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PubMed2005

Canonical transient receptor potential 1 plays a role in basic fibroblast growth factor (bFGF)/FGF receptor-1-induced Ca2+ entry and embryonic rat neural stem cell proliferation.

Basic fibroblast growth factor (bFGF) and its major receptor FGF receptor-1 (FGFR-1) play an important role in the development of the cortex. The mechanisms underlying the mitogenic role of bFGF/FGFR-1 signaling have not been elucidated. Intracellular Ca2+ concentrations ([Ca2+]i) in proliferating cortical neuroepithelial cells are markedly dependent on Ca2+ entry (Maric et al., 2000a). The absence of voltage-dependent Ca2+ entry channels, which emerge later, indicates that other membrane mechanisms regulate [Ca2+]i during proliferation. Canonical transient receptor potential (TRPC) family channels are candidates because they are voltage independent and are expressed during CNS development (Strübing et al., 2003). Here, we investigated the involvement of TRPC1 in bFGF-mediated Ca2+ entry and proliferation of embryonic rat neural stem cells (NSCs). Both TRPC1 and FGFR-1 are expressed in the embryonic rat telencephalon and coimmunoprecipitate. Quantitative fluorescence-activated cell sorting analyses of phenotyped telencephalic dissociates show that approximately 80% of NSCs are TRPC1+, proliferating, and express FGFR-1. Like NSCs profiled ex vivo, NSC-derived progeny proliferating in vitro coexpress TRPC1 and FGFR1. Antisense knock-down of TRPC1 significantly decreases bFGF-mediated proliferation of NSC progeny, reduces the Ca2+ entry component of the Cai2+ response to bFGF without affecting Ca2+ release from intracellular stores or 1-oleoyl-2-acetyl-sn-glycerol-induced Ca2+ entry, and significantly blocks an inward cation current evoked by bFGF in proliferating NSCs. Both Ca2+ influx evoked by bFGF and NSC proliferation are attenuated by Gd3+ and SKF96365 two antagonists of agonist-stimulated Ca2+ entry. Together, these results show that TRPC1 contributes to bFGF/FGFR-1-induced Ca2+ influx, which is involved in self-renewal of embryonic rat NSCs.

Animals↗

PubMed2002

Early patterning of the mouse embryo--contributions of sperm and egg.

The first cleavage of the fertilised mouse egg divides the zygote into two cells that have a tendency to follow distinguishable fates. One divides first and contributes its progeny predominantly to the embryonic part of the blastocyst, while the other, later dividing cell, contributes mainly to the abembryonic part. We have previously observed that both the plane of this first cleavage and the subsequent order of blastomere division tend to correlate with the position of the fertilisation cone that forms after sperm entry. But does sperm entry contribute to assigning the distinguishable fates to the first two blastomeres or is their fate an intrinsic property of the egg itself? To answer this question we examined the distribution of the progeny of early blastomeres in embryos never penetrated by sperm - parthenogenetic embryos. In contrast to fertilised eggs, we found there is no tendency for the first two parthenogenetic blastomeres to follow different fates. This outcome is independent of whether parthenogenetic eggs are haploid or diploid. Also unlike fertilised eggs, the first 2-cell blastomere to divide in parthenogenetic embryo does not necessarily contribute more cells to the blastocyst. However, even when descendants of the first dividing blastomere do predominate, they show no strong predisposition to occupy the embryonic part. Thus blastomere fate does not appear to be decided by differential cell division alone. Finally, when the cortical cytoplasm at the site of sperm entry is removed, the first cleavage plane no longer tends to divide the embryo into embryonic and abembryonic parts. Together these results indicate that in normal development fertilisation contributes to setting up embryonic patterning, alongside the role of the egg.

Animals↗

PubMed2006

[Effect of latrunculin B, jasplakinolide and brefeldin A on the store-dependent Ca2+ entry in macrophages].

