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1.
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 Ca2+-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 Ca2+-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 Ca2+-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   

2.
Release of γ-aminobutyric acid (GABA) can be elicited by electrical field stimulation even in the absence of external Ca2+. Indeed, the release of GABA under such conditions is even higher than in the presence of Ca2+. To investigate the underlying mechanism of this phenomenon, the release of endogenous GABA from rat striatal slices was measured by high performance liquid chromatography with electro- chemical detection. Electrical stimulation at 2 Hz for 3 min elevated GABA efflux by 4.5-fold. Withdrawing external Ca2+ and adding 1 mM EGTA produced a small, transient increase in the basal efflux of GABA and increased electrically-evoked overflow 3-fold. Tetrodotoxin (5 μM) did not affect basal efflux in either normal or Ca2+-free conditions, but abolished electrically-evoked release. In the presence of normal Ca2+, nipecotic acid (1 mM) enhanced both spontaneous efflux and evoked overflow. Nipecotic acid also increased spontaneous release when external Ca2+ was removed. However, in the absence of Ca2+, nipecotic acid failed to increase electrically evoked GABA overflow. These results suggest that there exists a Ca2+-independent process for GABA release via the same carrier system that is utilized for high affinity GABA uptake.  相似文献   

3.
Light-dependent Ca2+ efflux via the Ca2+/H+ antiport in the photosynthetic purple sulfur bacterium Chromatium vinosum was inhibited by three phenothiazines: chlorpromazine; trifluoperazine and phenothiazine. The inhibitors had no effect on Ca2+ uptake by C. vinosum in the dark nor any effect on the light-dependent efflux of either Na+ or Tl+ catalyzed, respectively, by the C. vinosum Na+/H+ or K+/H+ antiports. Ruthenium red and LaCl3, neither of which inhibited light-dependent Ca2+ efflux in C. vinosum, markedly inhibited Ca2+ uptake in the dark by C. vinosum cells. Ruthenium red had no effect on the uptake of either Na+or the K+ analog T1+ by C. vinosum cells in the dark. These results have been interpreted in terms of two separate Ca2+ transport systems in C. vinosum: (i) a phenothiazine-sensitive and ruthenium red, La3+-insensitive Ca2+/H+ antiport responsible for Ca2+ efflux in the light; and (ii) a ruthenium red and La3+-sensitive but phenothiazine-insensitive Ca2+ uptake system.  相似文献   

4.

1. 1. (Mg2+ + Ca2+) ATPases of microsomal and synaptic membrane preparations from immature and adult rat brain were activated by calcium (0.1–10 μM), maximal activation was found at 3 μM. The increase in (Mg2+ + Ca2+) ATPase seen during development was greatest in the synaptic membrane preparations.

2. 2. At 37°C both Na+ or K+ at concentrations higher than 30 mM inhibited the microsomal Mg2+ ATPase, but the (Mg2+ + Ca2+) ATPase was stimulated by both Na+ and K+. Synaptic membrane Mg2+ ATPase was inhibited by concentrations higher than 100 mM K+; Na+ however stimulated this enzyme at all concentrations. Much of this Na+ stimulated activity was ouabain sensitive. Synaptic membrane (Mg2+ + Ca2+) ATPase was stimulated by Na+ or K+, this stimulation follows approximate saturation kinetics with an apparent Km of 18.8 mM Na+ or K+.

3. 3. Arrhenius plots of microsomal (Mg2+ + Ca2+) ATPase were curvilinear, but two intersecting lines with a break at 20°C could be fitted. The calculated energies of activation from these lines were very similar in immature and adult preparations. The synaptic membrane preparation (adult) also gave a curvilinear plot; but two intersecting lines with a break at 25°C could be fitted to the data. These lines had slopes of 21 and 28 Kcal mole−1 above and below the break, respectively. The immature preparation when made using EDTA gave a Arrhenius plot of very similar form to the adult preparation. Without EDTA however the Arrhenius plot was complex with a plateau at 25–32°C. Pretreatment with EDTA activated the synaptic membrane (Mg2+ + Ca2+) ATPase from both immature and adult brain.

