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PubMed1978

Dextran T 500--induction of spreading in Ehrlich ascites tumour cells on glass surface.

The experiments were carried out in order to find factors which could induce attachment and spreading of Ehrlich ascites tumour (EAT) cells on solid substrata. In normal culture media, serum-free as well as serum-containing, these cells did not spread and very weakly attached onto glass. It was found that after coating the cell surfaces with dextran T 500 the EAT cells strongly attached and spread extensively on glass. This spreading could be inhibited or reversed by washing out the dextran or adding calf serum. Dextran T 500 caused rapid spreading also in chick embryo fibroblasts and mouse lymphocytes. Some aspects of these results in connection with contemporary views concerning the processes of cell attachment and spreading are discussed.

Animals↗
PubMed1983

Anchorage and lymphocyte function. Spreading-capacity distinguishes common thymocytes and peripheral T lymphocytes.

Contact of T-enriched human blood lymphocytes with an adhesive surface in the presence of Concanavalin A (Con A) almost immediately induced a sequence of motile changes in virtually all cells. The initial event in this spreading process was the formation of filopodia distinct from the microvilli of lymphocytes in suspension. The filopodia were accompanied by lamellipodia, ruffles and flattening of the nucleus. Contact with a nonadhesive substratum in the presence of Con A did not trigger this sequence of changes. Cytochalasin B and D or low temperature inhibited the contact-induced changes. With the exception of a small number of cells (5-15%), T-enriched lymphocytes that were allowed to settle in the absence of Con A showed a radius of action (area occupied by the cells/translational movement per hr) of 39 micrometers 2/ less than 1 micrometer. The small 'motile' population showed a radius of action of 74 micrometers 2/8 micrometers. The Con-A-mediated spreading-process yielded a radius of action of the lymphocytes of 117 micrometers 2/6 micrometers. This augmented radius of action markedly facilitated cell-cell interaction in a high frequency of the cells and appeared to be a prerequisite for such interactions at 'low' cell density. Thymocytes reactive with OKT 6 antibodies or belonging to the 'high-density' fraction of cells attached to a Con-A-coated surface to the same extent as peripheral OKT 3 positive lymphocytes, but did not exhibit the morphological changes characteristic of a spreading-process. In contrast, OKT 6 negative thymocytes or thymocytes with a relatively low density showed spreading indistinguishable from that of OKT 3 positive peripheral lymphocytes. These results characterize the spreading-process in human T lymphocytes and demonstrate its functional importance for interactions with the environment. Spreading-capacity appears to reflect the stage of maturation of T cells.

Animals↗
PubMed1981

Extrajunctional spread of acetylcholine depolarization on frog skeletal muscle membrane.

1. The extrajunctional spread of end-plate depolarization induced by acetyl) choline (ACh) applied in the bathing solution was studied on frog (Rana esculenta-skeletal muscle fibers. 2. The characteristics of this spread were determined on sartorius muscles mounted in a chamber where the end-plate free pelvic part was separated by a rubber membrane from the end-plate containing tibial one. There was no change in membrane potential if ACh was applied selectively on the pelvic part, even at a concentration of 10 mmol/l. However, on applying 1 mmol/l ACh on the tibial part, depolarization spreading over to the pelvic part was observed. 3. The peak values of ACh depolarization were not modified by tetrodotoxin (TTX) at a concentration of 32 nmol/l, whereas it was decreased by 35% in the presence of 3.1 mumol/l TTX. 4. ACh depolarization measured on the extrajunctional membrane in the presence of TTX is the result of the electronic spread of end-plate depolarization. The length constant of this spread was about the same as the length constant determined by square pulse analysis. 5. When the generation and propagation of action potentials accompanying ACh depolarization were not blocked either by TTX or Na-free Ringer solution, the depolarization values observed on the pelvic part were slightly higher than what could have been expected on the basis of electrotonic behaviour. 6. The above results imply the absence of ACh receptors from the extrajunctional membrane of twitch fibres. Deviations from the electrotonic spread are due to the action potentials accompanying ACh depolarization.

Acetylcholine↗
PubMed1980

Induction of an attachment and spreading on glass of Ehrlich ascites tumour cells by alpha-saturated polyprenols.