Using Fura-2AM microfluorimetry, effect of actin filament modifiers and vesicular trafficking inhibitor on the store-dependent Ca2+ entry induced by purinergic agonists (ATP, UTP) and endoplasmic Ca2+-ATPase inhibitors (thapsigargin, cyclopiazonic acid) in rat peritoneal macrophages was investigated. It was shown that inhibition of actin polymerization by latrunculin B had a biphasic time-dependent effect on Ca2+ entry, showing an initial potentiation followed by inhibition of Ca2+ entry. Moreover, addition of latrunculin B after induction of store-dependent Ca2+ entry inhibited the Ca2+ influx. Jasplakinolide, which reorganizes actin filaments into a tight cortical layer adjacent to the plasma membrane, prevented activation of store-dependent Ca2+ entry but did not modify this process after its activation. Vesicular transport inhibitor brefeldin A, which inactivates arfproteins, inhibited activation of store-dependent Ca2+ entry but did not alter this mechanism once being initiated. These data are compatible with the sectretion-like coupling model for store-dependent Ca2+ entry in macrophages based on a reversible trafficking and coupling of Ca2+ store with the plasma membrane.

Animals↗

PubMed1993

Effect of diazepam on cortical 5-HT release and behaviour in the guinea-pig on exposure to the elevated plus maze.

Previous studies have used the elevated plus maze to test for "anxiolytic" drugs in rats. The present study demonstrates that guinea-pigs handled daily from birth exhibit similar behaviour to rats on the plus maze. Pretreatment with diazepam (1.0 mg/kg) significantly increased the time the animals spent in the open arms and amount of entries into the open arms. Using intra-cortical microdialysis on exposure of the guinea-pig to the elevated plus maze resulted in increased extracellular 5-HT in the frontal cortex. Diazepam reduced, but not significantly, the increase in extracellular 5-HT and produced an "anxiolytic" profile of behaviour. Pretreatment with the benzodiazepine antagonist flumazenil (10.0 mg/kg) fully antagonised the behavioural effects of diazepam. Flumazenil also reduced the effect of diazepam on the increase in extracellular 5-HT observed on exposure of the guinea-pig to the elevated plus maze. Flumazenil alone decreased basal extracellular cortical 5-HT but had no effect on behaviour in the elevated plus maze. The results show that an increase in extracellular 5-HT occurs in the guinea-pig exposed to aversive conditions. While it remains to be determined whether the "anxiolytic" effects of diazepam in the guinea-pig are causally associated with decreased extracellular 5-HT, it is of interest that the selective benzodiazepine antagonist also prevented the increase in basal extracellular 5-HT produced by the exposure to the elevated plus maze but had no effect on behaviour. Results indicate that there is no simple relationship between inhibition of 5-HT release and the "anxiolytic" action of benzodiazepines.

Animals↗

PubMed1996

Comparison of rear-entry (two-incision) and endoscopic techniques for reconstruction of the anterior cruciate ligament.

In this series of patients having reconstruction of the anterior cruciate ligament (ACL), the rear-entry (two-incision) technique with fixation from lateral incision into cortical bone was compared with the endoscopic technique with fixation from inside to more cancellous bone. The rear-entry technique was used in 44 cases of ACL deficiency (8 chronic and 36 acute), and the endoscopic technique was used in 42 cases (19 chronic and 23 acute). Both groups had similar demographics. Objective and subjective criteria were evaluated at an average of 22 months postoperatively. Follow-up KT-1000 arthrometer findings, range of motion, and results of the Lachman and pivot shift tests were compared. There were no significant differences between the two groups at 22 months' follow-up. Subjective assessment of intensity of pain, swelling, and giving way was done by visual analog scales (0 to 10 rating). None of these parameters showed any statistically significant differences between the two techniques. This study shows that both of these techniques for reconstruction of the ACL render satisfactory objective and subjective results.

Adult↗

PubMed2000

Protein kinase C activates non-capacitative calcium entry in human platelets.

