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1.
In the present study we characterize the optimal experimental conditions under which to investigate the cholinergic regulation of endogenous electrically evoked γ-aminobutyric acid (GABA) release from guinea pig cortical slices. Superfusion with the neuronal GABA reuptake inhibitor, SKF89976A (10 μM) caused cortical GABA release to be linearly correlated with the frequency of electrical stimulation (5, 10, 20 Hz). Electrically evoked GABA release (10 Hz) was tetrodotoxin-sensitive and Ca 2+-dependent and was under GABA B autoreceptor control. Under these experimental conditions, acetylcholine (0.1–10 μM) and physostigmine (30 μM) decreased the electrically evoked GABA release while the M 2 receptor antagonist AFDX-116 (0.01–0.1 μM) counteracted these effects. Similar results were also observed in a cortical synaptosomal preparation stimulated with K + (10 mM). These findings demonstrate an inhibitory cholinergic regulation of electrically evoked GABA release via M 2 receptors located on cortical GABAergic terminals. 相似文献
2.
The effects of dithiothreitol (DTT) and, reduced (GSH) and oxidized (GSSG), glutathione on the release of [ 3H]GABA evoked by glutamate and its agonists were studied in rat hippocampal slices. DTT had no effect on the basal release of [ 3H]GABA but it enhanced and prolonged the glutamate agonist-evoked release. This effect was abolished by (+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)cyclohept-5,10-imine hydrogen maleate (MK-801), a noncompetitive NMDA antagonist, and blocked by Mg 2+ ions. It was only slightly attenuated by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a non-NMDA receptor antagonist, and not affected by
-(+)-2-amino-3-phosphonopropionate (
-AP3), a selective antagonist of the metabotropic glutamate receptor. The effect of DTT on the NMDA-evoked release of GABA was only slightly affected by extracellular Ca 2+ but completely blocked by verapamil even in the absence of Ca 2+. GSH and GSSG attenuated or abolished the effects of DTT on the agonist-induced release of [ 3H]GABA. The results imply that the enhanced and prolonged release of GABA evoked by the coexistence of DTT and excitatory amino acids and attenuated by endogenous GSH and GSSG is a consequence of sustained activation of the NMDA receptor-governed ionophores, which contain functional thiol groups. DTT, GSH and GSSG may regulate the redox state and accessibility of these groups. In addition to the influx of extracellular Ca 2+, DTT mobilizes Ca 2+ from intracellular pools distinct from those regulated by metabotropic glutamate receptors. 相似文献
3.
Extracellular ATP dose dependently stimulated 45Ca 2+ influx even in the presence of nifedipine, a Ca 2+ antagonist that inhibits voltage-dependent Ca 2+ channel, in osteoblast-like MC3T3-E1 cells. ATP stimulated arachidonic acid release and the synthesis of prostaglandin E 2 (PGE 2). However, the ATP-induced arachidonic acid release was significantly reduced by chelating extracellular Ca 2+ with EGTA. On the other hand, ATP induced DNA synthesis of these cells in a dose-dependent manner in the range between 1μM and 1 mM. The pretreatment with indomethacin, a cyclooxygenase inhibitor, suppressed both ATP-induced PGE 2 synthesis and DNA synthesis in these cells. The inhibitory effect by 50μM indomethacin on the DNA synthesis was reversed by adding 10μM PGE 2. These results strongly suggest that extracellular ATP stimulates Ca 2+ influx resulting in the release of arachidonic acid in osteoblast-like cells and that extracellular ATP-induced proliferative effect is mediated, at least in part, by ATP-stimulated PGE 2 synthesis. 相似文献
4.
The intracellular free Ca 2+ ion concentration ([Ca 2+]i) was measured using fura-2 microspec-trofluorimetry in individual rat pancreatic β-cells prepared by enzymatic digestion and fluorescence-activated cell sorting. The mean basal concentration of [Ca 2+]i in β-cells in the presence of 4.4 mM glucose and 1.8 mM Ca 2+ was 112±1.6 nM (n=207). The action of acetylcholine (ACh) was concentration-dependent, and raising the concentration resulted in [Ca 2+]i spikes of increasing amplitude and duration in some, but not all of the β-cells. In addition, the β-cells demonstrated variable sensitivity to ACh. The increases in [Ca 2+]i were rapid, transient and were blocked by atropine at 10 -6M. A brief exposure to 50 mM K + resulted in a transient increase in [Ca 2+]i similar to that induced by ACh, but resistant to atropine. A high concentration of ACh (100μL 10 -4M or 10 -3M) induced [Ca 2+]i oscillations in 11 out of 57 β-cells in the presence of 4.4 mM glucose. Using calcium channel blockers and Ca 2+ free medium, the source of the increase in [Ca 2+]i was deduced to be from extracellular spaces. Changing the temperature from 22 to 37°C did not affect the action of ACh on [Ca 2+]i. These data strongly suggest that ACh exerted a direct action on [Ca 2+]i in normal rat pancreatic β-cells and support a role for Ca 2+ as a second messenger in the action of ACh. 相似文献
5.
