the ratio in the cells. Addition of PAMP[1–20]NH2 inhibited carbachol-induced 22 Na+ influx via nicotinic receptors (IC50 = 2.5 µ M ) in a noncompetitive manner and thereby reduced carbachol-induced 45 Ca2+ influx via voltage-dependent Ca2+ channels (IC50 = 1.0 µ M ) and catecholamine secretion (IC50 = 1.6 µ M ). It did not alter high K+ -induced 45 Ca2+ influx via voltage-dependent Ca2+ channels or veratridine-induced 22 Na+ influx via voltage-dependent Na+ channels. PAMP seems to be a novel antinicotinic peptide cosecreted with catecholamines by a Ca2+ -dependent exocytosis in response to nicotinic receptor stimulation. 相似文献
9.
Modulation of Ion Gradients and Glutamate Release in Cultured Cerebellar Granule Cells by Ouabain 总被引:8,自引:0,他引:8
Abstract: Upon addition of the cardiac glycoside ouabain to cultured cerebellar granule cells, an immediate increase in intracellular free sodium is evoked mediated by two pathways, a voltage-sensitive channel blocked by tetrodotoxin and a channel sensitive to flunarizine. Ouabain induces a steady plasma membrane depolarization in low Ca2+ medium; whereas in the presence of Ca2+ , a distinct discontinuity is observed always preceded by a large increase in intracellular free Ca2+ ([Ca2+ ]c ). The plateau component of the increase can be inhibited additively by the L-type Ca2+ channel antagonist nifedipine, the spider toxin Aga-Gl, and the NMDA receptor antagonist MK-801. Single-cell imaging reveals that the [Ca2+ ]c increase occurs asynchronously in the cell population and is not dependent on a critical level of extracellular glutamate or synaptic transmission between the cells. A prolonged release of glutamate is also observed that is predominantly Ca2+ dependent for the first 6–10 min after the evoked increase in [Ca2+ ]c . This release is four times as large as that observed with 50 m M KCl and is predominantly exocytotic because release was inhibited by tetanus toxin, the V-type ATPase inhibitor bafilomycin, and Aga-Gl. It is proposed, therefore, that ouabain induces a period of membrane excitability culminating in a sustained exocytosis above that observed upon permanent depolarization with KCl. 相似文献
10.
Abstract: In the present communication we report that Ca2+ -dependent acetylcholine release from K+ -depolarized Torpedo electric organ synaptosomes is inhibited by morphine, and that this effect is blocked by the opiate antagonist naloxone. This finding suggests that the purely cholinergic Torpedo electric organ neurons contain pre-synaptic opiate receptors whose activation inhibits acetylcholine release. The mechanisms underlying this opiate inhibition were investigated by comparing the effects of morphine on acetylcholine release induced by K+ depolarization and by the Ca2+ ionophore A23187 and by examining the effect of morphine on 45 Ca2+ influx into Torpedo nerve terminals. These experiments revealed that morphine inhibits 45 Ca2+ influx into K+ -depolarized Torpedo synaptosomes and that this effect is blocked by naloxone. The effects of morphine on K+ depolarization-mediated 45 Ca2+ influx and on acetylcholine release have similar dose dependencies (half-maximal inhibition at 0.5–1 μ M ), suggesting that opiate inhibition of release is due to blockage of the presynaptic voltage-dependent Ca2+ channel. This conclusion is supported by the finding that morphine does not inhibit acetylcholine release when the Ca2+ channel is bypassed by introducing Ca2+ into the Torpedo nerve terminals via the Ca2+ ionophore. 相似文献
11.
The correct spatial and temporal control of Ca2+ signaling is essential for such cellular activities as fertilization, secretion, motility, and cell division. There has been a long-standing interest in the role of caveolae in regulating intracellular Ca2+ concentration. In this review we provide an updated view of how caveolae may regulate both Ca2+ entry into cells and Ca2+ -dependent signal transduction 相似文献
12.
Characterization of the Exocytotic Release of Glutamate from Guinea-Pig Cerebral Cortical Synaptosomes 总被引:12,自引:9,他引:3
Jose Sanchez-Prieto Talvinder S. Sihra David G. Nicholls 《Journal of neurochemistry》1987,49(1):58-64
Abstract: A continuous enzyme-linked fluorometric assay was used for determining the characteristics for glutamate exocytosis from guinea-pig cerebrocortical synaptosomes. Ca2+ -dependent release can be induced not only by K+ , but also by the Na+ channel activator veratridine and the Ca2+ ionophore ionomycin. K+ -induced release can be inhibited by the Ca2+ channel inhibitor verapamil. Sr2+ and Ba2+ substitute for Ca2+ in promoting K+ -induced release. Agents that would be predicted to transform the transvesicular pH gradient into a membrane potential are without effect on glutamate release. However, the protonophore carbonylcy-anide p -trifluoromethoxyphenylhydrazone causes a time-dependent loss of exocytosis that is oligomycin insensitive and may be due to depletion of vesicular glutamate. The Ca2+ -independent release of glutamate from the cytosol on depolarization is unchanged or promoted by metabolic inhibitors that lower the ATP/ADP ratio. In contrast, Ca2+ -dependent release is ATP dependent and is blocked by the combined inhibition of oxidative phosphorylation and glycolysis. 相似文献
13.