1. In many non-excitable cells Ca2+ influx is mainly controlled by the filling state of the intracellular Ca2+ stores. It has been suggested that this store-mediated or capacitative Ca2+ entry is brought about by a physical and reversible coupling of the endoplasmic reticulum with the plasma membrane. Here we provide evidence for an additional, non-capacitative Ca2+ entry mechanism in human platelets. 2. Changes in cytosolic Ca2+ and Sr2+ were measured in human platelets loaded with the fluorescent indicator fura-2. 3. Depletion of the internal Ca2+ stores with thapsigargin plus a low concentration of ionomycin stimulated store-mediated cation entry, as demonstrated upon Ca2+ or Sr2+ addition. Subsequent treatment with thrombin stimulated further divalent cation entry in a concentration-dependent manner. 4. Direct activation of protein kinase C (PKC) by phorbol-12-myristate-13-acetate or 1-oleoyl-2-acetyl-sn-glycerol also stimulated divalent cation entry, without evoking the release of Ca2+ from intracellular stores. Cation entry evoked by thrombin or activators of PKC was abolished by the PKC inhibitor Ro-31-8220. 5. Unlike store-mediated Ca2+ entry, jasplakinolide, which reorganises actin filaments into a tight cortical layer adjacent to the plasma membrane, did not inhibit divalent cation influx evoked by thrombin when applied after Ca2+ store depletion, or by activators of PKC. Thrombin also activated Ca2+ entry in platelets in which the release from intracellular stores and store-mediated Ca2+ entry were blocked by xestospongin C. 6. These results indicate that the non-capacitative divalent cation entry pathway is regulated independently of store-mediated entry and does not require coupling of the endoplasmic reticulum and the plasma membrane. These results support the existence of a mechanism for receptor-evoked Ca2+ entry in human platelets that is independent of Ca2+ store depletion. This Ca2+ entry mechanism may be activated by occupation of G-protein-coupled receptors, which activate PKC, or by direct activation of PKC, thus generating non-capacitative Ca2+ entry alongside that evoked following the release of Ca2+ from the intracellular stores.

Blood Platelets↗

PubMedDate not supplied

Elucidating penetration pathways into the hair fiber using novel microscopic techniques.

Much controversy exists regarding the route of penetration of molecules into hair fibers. In brief, there are two schools of thought. The first argument is that molecules enter the hair fiber via the cell membrane complex (cmc) of the cuticle and then diffuse throughout the cortex via both the intercellular cement and the bulk of individual cortical cells. The second approach concludes that entry to the fiber is via the endocuticle and other non-keratinous parts of the fiber. In the latter case the cmc is definitely not considered to have a role in the penetration of molecules into the fiber. The tools available for studying penetration into the fiber, e.g., light and electron microscopy, mean that it is usually only possible to extract static information from a dynamic process. Similarly, great care is needed in the interpretation of images produced by the various techniques. Where a molecule is seen to end up does not always indicate how it got there! In these studies I have used novel derivations of conventional electron microscopic techniques, combined with early photographic chemistry, to elucidate further the pathways of penetration into the hair fiber. From these studies one can conclude that both arguments describing penetration into the fiber are complementary, valid, and highly relevant. The techniques allow one to visualize material within the cell membrane complex of the cuticle. In addition, these studies show that the high-sulphur proteins of the cuticle, usually considered as highly cross-linked and inaccessible, are easily penetrated. Therefore, all of the structures within a hair fiber should be considered as penetration routes into the hair fiber for the delivery of industrial and cosmetic materials, even though they may not form continuous pathways throughout the hair. The hair should be viewed as a structure composed of a number of compartments of differing capacity, chemistry, and accessibility, rather than as continuous pathways from the surface to the center of the fiber.

Animals↗

PubMed1990

Alcohol exposure and undernutrition: effects on lipid metabolism and alcohol partitioning in rat brain regions in vitro.

The effects of maternal alcohol consumption and undernutrition on lipid metabolism and alcohol partitioning in brain cortical and stem slices of pups were studied under in vitro conditions. Alcohol administration along with a normal diet during gestation and lactation resulted in an increase in the synthesis of cholesterol in cortical and stem slices associated with decreased entry of alcohol. Phospholipid metabolism was not affected in the cortex, whereas the incorporation of [32P] was found to be altered in the brain stem, indicating regional differences with respect to alcohol effects. Undernutrition induced by feeding the mothers a low protein diet, on the other hand, decreased the incorporation of labelled precursors into lipids in cortex and stem. The changes in lipid metabolism observed in the high protein alcohol pups were not evident in the brain regions of undernourished pups exposed to alcohol and the partitioning of alcohol was not altered.

Acetates↗

PubMed2005

[Technique for percutaneous iliosacral screw insertion with conventional C-arm radiography].