Purified synaptic vesicles were isolated from hog cerebral cortex by a rapid procedure consisting of homogenization of cerebral cortex slices in iso-osmotic sucrose, differential centrifugation and sucrose density-gradient centrifugation. The purity of the vesicles was evaluated both biochemically and morphologically. The vesicles contained high amounts of γ-aminobutyrate (GABA) and acetylcholine at specific concentrations of 390 nmol/mg protein and 7.2 nmol/mg protein respectively. Glutamate decarboxylase, the enzyme which catalyses GABA formation, binds to the synaptic vesicles in a calcium-dependent manner. The percentage of glutamate decarboxylase bound to the vesicles increases from about 5% without calcium, reaching a plateau of about 60% at 4 mM Ca2+. Magnesium in concentrations 0.2–10 mM has no significant effect on glutamate decarboxylase binding. Also in phospholipid vesicles (small unilamellar phosphatidylserine-phosphatidylcholine. 2:1 liposomes) Ca2+, but not Mg2+, induced the binding of glutamate decarboxylase, reaching a plateau of 50% at 2 mM Ca2+. Both in synaptic vesicles and in phospholipid vesicles the calcium-dependent glutamate decarboxylase binding seems to be specific, and not caused by unspecific association of proteins, since the specific binding (bound enzyme activity/mg bound protein) increases 3-fold from 0 to 4 mM Ca2+. The functional role of this binding was studied in GAD containing vesicles by measuring the relationship between the accumulation of [3H]GABA, newly synthetized from [3H]glutamate, and the uptake of added [14C]GABA. No significant uptake of [14C]GABA was found under the experimental conditions used, whereas large amounts of [3H]GABA were found within the vesicles. It appears that the [3H]GABA accumulation process is functionally linked to [3H]GABA synthesis and is mediated by the membrane-bound glutamate decarboxylase. This synthesis-coupled uptake of GABA into synaptic vesicles possibly serves to bring about a plasticity effect in previously stimulated GABAergic nerve endings. 相似文献
6.
We have studied the effects of cholinegic agonists on the rates of insulin release and the concentrations of diacylglycerol (DAG) and intracellular free Ca 2+ ([Ca 2+] i) in the β-cell line MIN6. Insulin secretion was stimulated by glucose, by glibenclamide and by bombesin. In the presence of glucose, both acetylcholine (ACh) and carbachol (CCh) produced a sustained increase in the rate of insulin release which was blocked by EGTA or verapamil. The DAG content of MIN6 β-cells was not affected by glucose. Both CCh and ACh evoked an increase in DAG which was maximal after 5 min and returned to basal after 30 min; EGTA abolished the cholinergic-induced increased in DAG. ACh caused a transient rise in [Ca 2+] i which was abolished by omission of Ca 2+ or by addition of devapamil. Thus, cholinergic stimulation of β-cell insulin release is associated with changes in both [Ca 2+] i and DAG. The latter change persists longer than the former and activation of protein kinase C and sensitization of the secretory process to Ca 2+ may underlie the prolonged effects of cholinergic agonists on insulin release. However, a secretory response to CCh was still evident after both [Ca 2+] i and DAG had returned to control values suggesting that additional mechanisms may be involved. 相似文献
7.
A spontaneous efflux of choline originating from the cytoplasmic free choline compartment and, partly, from metabolized form was measured from neurons and glial cells in culture. The efflux was stimulated by an excess of K + and by the absence of Ca 2+ ions from the incubation medium in both types of culture. The two effects did not appear to be synergistic. The stimulation produced by an excess of K+ (100 mM) was blocked in neurons by 0.5 μM BaCl2 and in glia cells by 0.1 μM BaCl2 (in the presence of 30 mM K+). The stimulation produced by the absence of Ca2+ instead was not blocked by Ba2+ ions in either of the two types of culture. The results suggest that the stimulation induced by K+ (high concentration and long time of incubation) might be of biochemical rather than physiological nature and that choline may be driven out of the cells in correlation with the K+ gradient. The greater sensitivity of glial cells to K+ ions may also suggest a supportive role of these cells with respect to neurons, as they seem capable of furnishing choline for neuronal needs during depolarization. 相似文献
8.