Author Keywords: Brain; ATPase; temperature; development; synaptic membranes  相似文献   


5.
通过盆栽试验,采用原子吸收分光光度法和非损伤微测技术,研究了NaHCO3胁迫(300 mmol·L-1)对大洋洲滨藜、四翅滨藜和宁夏枸杞3种灌木离子吸收及运转的影响.结果表明: 随着NaHCO3浓度升高,两种滨藜和宁夏枸杞叶片中Na+含量升高,300 mmol·L-1NaHCO3胁迫下,宁夏枸杞叶肉细胞Na+的外排增加,两种滨藜净Na+外排降低;随着胁迫时间的延长,大洋洲滨藜和宁夏枸杞叶片的K+含量下降,Na+/K+升高,四翅滨藜叶片K+含量升高,Na+/K+降低;随着浓度的升高,宁夏枸杞叶片积累Ca2+减少,Na+/Ca2+高于对照,叶肉细胞Ca2+外排;两种滨藜叶Ca2+含量总体呈升高趋势,叶肉细胞Ca2+表现为内流.在NaHCO3胁迫下,3种灌木通过不同的策略来消除Na+毒害.宁夏枸杞叶片Na+的积累抑制了对Ca2+的吸收;两种滨藜Ca2+的内流促使细胞质中游离Ca2+增加,增加的细胞质\[Ca2+\]cyt防治质膜H+ ATPase去极化,限制K+的外排,从而维持细胞内Na+/K+的平衡,其中四翅滨藜调控Na+/K+平衡的能力较强.  相似文献   

6.
通过盆栽试验,采用原子吸收分光光度法和非损伤微测技术,研究了NaHCO3胁迫(300 mmol·L-1)对大洋洲滨藜、四翅滨藜和宁夏枸杞3种灌木离子吸收及运转的影响.结果表明: 随着NaHCO3浓度升高,两种滨藜和宁夏枸杞叶片中Na+含量升高,300 mmol·L-1NaHCO3胁迫下,宁夏枸杞叶肉细胞Na+的外排增加,两种滨藜净Na+外排降低;随着胁迫时间的延长,大洋洲滨藜和宁夏枸杞叶片的K+含量下降,Na+/K+升高,四翅滨藜叶片K+含量升高,Na+/K+降低;随着浓度的升高,宁夏枸杞叶片积累Ca2+减少,Na+/Ca2+高于对照,叶肉细胞Ca2+外排;两种滨藜叶Ca2+含量总体呈升高趋势,叶肉细胞Ca2+表现为内流.在NaHCO3胁迫下,3种灌木通过不同的策略来消除Na+毒害.宁夏枸杞叶片Na+的积累抑制了对Ca2+的吸收;两种滨藜Ca2+的内流促使细胞质中游离Ca2+增加,增加的细胞质\[Ca2+\]cyt防治质膜H+ ATPase去极化,限制K+的外排,从而维持细胞内Na+/K+的平衡,其中四翅滨藜调控Na+/K+平衡的能力较强.  相似文献   

7.
The store-mediated Ca2+ entry was detected in single and cluster of rat submandibular acinar cells by measuring the Ca2+ activated ionic membrane currents. In the cells where intracellular Ca2+ was partly depleted by stimulation with submaximal concentration of acetylcholine (ACh) under a Ca2+-free extracellular condition, an employment of external Ca2+ in the absence of ACh caused a sustained increase of the K+ current without affecting the Cl current. A renewed ACh challenge without external Ca2+ caused repetitive spikes of both K+ and Cl currents due to the Ca2+ release. SK & F 96365 inhibited the generation of the sustained K+ current and refilling of the Ca2+ store following the Ca2+ readmission. It is suggested that the Ca2+ enters the cell through the store-mediated pathway near the K+ channels and is taken up by the store. Thus, only Ca2+ released from the store can activate both the K+ and Cl currents.  相似文献   

8.
A self-referencing and non-invasive Ca2+-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 Ca2+ 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 Ca2+ 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 Ca2+ regulatory mechanisms in the plasmalemma. No morphological changes were observed in cells challenged with 0.0025 mM hydrogen peroxide and the enhanced rate of Ca2+ efflux rapidly decreased to pre-exposure values. Sustained and enhanced Ca2+ effluxes from those cells exposed to 0.005 mM or 0.01 mM hydrogen peroxide were also consistent with regulatory pumping of Ca2+ 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 Ca2+ 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   