BACKGROUND: During percutaneous iliosacral screw fixation, fluoroscopy with a conventional C-arm X-ray unit is still the standard procedure for intraoperative orientation. Lateral sacral images in combination with the inlet and outlet view are always necessary. Nevertheless, the complex pelvic anatomy makes it difficult to prevent malpositioning of screws. OPERATIVE TECHNIQUE: Defining the correct entry into the bone is the decisive step for ideal screw placement. The better this is defined, the larger safety margins will be concerning cortical perforation by the screws. In the lateral view, an entry ventral to the sacral canal has to be avoided as well as an entry into the cranial half of the first sacral vertebra. To improve the surgeon's three-dimensional orientation with the help of his personal experience and two-dimensional images, it is recommended to place the tip of the screws in the center of the sacrum (in AP view) whenever possible. Routinely performed postoperative CT imaging of 24 screws, consecutively implanted according to the standards described, revealed no case of malpositioning. CONCLUSION: Standard X-ray views in combination with standardized aiming of screw entry position and final screw thread position enable the surgeon to find the "safe zone" for iliosacral screw insertion and to prevent iliosacral screw malpositioning with high accuracy.

Bone Screws↗

PubMed1989

Polarity of sperm entry in the ascidian egg.

We have investigated the point of sperm entry in denuded eggs of the ascidian Phallusia mammillata. In contrast to what is generally believed, the sperm show a strong tendency to enter the animal hemisphere rather than the vegetal hemisphere. After entry, the sperm nucleus is carried toward the vegetal pole of the egg during the cortical contraction which occurs within a few minutes after fertilization. This polarity of sperm entry is abolished and the entry point is randomized by pretreating the eggs with cytochalasin D. We suggest that cytochalasin may act by randomizing components needed for sperm attachment or fusion, or structures needed for sperm entry.

Animals↗

PubMed1987

Effects of calcium entry blocker emopamil on postischemic energy metabolism of the isolated perfused rat brain.

The effects of emopamil on postischemic energy metabolism and electroencephalographic (EEG) recovery were investigated in the isolated rat brain perfused at either constant pressure or, alternatively, at constant flow rate. Flow rate and perfusion pressure were monitored continuously. The brains were perfused with a fluorocarbon emulsion for 30 min, and after 30 min of ischemia, perfusion was reinstituted for 5, 30, or 60 min. Global cerebral perfusion rate was increased by emopamil throughout the perfusion period and, accordingly, in brains perfused at a constant flow rate, perfusion pressure was reduced by the drug. At constant pressure perfusion, after 5 min after ischemia, cortical levels of creatine-phosphate, adenosine triphosphate (ATR), glucose, glucose-6-phosphate, and fructose-6-phosphate were higher in emopamil-treated brains than in controls, although the levels of adenosine diphosphate (ADP) and adenosine monophosphate (AMP) were reduced. When brains were perfused at constant flow rate, however, emopamil exhibited no effect on brain energy metabolism in the early reperfusion period. Postischemic restoration of high-energy phosphates proved to depend on the flow rate used. After 30 min of postischemic reperfusion, cortical levels of lactate were lower in emopamil-treated brains compared to controls at both constant pressure and constant volume perfusion. Postischemic lactate levels were independent of flow rate and were also reduced when emopamil was only present during reperfusion. The postischemic restoration of cortical EEG activity was improved by the calcium entry blocker.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Changes in the blood-thymus barrier of adult rats after estradiol-treatment.

The accessibility of the thymus parenchyma for relatively large Mw (+/- 150 Kd) proteins has been studied by the intravenous injection of monoclonal antibodies (mAbs) specific either for all T cells (His-17) or MHC class II molecules (His-19) in control and estradiol benzoate (EB)-treated adult Wistar rats. In controls, the transcapsular route rather than cortical capillaries seems to be involved in the entry of molecules into the thymus. By contrast, a specific staining for either T cells (His-17) or MHC class II molecules (His-19 positive cells) disappears almost completely from the thymic cortex of EB-treated rats except in the immediate subcapsular epithelial cell layer. In these rats, T cells and epithelial cells intimately associated to blood vessels from both inner cortex and corticomedullary border showed additional staining with the respective mAbs confirmed by electron microscopy. The disappearance of the transcapsular route together with the increased vascular permeability of cortical blood vessels would be related to the reinforcement of the subcapsular epithelial cell layer and to direct effects of EB on vascular endothelia, respectively. These results are discussed in relationship to the cell migration into and out of adult thymus, as suggested by the changes in intrathymic T cell subsets evaluated by flow cytometry.