Abstract: Following incubation with [ 14C]y-aminobutyric acid (GABA) or [ 3H]dopamine, slices of rat striatum were superfused with media containing 36 mM K + or ethylenediamine (EDA), 1 or 5 mM. Both K + and EDA induced a release of [ 14C]GABA, the K +-induced release being largely Ca 2+-dependent, while the EDA-induced release was not. Whereas K + also evoked a Ca 2+-dependent release of [ 3H]dopamine, EDA evoked no release of dopamine. EDA may therefore have potential as a specific GABA releasing agent. 相似文献
9.
A self-referencing and non-invasive Ca 2+-sensitive vibrating electrode was used to assess the effects of hydrogen peroxide-induced oxidative challenges on the efflux and influx of calcium across the plasma membrane of single nerve cells cultured from abdominal ganglion of Aplysia californica. A reduced net efflux of Ca 2+ from the cell soma occurred immediately after the addition of hydrogen peroxide (0.0025 mM, 0.005 mM or 0.01 mM) to the culture medium, indicating damage to the cell membrane or Ca 2+ transport mechanism. There then followed a marked efflux, the extent and duration of which was related to the concentration of hydrogen peroxide used and which may reflect compensatory activity by the Ca 2+ regulatory mechanisms in the plasmalemma. No morphological changes were observed in cells challenged with 0.0025 mM hydrogen peroxide and the enhanced rate of Ca 2+ efflux rapidly decreased to pre-exposure values. Sustained and enhanced Ca 2+ effluxes from those cells exposed to 0.005 mM or 0.01 mM hydrogen peroxide were also consistent with regulatory pumping of Ca 2+ out of the cell although contraction and blebbing of neurites and swelling of the soma may indicate that a proportion of the efflux arose from release of Ca 2+ from disrupted intracellular stores. The vibrating electrode is a useful additional technique for the study of the pathogenesis of neurological conditions, as ionic fluxes across single nerve cells exposed to physiologically-relevant concentrations of free radicals can be monitored non-invasively for prolonged periods. 相似文献
10.
We previously demonstrated that oxysterols added to the culture medium of NRK 49F cells labelled with [ 14C] arachidonic acid potentiated arachidonic acid (AA) release and prostaglandin (PG) E 2 biosynthesis induced by the activation of these cells with fetal calf serum (FCS). In the absence of FCS, oxysterols had no effect on AA release. As phospholipase (Plase) A 2 activity is Ca 2+-dependent, we investigated whether oxysterol potentiating effect on AA release was related to an effect of these compounds on cell Ca 2+ concentration. In this paper, we show that the intensity of potentiation by oxysterol varies with the external cell Ca 2+ concentration; when external Ca 2+ is chelated by EGTA, the oxysterol effect persists, though it is decreased. The Ca 2+ channel inhibitor nifedipine does not decrease the potentiating effect of 25-OH cholesterol, indicating that, if oxysterol favours Ca 2+ entry into the cell, the nifedipine inhibited channel is not involved. At the usual concentration (5 μm/ml), oxysterols are not able to increase, mimmediately or after a short time of contact (90 min) the concentration of intracellular free Ca 2+ ([Ca 2+]) i measured by fluorescence of Quinn-2; at very high concentration of oxysterol (25 μm/ml), [Ca 2+] i only slightly increases (+30%). The liberation of AA induced by cell activation with the Ca 2+ ionophore ionomycin is also potentiated by 25-OH cholesterol. All these observations are not in favour of a proper effect o oxysterols on cell Ca 2+ level. 相似文献
11.