It has been observed that a dolichol, alpha dihydro-undecaprenol, induces phenotypic changes in Ehrlich ascites tumour [EAT] cells. In the presence of this dolichol in the medium. EAT cells attach to glass and spread on it but grow in an overlapping pattern. This spreading takes place after a lag of between 72-96 hours at continuous exposure to the dolichol. When cells, once induced to spread, are trypsinized, they can spread once more within 3-6 hours in the dolichol-free medium. It is suggested that dolichols, which act as lipid intermediates in protein glycosylation, may represent a class of compounds which by interference with the biosynthesis of plasma membrane constituents influence surface properties of EAT cells and induce spreading. The results presented in this paper support the view that sugar moieties of plasma membrane constituents play a role in controlling cell attachment, spreading, and intercellular communication.

Animals↗
PubMedDate not supplied

Do patient variables influence the subarachnoid spread of hyperbaric lidocaine in the postpartum patient?

BACKGROUND AND OBJECTIVES: Age, height, weight, body mass index (weight/height2), and vertebral column length may affect the subarachnoid spread of local anesthetics. Little information exists concerning the relationship between these variables and the spread of hyperbaric lidocaine. The authors studied the influence of patient demographics on the block produced by hyperbaric lidocaine in women undergoing postpartum tubal ligation. METHODS: Within 48 hours of vaginal delivery, the authors studied 44 ASA class 1-2 women agreeing to spinal anesthesia for postpartum tubal ligation. Before induction of anesthesia, the authors weighed each patient, measured her height and vertebral column length, and calculated body mass index. In a standardized manner, the authors induced spinal anesthesia with 5% lidocaine 75 mg. An observer, blinded to the measured variables, evaluated loss-of-temperature sensation and loss-of-sensation of sharpness to pinprick bilaterally every 5 minutes for 30 minutes and again at 45 and 60 minutes. RESULTS: There was no correlation between age, weight, body mass index, vertebral column length, or time from delivery to placement of the block, and the spread of sensory block after subarachnoid injection of hyperbaric lidocaine. Only height weakly correlated with the spread of block (r2 = 0.15). CONCLUSIONS: While height may have some small influence on the spread of sensory block, the variation in spread of block within patients of the same height is large. The data suggest that adjusting the dose of local anesthetic injected based on differences in patient height would provide no clinically significant benefit.

Adult↗
PubMed1994

Fibroepithelioma of Pinkus. Eccrine duct spread of basal cell carcinoma.

The spread of basal cell carcinoma (BCC) directly into the dermis or down the sides of hair follicles is a common-place pathologic observation. BCC spread via eccrine ducts, which has received less recognition, is the subject of this investigation. We specifically address the question of whether eccrine duct spread accounts for the histologic pattern of the fibroepithelioma of Pinkus (feP) type of BCC. Twenty-five BCC, including 12 feP, five superficial BCC, six ordinary BCC, one BCC of the sole of the foot, and one BCC with prominent hair follicle spread were studied with H&E sections; 11 were immunostained for carcinoembryonic antigen. In ordinary BCC, occasional entrapped eccrine ducts were present. One superficial BCC surrounded the proximal portion of an eccrine duct. The BCC from the sole of the foot showed advanced spread down eccrine ducts; focal obliteration of duct epithelium and lumen was seen, as was transition to strands of solid BCC. Nine of the 12 feP showed one or several eccrine duct foci with tumor strands. These findings suggest that eccrine ducts serve as an initial template in feP and subsequently are replaced by the BCC. However, eccrine duct spread of BCC may occur without necessarily imparting an feP histologic pattern.

Carcinoembryonic Antigen↗
PubMed1993

Characterization of FN-C/H-V, a novel synthetic peptide from fibronectin that promotes rabbit corneal epithelial cell adhesion, spreading, and motility.