Animals↗

PubMed2001

Presynaptic Ca2+ channels and neurotransmitter release at the terminal of a mouse cortical neuron.

Regional variation in synaptic efficacy is an important determinant of associative processing as information flows through major circuits of the brain. The perforant path is the principal route of entry from cortex to the hippocampus and contains the first synapse in the cortical-hippocampal projection pathway. We used optical imaging techniques to analyze presynaptic Ca(2+) entry and neurotransmitter release at synapses in the medial perforant path linking stellate neurons located in layer II of the entorhinal cortex to granule cells in the dentate gyrus. Similar to other excitatory central synapses, the relationship between neurotransmitter release and the amount of Ca(2+) influx can be best described by a Hill equation with a Hill coefficient of 3.5. Our Ca(2+) channel toxin studies indicate that P/Q-type channels are the predominant Ca(2+) source triggering neurotransmitter release in this pathway, as shown by a potent inhibition of Ca(2+) entry and synaptic transmission by the P/Q-type channel blocker omega-agatoxin IVA. However, compared with the downstream hippocampal pyramidal neuron CA3-CA1 synapse, neurotransmitter release was less sensitive to the N-type Ca(2+) channel blocker omega-conotoxin GVIA, although the amount of N-type Ca(2+) current is comparable. The contribution of N-type channels to neurotransmitter release approximates that found at the CA3-CA1 synapse when tested under lower [Ca(2+)](o), which effectively reduces the size of the Ca(2+) microdomain surrounding each channel. These results suggest that P/Q-type channels are more closely associated with release machinery then N-type channels at this synapse and that cooperativity differences for each channel subtype may characterize variations in signaling at central synapses.

Animals↗

PubMed1993

Feedback regulation of Na channels in rat CCT. II. Effects of inhibition of Na entry.

Na channels in the apical membrane of the rat renal cortical collecting tubule were studied using the patch-clamp technique. Channel activity was monitored in cell-attached patches on tubules that were split open to expose the luminal surface. Channel number (N), open probability (Po), and single-channel currents (i) were measured at 37 degrees C during continuous superfusion of the tubule. Addition of amiloride (10 microM) or benzamil (0.5 microM) to the superfusate resulted in a twofold increase in the mean number of open channels (NPo) after 2 min. The effect closely paralleled an increase in i, presumably reflecting membrane hyperpolarization. The effects on both i and NPo reversed within 3 min after removal of amiloride. The increase in NPo was accounted for, at least in part, by an increase in Po. Several cellular events may contribute to this phenomenon. Channels could be activated directly by membrane hyperpolarization and by cell shrinkage, both of which are known to occur during acute administration of amiloride. In addition, benzamil elicited a 30% decrease in intracellular Ca compared with control levels as measured by fura-2 fluorescence. A comparable decrease observed after reducing extracellular Ca did not increase NPo. No changes in cell pH, measured with 2',7'-bis-(carboxyethyl)-5(6)-carboxyfluorescein fluorescence, were observed. The modulation of channel Po by the rate of Na entry into the cell will act as a feedback mechanism to maintain cellular ion homeostasis, and this may also serve to distribute Na reabsorption more evenly along the nephron.

Amiloride↗

PubMed2000

A role for the actin cytoskeleton in the initiation and maintenance of store-mediated calcium entry in human platelets. Evidence for conformational coupling.

The nature of the mechanism underlying store-mediated Ca(2+) entry has been investigated in human platelets through a combination of cytoskeletal modifications. Inhibition of actin polymerization by cytochalasin D or latrunculin A had a biphasic time-dependent effect on Ca(2+) entry, showing an initial potentiation followed by inhibition of Ca(2+) entry. Moreover, addition of these agents after induction of store-mediated Ca(2+) entry inhibited the Ca(2+) influx mechanism. Jasplakinolide, which reorganizes actin filaments into a tight cortical layer adjacent to the plasma membrane, prevented activation of store-mediated Ca(2+) entry but did not modify this process after its activation. In addition, jasplakinolide prevented cytochalasin D-induced inhibition of store-mediated Ca(2+) entry. Calyculin A, an inhibitor of protein serine/threonine phosphatases 1 and 2 which activates translocation of existing F-actin to the cell periphery without inducing actin polymerization, also prevented activation of store-mediated Ca(2+) entry. Finally, inhibition of vesicular transport with brefeldin A inhibited activation of store-mediated Ca(2+) entry but did not alter this mechanism once initiated. These data suggest that store-mediated Ca(2+) entry in platelets may be mediated by a reversible trafficking and coupling of the endoplasmic reticulum with the plasma membrane, which shows close parallels to the events mediating secretion.