Abstract: To see the effect of a γ-aminobutyric acid GABA uptake inhibitor on the efflux and content of endogenous and labeled GABA, rat cortical slices were first labeled with [ 3H]GABA and then superfused in the absence or presence of 1 m M nipecotic acid. Endogenous GABA released or remaining in the slices was measured with high performance liquid chromatography, which was also used to separate [ 3H]GABA from its metabolites. In the presence of 3 m M K +, nipecotic acid released both endogenous and [ 3H]GABA, with a specific activity four to five times as high as that present in the slices. The release of labeled metabolite(s) of [ 3H]GABA was also increased by nipecotic acid. The release of endogenous GABA evoked by 50 m M K + was enhanced fourfold by nipecotic acid but that of [ 3H]GABA was only doubled when expressed as fractional release. In a medium containing no Ca 2+ and 10 m M Mg 2+, the release evoked by 50 m MK+ was nearly suppressed in either the absence or the presence of nipecotic acid. In the absence of nipecotic acid electrical stimulation (bursts of 64 Hz) was ineffective in evoking release of either endogenous or [ 3H]GABA, but in the presence of nipecotic acid it increased the efflux of endogenous GABA threefold, while having much less effect on that of [ 3H]GABA. Tetrodotoxin (TTX) abolished the effect of electrical stimulation. Both high K + and electrical stimulation increased the amount of endogenous GABA remaining in the slices, and this increase was reduced by omission of Ca 2+ or by TTX. The results suggest that uptake of GABA released through depolarization is of major importance in removing GABA from extracellular spaces, but the enhancement of spontaneous release by nipecotic acid may involve intracellular heteroexchange. Depolarization in the presence of Ca 2+ leads to an increased synthesis of GABA, in excess of its release, but the role of this excess GABA remains to be established. 相似文献
12.
In order to examine intracellular modulation of CNS catecholamine release, cerebrocortical synaptosomes were prelabeled with [ 3H]noradrenaline and permeabilized with streptolysin-O in the absence or presence of Ca 2+. Plasma membrane permeabilization allowed efflux of cytosol and left a compartmentalized pool of [ 3H]noradrenaline intact, approximately 10% of which was released by addition of 10 −5 M Ca 2+. Addition of activators or inhibitors of protein kinase C, as well as inhibitors of Ca 2+-calmodulin kinase II or calcineurin, failed to change Ca 2+-induced noradrenaline release. Evoked release from permeabilized synaptosomes deficient in the vesicle-associated phosphoprotein synapsin I was also unchanged. In contrast, addition of a synthetic ‘active domain’ peptide from the myristoylated, alanine-rich C-kinase substrate (MARCKS) protein increased, while addition of calmodulin decreased Ca 2+-induced release from the permeabilized synaptosomes, the latter effect being reversed by a peptide inhibitor of calcineurin. Moreover, addition of the actin-destabilizing agent DNase I, as well as antibodies to MARCKS, appeared to increase spontaneous, Ca 2+-independent release from noradrenergic vesicles. These results indicate that the MARCKS protein may modulate release from permeabilized noradrenergic synaptosomes, possibly by modulating calmodulin levels and/or the actin cytoskeleton. 相似文献
13.
We investigated the restoration of [Ca 2+] i in fura-2-loaded human platelets following discharge of internal Ca 2+ stores in the absence of external Ca 2+. After stimulation by thrombin [Ca 2+] i returned from a peak level of 0.6 μM to resting levels within 4 min. When ionomycin discharged the internal stores the recovery was slower with [Ca 2+] i still elevated at around 0.5 μM after 5 min. Thrombin added shortly after ionomycin could accelerate the recovery of [Ca 2+] i and restore resting levels within 5 min, an effect that was mimicked by phorbol-12-myristate-13-acetate (PMA). Since the continued presence of ionomycin precluded reuptake into the internal stores we conclude that thrombin and PMA stimulate Ca 2+ efflux, perhaps via protein kinase C actions on a plasma membrane Ca 2+ pump. 相似文献
14.
The effect of clomiphene, an ovulation-inducing agent, on cytosolic free Ca 2+ levels ([Ca 2+] i) in populations of PC3 human prostate cancer cells was explored by using fura-2 as a Ca 2+ indicator. Clomiphene at concentrations between 10-50 μM increased [Ca 2+] i in a concentration-dependent manner. The [Ca 2+] i signal was biphasic with an initial rise and a slow decay. Ca 2+ removal inhibited the Ca 2+ signal by 41%. Adding 3 mM Ca 2+ increased [Ca 2+] i in cells pretreated with clomiphene in Ca 2+-free medium, confirming that clomiphene induced Ca 2+ entry. In Ca 2+-free medium, pretreatment with 50 μM brefeldin A (to permeabilize the Golgi complex), 1 μM thapsigargin (to inhibit the endoplasmic reticulum Ca 2+ pump), and 2 μM carbonylcyanide m-chlorophenylhydrazone (to uncouple mitochondria) inhibited 25% of 50 μM clomiphene-induced store Ca 2+ release. Conversely, pretreatment with 50 μM clomiphene in Ca 2+-free medium abolished the [Ca 2+] i increase induced by brefeldin A, thapsigargin or carbonylcyanide m-chlorophenylhydrazone. The 50 μM clomiphene-induced Ca 2+release was unaltered by inhibiting phospholipase C with 2 μM 1-(6-((17β-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122). Trypan blue exclusion assay suggested that incubation with clomiphene (50 μM) for 2-15 min induced time-dependent decrease in cell viability by 10-50%. Collectively, the results suggest that clomiphene induced [Ca 2+] i increases in PC3 cells by releasing store Ca 2+ from multiple stores in an phospholipase C-independent manner, and by activating Ca 2+ influx; and clomiphene was of mild cytotoxicity. 相似文献
15.