9.
Fluoxetine, a selective 5-HT uptake inhibitor, inhibited 15 mM K+-induced [3H] 5-HT release from rat spinal cord and cortical synaptosomes at concentrations > 0.5 uM. This effect reflected a property shared by another selective 5-HT uptake inhibitor paroxetine but not by less selective uptake inhibitors such as amitriptyline, desipramine, imipramine or nortriptyline. Inhibition of release by fluoxetine was inversely related to both the concentration of K+ used to depolarize the synaptosomes and the concentration of external Ca2+. Experiments aimed at determining a mechanism of action revealed that fluoxetine did not inhibit voltage-independent release of [3H] 5-HT release induced by the Ca2+-ionophore A 23187 or Ca2+-independent release induced by fenfluramine. Moreover the 5-HT autoreceptor antagonist methiothepin did not reverse the inhibitory actions of fluoxetine on K+-induced release. Further studies examined the effects of fluoxetine on voltage-dependent Ca2+ channels and Ca2+ entry. Whereas fluoxetine and paroxetine inhibited binding of [3H] nitrendipine to the dihydropyridine-sensitive L-type Ca2+ channel, the less selective uptake inhibitors did not alter binding. The dihydropyridine antagonist nimodipine partially blocked fluoxetine-induced inhibition of release. Moreover enhanced K+-stimulated release due to the dihydropyridine agonist Bay K 8644 was reversed by fluoxetine. Fluoxetine also inhibited the K+-induced increase in intracellular free Ca2+ in fura-2 loaded synaptosomes. These data are consistent with the suggestion that fluoxetine inhibits K+-induced [3H] 5-HT release by antagonizing voltage-dependent Ca2+ entry into nerve terminals.  相似文献   

10.
The intracellular free Ca2+ ion concentration ([Ca2+]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 [Ca2+]i in β-cells in the presence of 4.4 mM glucose and 1.8 mM Ca2+ was 112±1.6 nM (n=207). The action of acetylcholine (ACh) was concentration-dependent, and raising the concentration resulted in [Ca2+]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 [Ca2+]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 [Ca2+]i similar to that induced by ACh, but resistant to atropine. A high concentration of ACh (100μL 10-4M or 10-3M) induced [Ca2+]i oscillations in 11 out of 57 β-cells in the presence of 4.4 mM glucose. Using calcium channel blockers and Ca2+ free medium, the source of the increase in [Ca2+]i was deduced to be from extracellular spaces. Changing the temperature from 22 to 37°C did not affect the action of ACh on [Ca2+]i. These data strongly suggest that ACh exerted a direct action on [Ca2+]i in normal rat pancreatic β-cells and support a role for Ca2+ as a second messenger in the action of ACh.  相似文献   

11.
以冰叶日中花(Mesembryanthemum crystallinum L.)实生苗为材料,经NaCl、NaCl+ CaCl_2、NaCl+LaCl_3处理后,利用电感耦合等离子发射光谱仪检测叶、茎、根中Na~+、K~+、Ca~(2+)、Mg~(2+)含量,计算K~+/Na~+、Ca~(2+)/Na~+和Mg~(2+)/Na~+比值,利用非损伤微测技术测定根尖Na~+流和K~+流,研究盐胁迫下钙在维持离子平衡中的作用。结果显示,NaCl处理后,冰叶日中花各器官中Na~+含量增加,K~+、Ca~(2+)、Mg~(2+)含量降低,离子比值降低;CaCl_2处理降低了Na~+含量,提高了K~+、Ca~(2+)、Mg~(2+)含量,离子比值升高,而LaCl_3处理后的结果相反。经NaCl处理24 h后,冰叶日中花根尖Na~+和K~+明显外流,加入CaCl_2后,Na~+外流速度显著增加,K~+外流速度受到抑制,而加入LaCl_3后则降低了Na~+的外流速度,促进了K~+的外流。研究结果表明冰叶日中花受到盐胁迫后,钙参与了促进根部Na~+外排、抑制K~+外流的过程,进而保持各器官中较低的Na~+含量,表明钙在维持和调控离子平衡中起到重要作用。  相似文献   

12.
The effect of clomiphene, an ovulation-inducing agent, on cytosolic free Ca2+ levels ([Ca2+]i) in populations of PC3 human prostate cancer cells was explored by using fura-2 as a Ca2+ indicator. Clomiphene at concentrations between 10-50 μM increased [Ca2+]i in a concentration-dependent manner. The [Ca2+]i signal was biphasic with an initial rise and a slow decay. Ca2+ removal inhibited the Ca2+ signal by 41%. Adding 3 mM Ca2+ increased [Ca2+]i in cells pretreated with clomiphene in Ca2+-free medium, confirming that clomiphene induced Ca2+ entry. In Ca2+-free medium, pretreatment with 50 μM brefeldin A (to permeabilize the Golgi complex), 1 μM thapsigargin (to inhibit the endoplasmic reticulum Ca2+ pump), and 2 μM carbonylcyanide m-chlorophenylhydrazone (to uncouple mitochondria) inhibited 25% of 50 μM clomiphene-induced store Ca2+ release. Conversely, pretreatment with 50 μM clomiphene in Ca2+-free medium abolished the [Ca2+]i increase induced by brefeldin A, thapsigargin or carbonylcyanide m-chlorophenylhydrazone. The 50 μM clomiphene-induced Ca2+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 [Ca2+]i increases in PC3 cells by releasing store Ca2+ from multiple stores in an phospholipase C-independent manner, and by activating Ca2+ influx; and clomiphene was of mild cytotoxicity.  相似文献   