Actins↗

PubMed1978

Visual orientation in the rat: a dissociation of deficits following cortical and collicular lesions.

Rats with either bilateral ablations of superior colliculus, bilateral ablations of visual cortex, or sham operations were trained to run across a large arena towards a small illuminated target which varied in location from trial to trial. An impairment in this visually-guided running was apparent in the cortical group, but not in the collicular group. When, in a second experiment, the spatial relationships within the apparatus were changed by extending the entry-tunnel some distance into the arena, the running of the cortical group became even more impaired, while the collicular animals continued to run towards the targets under efficient visual control. In a third experiment, the effect of introducing a novel flashing light in various locations around the perimeter of the arena was investigated. It was found that unlike the other two groups, the collicular animals showed no orienting reflex to the novel stimulus when it was presented outside a broad central area of the visual field.

Animals↗

PubMed2000

Sperm entry induces polarity in fucoid zygotes.

Fucoid zygotes establish a rhizoid-thallus growth axis in response to environmental signals; however, these extrinsic cues are not necessary for polarization, suggesting that zygotes may have inherent polarity. The hypothesis that sperm entry provides a default pathway for polarization of zygotes cultured in the absence of environmental signals was tested, and was supported by several lines of evidence. First, an F-actin patch, a cortical marker of the rhizoid pole, formed at the sperm entry site within minutes of fertilization. Second, the sperm entry site predicted the site of polar adhesive secretion (the first morphological manifestation of the rhizoid pole) and the position of rhizoid outgrowth. Third, when fertilization was restricted to one hemisphere of the egg, rhizoid outgrowth always occurred from that hemisphere. Fourth, delivery of sperm to one location within a population of eggs resulted in polarization of both adhesive secretion and rhizoid outgrowth toward the sperm source. Finally, induction of polyspermy using low sodium seawater increased the frequency of formation of two rhizoids. Sperm entry therefore provides an immediate default axis that can later be overridden by environmental cues.

Actins↗

PubMed1998

Cortical granule exocytosis is triggered by different thresholds of calcium during fertilisation in sea urchin eggs.

In sea urchin eggs, fertilisation is followed by a calcium wave, cortical granule exocytosis and fertilisation envelope elevation. Both the calcium wave and cortical granule exocytosis sweep across the egg in a wave initiated at the point of sperm entry. Using differential interference contrast (DIC) microscopy combined with laser scanning confocal microscopy, populations of cortical granules undergoing calcium-induced exocytosis were observed in living urchin eggs. Calcium imaging using the indicator Calcium Green-dextran was combined with an image subtraction technique for visual isolation of individual exocytotic events. Relative fluorescence levels of the calcium indicator during the fertilisation wave were compared with cortical fusion events. In localised regions of the egg, there is a 6s delay between the detection of calcium release and fusion of cortical granules. The rate of calcium accumulation was altered experimentally to ask whether this delay was necessary to achieve a threshold concentration of calcium to trigger fusion, or was a time-dependent activation of the cortical granule fusion apparatus after the 'triggering' event. Calcium release rate was attenuated by blocking inositol 1,4,5-triphospate (InsP3)-gated channels with heparin. Heparin extended the time necessary to achieve a minimum concentration of calcium at the sites of cortical granule exocytosis. The data are consistent with the conclusion that much of the delay observed normally is necessary to reach threshold concentration of calcium. Cortical granules then fuse with the plasma membrane. Further, once the minimum threshold calcium concentration is reached, cortical granule fusion with the plasma membrane occurs in a pattern suggesting that cortical granules are non-uniform in their calcium sensitivity threshold.

Animals↗