Rabbit retinac preloaded with [ 3H]adenosine were superfused in vitro and the effect of neurotransmitter agonists and antagonists on the release of [ 3H]purines was studied. Glutamic acid, aspartic acid, kainic acid (KA), quisqualic acid (QUIS) and
acid (NMDA) all stimulated the efflux of [ 3H] labelled and endogenous purines. Their effect was reduced in a Ca 2+-free medium except when using a high concentration (100 μM) of KA, QUIS and NMDA. The effect of aspartic acid and of NMDA were blocked by 2-amino-7-phosphono-heptanoic acid (APH) and 2-amino-5-phosphono-valeric acid (APV). Carbachol also increased the release of adenosine-derived radioactivity and this effect was reduced by the removal of Ca 2+ and by pretreatment with atropine. τ-Aminobutyric acid (GABA) and muscimol, induced a small increase in the release which was Ca 2+-dependent and was blocked by bicuculline and picrotoxin. Dopamine elicited an increase in the release which was partially reduced in a Ca 2+-free medium and was blocked by haloperidol. Glycine and 5-hydroxytryptamine (5-HT) also induced small but significant increases. The neurotransmitter antagonists had an effect of their own. Superfusion with APH and APV depressed the outflow of radioactivity whereas bicuculline, picrotoxin, strychnine and haloperidol enhanced it. The K +-evoked release of [ 3H]purines was reduced by haloperidol and by 5-HT. The observations indicate that stimulation of several important neurotransmitter receptors in the retina elicits the release of adenosine derivatives. The results with the antagonists also suggest that purines are continuously released as a result of a tonic activation of the respective membrane receptors. 相似文献
16.
The effect of five lignans isolated from Hernandia nymphaeifolia on estrogenic compounds (17β-estradiol, tamoxifen and clomiphene)-induced Ca 2+ mobilization in human neutrophils was investigated. The five lignans were epi-yangambin, epi-magnolin, epi-aschantin, deoxypodophyllotoxin and yatein. In Ca 2+–containing medium, the lignans (50–100 μM) inhibited 10 μM 17β-estradiol- and 5 μM tamoxifen-induced increases in intracellular free Ca 2+ levels ([Ca 2+] i) without changing 25 μM clomiphene-induced [Ca 2+] i increase. 17β-estradiol and tamoxifen increased [Ca 2+] i by causing Ca 2+ influx and Ca 2+ release because their responses were partly reduced by removing extracellular Ca 2+. In contrast, clomiphene solely induced Ca 2+ release. The effect of the lignans on these two Ca 2+ movement pathways underlying 17β-estradiol- and tamoxifen-induced [Ca 2+] i increases was explored. All the lignans (50–100 μM) inhibited 10 μM 17β-estradiol-and 5 μM tamoxifen-induced Ca 2+ release, and 17β-estradiol-induced Ca 2+ influx. However, only 100 μM epi-aschantin was able to reduce tamoxifen-induced Ca 2+ influx while the other lignans had no effect. Collectively, this study shows that the lignans altered estrogenic compounds-induced Ca 2+ signaling in human neutrophils in a multiple manner. 相似文献
17.