Abstract: The role of the Na+ /Ca2+ exchanger and intracellular nonmitochondrial Ca2+ pool in the regulation of cytosolic free calcium concentration ([Ca2+ ]i ) during catecholamine secretion was investigated. Catecholamine secretion and [Ca2+ ]i were simultaneously monitored in a single chromaffin cell. After high-K+ stimulation, control cells and cells in which the Na+ /Ca2+ exchange activity was inhibited showed similar rates of [Ca2+ ]i elevation. However, the recovery of [Ca2+ ]i to resting levels was slower in the inhibited cells. Inhibition of the exchanger increased the total catecholamine secretion by prolonging the secretion. Inhibition of the Ca2+ pump of the intracellular Ca2+ pool with thapsigargin caused a significant delay in the recovery of [Ca2+ ]i and greatly enhanced the secretory events. These data suggest that both the Na+ /Ca2+ exchanger and the thapsigargin-sensitive Ca2+ pool are important in the regulation of [Ca2+ ]i and, by modulating the time course of secretion, are important in determining the extent of secretion. 相似文献
14.
Abstract: We have found that modification of rat PC12 cells with pertussis toxin resulted in an ∼50% inhibition of a protein phosphatase 2A-like phosphatase. Protein phosphatase 2A (PP2A) is a major cellular serine/threonine-specific protein phosphatase. Treatment of extracts from pertussis toxin-modified PC12 cells with either immobilized alkaline phosphatase or Ca2+ reversed this inhibition. Reactivation of the PP2A-like phosphatase in Ca2+ appears to result from the dephosphorylation of a protein by the Ca2+ /calmodulin-dependent protein phosphatase calcineurin. The PP2A-like phosphatase in extracts from pertussis toxin-modified PC12 cells eluted from a Mono Q column at a higher ionic strength than did the PP2A-like phosphatase in extracts from control cells. After incubation in Ca2+ , the PP2A-like phosphatase in extracts from pertussis toxin-modified cells eluted from a Mono Q column at the same ionic strength as did the PP2A-like phosphatase in extracts from control cells. These results indicate that the effect of pertussis toxin on this PP2A-like activity results from the phosphorylation of either one of the subunits of the PP2A-like phosphatase or a protein that when phosphorylated binds to and inhibits this phosphatase. Pertussis toxin modification did not result in the phosphorylation of the catalytic subunit of PP2A. Because phosphorylation regulates the activities of many enzymes and cell surface receptors, a pertussis toxin-induced decrease in PP2A activity could alter signaling pathways and other cellular processes in which G proteins are not directly involved. 相似文献
15.
Subtoxic concentrations of the saponin digitonin. the polyene antibiotic amphotericin B and the bacterial phytotoxin syringomycin induce increased uptake of 45 Ca2+ into suspension-cultured plant cells and a rapid Ca2+ -dependent defense response, callose synthesis. Both reactions were inhibited by preincubation of the cells with okadaic acid, a specific inhibitor of type 1 and type 2A protein phosphatases. These results suggest that Ca2+ uptake induced by the above agents does not occur due to unspecific perturbation of plasma membrane permeability but involves transport proteins which are controlled by protein phosphorylation/dephosphorylation. Phosphoproteins appear also to be involved in the regulation of callose synthesis, although it remains open whether this control is effected at the level of Ca2+ transport or at the 1,3-ß-glucan synthase involved in deposition of the polymer. 相似文献
16.
Martin G. Klotz Alajos Bérczi László Erdei Bernd Liebermann 《Physiologia plantarum》1989,75(3):405-410
Purified plasmalemma vesicles were isolated in the presence of 250 m M sucrose from roots of 14-day-old seedlings of winter wheat ( Triticum aestivum L. Martonvásári-8) by phase partitioning of salt-washed microsomal fractions in a Dextran-polyethylene glycol two-phase system, and both Mg2+ - and Ca2+ -ATPase activities were detected. Orthovanadate-sensitive Mg2+ -ATPase activity associated with the inside of right side-out plasmalemma (PM) vesicles (latency 98%) was inhibited 76% by 0.3 m M Ca2+ , Ca2+ -dependent ATPase activity located partly on the inside and partly on the outside of plasmalemma vesicles (latency 47%) was not affected by Mg2+ .
Mg2+ -ATPase activity was inhibited by 68% and inhibition of Mg2+ activation by 0.3 m M Ca2+ partly disappeared in the presence of 10 p M tentoxin, a fungal phytotoxin. Mg2+ -ATPase activity remained inhibited up to 10 n M tentoxin while at 1 μ M tentoxin Mg2+ activation was as high as without tentoxin. K+ -stimulation and vanadate inhibition was increased and decreased, respectively, by 100 p M -10 n M tentoxin. Ca2+ -dependent ATPase activity was continuously increased by 1 p M -10 n M tentoxin, but at 1 μ M tentoxin the stimulation disappeared. The effects of p M tentoxin on plasma-lemma Mg2+ -ATPase are discussed in relation to its influence on K+ transport in wheat seedlings. 相似文献
Mg
17.