13.
The effects of K+ channel modulators, tetraethylammonium, 4-aminopyridine and diazoxide, and high extracellular K+ on cell growth and agonist-induced intracellular Ca2+ mobilization were investigated. Two human brain tumour cell lines, U-373 MG astrocytoma and SK-N-MC neuroblastoma, were used as model cellular systems. K+ channel modulators and increased extracellular K+ concentration inhibited tumour cell growth in a dose-related fashion in both cell lines. In addition, agonist (carbachol or serum)-induced intracellular Ca2+ mobilization was also blocked by the pretreatment of growth-inhibitory concentrations of K+ channel modulators and high extracellular K+. Thus, these results suggest that K+ channel modulators are effective inhibitors of brain tumour cell growth and that their growth regulation may be due to the interference with the intracellular Ca2+ signalling mechanisms.  相似文献   

14.
Glial fibrillary acidic protein (GFAP), which was purified from acetone powder of the bovine spinal cord, was reassembled in 0.1 M imidazole HCl buffer containing metallic cations, Ca2+, Mg2+, Na+ or K+ at physiological or more acidic pH. An electron microscopy revealed reassembled glial filaments at pH 6.8 without any cations but amorphous aggregates at pH 6.3 which were readily observed as a white precipitate by the naked eye. Under more alkaline pH (pH 7.4) only rod-shaped short filaments were formed. In the presence of mM concentrations of Ca2+ or Mg2+, thick bundles of glial filaments, detectable by light microscopy, were formed at acidic pH. At pH 7.4 long reassembled filaments could be formed in the buffer containing divalent cations. Na+ (0.1 M) made filament-like structures of GFAP but they are rather random compared to the filaments promoted by the divalent cations. K+ made only amorphous aggregation of the short filaments. These findings indicate that the reassembly of GFAP at physiological pH requires essentially divalent cations but not ionic strength.  相似文献   

15.
Glucose-induced insuline release, glucose-induced rises in intracellular free Ca2+ concentration ([Ca2+]i), and voltage-dependent Ca2+ channel activity were assessed in monolayer cultures of β-vells 3–5 day-old rats. The glucose-stimulated insulin secretory responses and [Ca2+]i rises were like those in adult rat β-cells rather than fetal rat β-cells. Voltage-dependent Ca2+ channel antagonists decreased glucose-induced insulin secretion, aborted the [Ca2+]2 rise and, like deprivation of extracellular Ca2+, prevented the glucose-induced rise in [Ca2+]i when added before the glucose challenge. The presence of nifedipine-sensitive, voltage-dependent Ca2+ channels was demonstrated directly by measuring Ca2+ currents using the whole-cell configuration of the patch-clamp technique and indirectly by measuring [Ca2+]1 after membrane depolarization by 45 mMm K+ or 200 μM tolbutamide. Thus, in cultured β-cells of 3–5 day-old rats the coupling of glucose stimulation to Ca2+ influx is essentially mature, in contrast to what has been reported for fetal or very early neonatal cells.  相似文献   

16.
Oxidative stress to B-cells is thought to be of relevance in declining B-cell function and in the process of B-cell destruction. In other tissues including heart, brain and liver, oxidative stress has been shown to elevate the intracellular free calcium concentration and to provoke potassium efflux. We studied the effect of oxidative stress on Ca2+ and K+ (Rb+) outflow from pancreatic islets using the thiol oxidants DIP and BuOOH. Both compounds reversibly increased 86Rb+ efflux in the presence of 3 and 16.7 mmol/l glucose. Stimulation of 86Rb+ efflux was also evident in the absence of calcium. DIP evoked release of 45Ca2+ from the pancreatic islets both in the presence or absence of extracellular calcium. Employing inhibitors of the calcium-activated potassium channel (KCa) and the high conductance K+-channel (BKCa), the effect of DIP on 86Rb+ efflux was slightly diminished. Tolbutamide had no effect on 86Rb+ efflux in the presence of DIP. On the other hand thapsigargin, a blocker of the Ca2+-ATPase of the endoplasmic reticulum, completely suppressed the DIP-mediated 86Rb+ outflow. The data suggest that thiol oxidant-induced potassium efflux from pancreatic islets is mainly mediated through liberation of intracellular calcium and subsequent stimulation of calcium-activated potassium efflux.  相似文献   