N-Acetylaspartate (NAA) is a largely neuron specific dianionic amino acid present in high concentration in vertebrate brain. Many fundamental questions concerning N-acetylaspartate in brain remain unanswered. One such issue is the predominantly neuronal synthesis and largely glial catabolism which implies the existence of a regulated efflux from neurons. Here we show that transient (5 min) NMDA-receptor activation (60 μM) induces a long lasting Ca 2+-dependent efflux of N-acetylaspartate from organotypic slices of rat hippocampus. The NMDA-receptor stimulated efflux was unaffected by hyper-osmotic conditions (120 mM sucrose) and no efflux of N-acetylaspartate was evoked by high K +-depolarization (50 mM) or kainate (300 μM). These results indicate that the efflux induced by NMDA is not related directly to either cell swelling or depolarization but is coupled to Ca 2+-influx via the NMDA-receptor. The efflux of N-acetylaspartate persisted at least 20 min after the omission of NMDA, similar to the efflux of the organic anions glutathione and phosphoethanolamine. The efflux of taurine and hypotaurine was also stimulated by NMDA but returned more quickly to basal levels. The NMDA-receptor stimulated efflux of N-acetylaspartate, glutathione, phosphoethanolamine, taurine and hypotaurine correlated with delayed nerve cell death measured 24 h after the transient NMDA-receptor stimulation. However, exogenous administration of high concentrations of N-acetylaspartate to the culture medium was non-toxic. The results suggest that Ca 2+-influx via the NMDA-receptor regulates the efflux of N-acetylaspartate from neurons which may have both physiological and pathological importance. 相似文献
18.
These studies examined the regulation by GABA of norepinephrine release from hypothalamus, preoptic area and frontal cortex. Using superfused brain slicesfrom female rats, we show that 100 μM GABA enhances both basal and electrically stimulated release of 3H-norepinephrine in all three brain regions. The GABA A agonist muscimol (100 μM) significantly augments 3H-norepinephrine release, but it is somewhat less effective than GABA. The GABA B agonist baclofen has little or no effect on basal 3H-norepinephrine efflux. GABA also augments both the magnitude and duration of electrically evoked 3H-norepinephrine release in slices from all three brain regions. GABA facilitation of electrically stimulated 3H-norepinephrine release is mediated through GABA A receptors as evidenced by its blockad by 10 μM bicuculline, a GABA A antagonist, but not by 200 μM 2-OH-saclofen, a GABA B antagonist. These data show that the inhibitory amino acid neurotransmitter GABA enhances both basal and evoked release of 3H-norepinephrine in brain slices from female rats. These effects are predominantly mediated by GABA A receptors. GABA modulation of hypothalamic norepinephrine release may play a role in the regulation of gonadotropin secretion and reproductive behaviors such as lordosis. 相似文献
19.
Abstract: The release processes of endogenous Acetylcholine (ACh), γ-aminobutyric acid (GABA), glutamate (Glu) and glutamine (GLN) were studied in superfused guinea-pig caudatal slices. Basal ACh release remained constant for up to 2 h, while the basal release of GABA, Glu and GLN declined to half or less of its initial values after 1 h of superfusion. Electrical stimulation increased the ACh release by 700–800% and that of GABA by 80% whereas it decreased the output of Glu by 50% and failed to modify the GLN efflux. KCl (25 mM) increased the output of ACh by 400%, that of GABA by approximately 500% and decreased that of Glu by 40%. Substituting of CaCl 2 by MgCl 2 in the superfusion medium reduced the basal ACh release by 70% whereas no differences were observed in the basal efflux of GABA, Glu and GLN. Under these conditions, no evoked release of ACh or of GABA was detected, following electrical or KCl stimulation. Tetrodotoxin 5 × 10 -7 M decreased the basal ACh release by 60% and increased the GABA efflux by 40%. The toxin abolished the stimulus-evoked ACh efflux but scarcely affected that of GABA. These results are consistent with a possible neurotransmitter role of ACh and GABA in the striatum and show some differences in the ionic mechanisms underlying GABA and ACh release. 相似文献
20.
The ability of vasopressin to elevate cytosolic Ca 2+ in small cell lung cancer (SCLC) cells was investigated. Ten nanomolar vasopressin elevated the cytosolic Ca 2+ in 6 of 8 SCLC cell lines that were loaded with Fura-2 AM. Using SCLC cell line NCI-H345, the effect of vasopressin was dose dependent, being maximal at 100 nM, where the cytosolic Ca 2+ was elevated from 150 to 210 nM. Because addition of 1 mM EGTA had no effect on the vasopressin response, vasopressin released Ca 2+ from intracellular pools. Also, oxytocin weakly elevated the cytosolic Ca 2+. The response to vasopressin was strongly blocked by [(β-mercapto-β,β-cyclopentamethylene propionic acid) 1,O-MeTyr 2,Arg 8]vasopressin and weakly blocked by [(β-mercapto-β,β-cyclopentamethylene propionic acid) 1,O-MeTyr 2,Orn 8]vasotocin. These data suggest that V 1 vasopressin receptors are present on SCLC cells. 相似文献
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