Abstract: The mechanism of glutamate release from cultured cerebellar granule neurones in response to a chemical model of ischaemia (10 m M 2-deoxyglucose plus 1 m M sodium cyanide) was investigated. In the first 2 min of ischaemia, release of preloaded d -[3 H]aspartate could be extensively attenuated by tetanus toxin and bafilomycin A1 and was dependent on the activation of Ca2+ channels sensitive to the "Q" type Ca2+ channel antagonist, ω-conotoxin-MVIIC. During this period, ATP/ADP ratios fell rapidly. The extent of release in the first 2 min was comparable to that evoked by 2-min depolarization by 50 m M KCl. Free Ca2+ concentrations, determined in neurites and somata, did not increase until after 2 min. The neurite increase in cellular Ca2+ precedes that of the cell somata. Release of d -[3 H]aspartate was partially inhibited by the NMDA receptor antagonist MK-801, which also delayed the increase in free Ca2+ concentration. Prolonging the period of ischaemia to 6 and 10 min produced no further increase in the apparently exocytotic component of release, but initiated an extensive nonexocytotic release of the amino acid. Studies with the synaptic vesicle membrane probe FM1-43 in which released amino acid was removed by superfusion indicated that Ca2+ -dependent exocytosis was delayed in this system. It is concluded that chemical ischaemia initiates an initial exocytotic followed by nonexocytotic release and that the former is facilitated by NMDA receptor activation. These events occur in cells that are still able to exclude propidium iodide, indicating that cell death has not yet occurred. 相似文献
18.
JAMES J. WASSENBERG KEVIN D. CLARK DAVID L. NELSON 《The Journal of eukaryotic microbiology》1997,44(6):574-581
ABSTRACT. Inhibitors of SERCA (sarcoplasmic/endoplasmic reticulum Ca2+ -dependent ATPase) calcium pumps were used to investigate the involvement of internal Ca2+ stores in the GTP response in Paramecium . External application of these inhibitors was found to dramatically alter the typical behavioral and electrophysiological responses of Paramecium to extracellular chemical stimulation. In particular, 2.5-di-tert-butylhydroquinone (BHQ) strongly inhibited the backward swimming response of paramecia to externally applied GTP, though it did not inhibit the associated whirling response. BHQ also prolonged the normally brief electrophysiological response of these cells to GTP. BHQ completely blocked the behavioral and electrophysiological responses of Paramecium to extracellular Ba2+ , but had no measurable effect on the behavioral or electrophysiological responses of these cells to another depolarizing stimulus, elevated external K+ concentration. These results suggest the involvement of nonciliary Ca2+ ions in the GTP and Ba2+ responses. 相似文献
19.
Abstract: The effect of tetanus toxin pretreatment on K+ -stimulated [3 H]γ-aminobutyric acid release from neuron-enriched cerebellar cell cultures at various stages during their development in vitro was assessed. Tetanus toxin had little inhibitory effect on immature (1-3-day-old) cultures, but markedly reduced K+ -evoked [3 H]γ-aminobutyric acid release from 7- and 14-day-old cultures (∼80% inhibition). It is suggested that cerebellar neurons in culture develop tetanus toxin-sensitive transmitter release mechanisms similar to their in vivo counterparts. 相似文献
20.
Abstract: Effects of concanavalin A on transmitter release were investigated in primary cultures of chick sympathetic neurons. The lectin reduced electrically evoked [3 H]noradrenaline release by up to 30% with half-maximal inhibition at 0.16 µ M . Concanavalin A also reduced the release triggered by extracellular Ca2+ in neurons depolarized by 25 m M K+ or rendered Ca2+ -permeable by the ionophore A23187. The inhibitory action of concanavalin A on electrically evoked release was additive to that of the α2 -adrenergic agonist UK 14,304. Inactivation of Gs and Gi /Go type G proteins by either cholera or pertussis toxin did not alter the inhibitory effect of the lectin. Concanavalin A failed to affect the resting membrane potential, action potential waveforms, or voltage-dependent K+ and Ca2+ currents. In contrast, the lectin efficiently blocked both the Ca2+ -dependent and -independent α-latrotoxin-induced transmitter release, but only when applied before the toxin. The reduction of electrically evoked, as well as α-latrotoxin-evoked, release by concanavalin A was attenuated in the presence of glucose and abolished by methyl α- d -mannopyranoside. The dimeric derivative, succinyl-concanavalin A, was significantly less active than tetrameric concanavalin A. In bovine adrenal chromaffin cells, which displayed only weak secretory responses to α-latrotoxin, concanavalin A failed to alter K+ -evoked catecholamine secretion. These results show that concanavalin A causes presynaptic inhibition in sympathetic neurons and indicate that cross-linking of α-latrotoxin receptors may reduce action potential-dependent transmitter release. 相似文献