17.
W K Pollock  S O Sage  T J Rink 《FEBS letters》1987,210(2):132-136
We investigated the restoration of [Ca2+]i in fura-2-loaded human platelets following discharge of internal Ca2+ stores in the absence of external Ca2+. After stimulation by thrombin [Ca2+]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 [Ca2+]i still elevated at around 0.5 μM after 5 min. Thrombin added shortly after ionomycin could accelerate the recovery of [Ca2+]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 Ca2+ efflux, perhaps via protein kinase C actions on a plasma membrane Ca2+ pump.  相似文献   

18.
At pH 7, addition of glucose under anaerobic conditions to a suspension of the yeast Saccharomyces cerevisiae causes both a transient hyperpolarization and a transient net efflux of K+ from the cells. Hyperpolarization shows a peak at about 3 min and a net K+ efflux at 4–5 min. An additional transient hyperpolarization and net K+ efflux are found after 60–80 and 100 min, respectively. Addition of 2-deoxyglucose instead of glucose does not lead to hyperpolarization of the cells or K+ efflux. At low pH, neither transient hyperpolarization nor a transient K+ efflux are found. With ethanol as substrate and applying aerobic conditions, both a transient hyperpolarization and a transient K+ efflux are found at pH 7. The fluorescent probe 2-(dimethylaminostyryl)-1-ethylpyridinium appears to be useful for probing changes in the membrane potential of S. cerevisiae. It is hypothesized that the hyperpolarization of the cells is due to opening of K+ channels in the plasma membrane. Accordingly, the hyperpolarization of the cells at pH 7 is almost completely abolished by 1.25 mM K+, whereas the same amount of Na+ does not reduce the hyperpolarization  相似文献   

19.
Markus Hoth 《FEBS letters》1996,390(3):285-288
Highly Ca2+ selective Ca2+ channels activated by store depletion have been recently described in several cell types and have been termed CRAC channels (for calcium release-activated calcium). The present study shows that following store depletion in mast and RBL-1 cells, monovalent outward currents could be recorded if the internal solution contained K+ but not Cs+. The activation of the outward K+ current correlated with the activation of ICRAC, in both time and amplitude, suggesting that the K+ current might be carried by CRAC channels. The amplitude of the outward current was increased if external Ca2+ was reduced or replaced by external Ba2+. The outward K+ conductance might have a physiological role in maintaining the driving force for Ca2+ entry during the activation of CRAC channels.  相似文献   

20.
Estrogen rapidly alters the excitability of hypothalamic neurons that are involved in regulating numerous homeostatic functions including reproduction, stress responses, feeding and motivated behaviors. Some of the neurons include neurosecretory neurons such as gonadotropin-releasing hormone (GnRH) and dopamine neurons, and local circuitry neurons such as proopiomelanocortin (POMC) and γ-aminobutyric acid (GABA) neurons. We have elucidated several non-genomic pathways through which the steroid alters synaptic responses in these hypothalamic neurons. We have examined the modulation by estrogen of the coupling of various receptor systems to inwardly-rectifying and small-conductance, Ca2+-activated K+ (SK) channels using intracellular sharp-electrode and whole-cell recording techniques in hypothalamic slices from ovariectomized female guinea pigs. Estrogen rapidly uncouples μ-opioid receptors from G protein-gated inwardly-rectifying K+ (GIRK) channels in POMC neurons and GABAB receptors from GIRK channels in dopamine neurons as manifested by a reduction in the potency of μ-opioid and GABAB receptor agonists to hyperpolarize their respective cells. This effect is blocked by inhibitors of protein kinase A (PKA) and protein kinase C (PKC). In addition, after 24 h following steroid administration in vivo, the GABAB/GIRK channel uncoupling observed in GABAergic neurons of the preoptic area is associated with reduced agonist efficacy. Conversely, estrogen enhances the efficacy of 1-adrenergic receptor agonists to inhibit apamin-sensitive SK currents in these preoptic GABAergic neurons, and does so in both a rapid and sustained fashion. Finally, we observed a direct, steroid-induced hyperpolarization of GnRH neurons. These findings indicate a richly complex yet coordinated steroid modulation of K+ channel activity in hypothalamic (POMC, dopamine, GABA, GnRH) neurons that are involved in regulating numerous homeostatic functions.  相似文献   

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