PURPOSE: Fibronectin promotes corneal epithelial cell adhesion and motility in vitro and plays an important role in corneal re-epithelialization during corneal wound healing. Multiple domains contribute to the adhesion- and motility-promoting activity of fibronectin. The aim of this study was to identify amino acid sequences that contribute to the rabbit corneal epithelial (RCE) cell adhesion- and motility-promoting activity of the 33 and 66 kD carboxy-terminal heparin-binding fragments of fibronectin. METHODS: Synthetic peptides derived from the 33/66 kD fragments of fibronectin were tested for their ability to directly promote RCE cell adhesion, spreading, and motility. To assess the contribution of these peptides to the activity of fibronectin and the 33/66 kD fragments of fibronectin, synthetic peptides, and antibodies against these peptides were tested for their ability to block RCE cell adhesion, spreading, and motility. RESULTS: In this study, we identified a novel peptide sequence derived from the 33/66 kD fragments of fibronectin, FN-C/H-V (WQPPRARI), that directly promotes the adhesion, spreading, and migration of RCE cells in a concentration-dependent manner. A second peptide from the 33/66 kD fragments of fibronectin, FN-C/H-IV (SPPRRARVT), promoted RCE cell adhesion and spreading, but did not promote RCE cell migration. In contrast, two synthetic peptides from the 33/66 kD fragments of fibronectin that were previously shown to promote RCE cell adhesion (FN-C/H-I and FN-C/H-III) did not promote RCE cell spreading or migration. Soluble FN-C/H-V inhibited RCE cell adhesion to surfaces coated with FN-C/H-V, the 33/66 kD fragments of fibronectin, and to fibronectin. In addition, polyclonal anti-FN-C/H-V IgG inhibited RCE cell adhesion to FN-C/H-V, the 33/66 kD fragments of fibronectin, and to fibronectin. Finally, polyclonal anti-FN-C/H-V IgG also inhibited RCE cell haptotactic migration on the 33/66 kD fragments. CONCLUSIONS: These data suggest that the amino acid sequence defined by peptide FN-C/H-V contributes to the adhesion-, spreading-, and motility-promoting activity of the 33/66 kD carboxy-terminal heparin-binding fragments of fibronectin. Given the important role of fibronectin in corneal wound healing, these findings provide additional insight into the complex molecular basis of corneal epithelial cell interactions with fibronectin and may be important in the context of corneal wound healing.

Amino Acid Sequence↗
PubMed1997

Signaling by adhesion in human neutrophils: activation of the p72syk tyrosine kinase and formation of protein complexes containing p72syk and Src family kinases in neutrophils spreading over fibrinogen.

Src family kinases are implicated in signaling by integrins in polymorphonuclear neutrophils (PMN). To identify proteins present in complexes with Src family kinases, we subjected p58(c-fgr) or p53/56(lyn) immunoprecipitates from Triton X-100 lysates of PMN incubated on fibrinogen-coated surfaces to in vitro kinase assays. Assays on p58(c-fgr) or p53/56(lyn) immunoprecipitates from Triton lysates of PMN induced to spread over fibrinogen in response to TNF-alpha showed that several proteins form complexes with Src family kinases and can be phosphorylated in vitro. Immunoblot analysis showed that the p72(syk) tyrosine kinase is one of these proteins. Formation of protein complexes containing Src family kinases and p72(syk) required PMN spreading because p72(syk) was not detected in p58(c-fgr) or p53/56(lyn) immunoprecipitates from PMN, which were stimulated with TNF-alpha, in suspension. In addition, induction of PMN spreading with Mn2+ in the absence of TNF-alpha promoted the formation of protein complexes containing Src family kinases and p72(syk). We also found that p72(syk)-autophosphorylating kinase activity was enhanced, and a fraction of p72(syk) was translocated to a Triton-insoluble cytoskeletal fraction in PMN induced to spread over fibrinogen by TNF-alpha or Mn2+. In vitro kinase assays on CD18 (beta 2 integrin subunit) immunoprecipitates from Triton lysates of spread PMN showed that several proteins formed complexes with CD18 and could be phosphorylated in vitro. Immunoblot analysis of CD18 immunoprecipitates allowed us to identify p72(syk) as one of these proteins. These findings show that PMN spreading is accompanied by activation of p72(syk) and formation of multimolecular complexes in which Src family kinases and p72(syk) colocalize.

CD18 Antigens↗
PubMed1977

In vitro suppression of macrophage spreading caused by supernatants of tumour, thymus, and lymph node cells.

Peritoneal macrophages washed out from C3Hf/Bu mice were cultivated in medium 199 supplemented with 35% foetal calf serum. If the pH of the medium was adjusted to 7.2, there were 70% spread macrophages after six hours of incubation at 37 degrees C. We investigated the effect of tumour cells on macrophage spreading. Supernatants from cell cultures of a fibro-sarcoma of C57BL mice and lymphoma of C3Hf/Bu mice were used to determine the number of spread macrophages after 6 hours of culture in these supernatants. Supernatants from cell cultures of the kidney, thymus and lymph nodes of normal C57BL or C3Hf/Bu mice and peritoneal cells of normal C3Hf/Bu mice in medium 199 alone served as control. We observed that supernatants from both allogeneic and syngeneic tumour cell cultures reduced significantly the percentage of spread macrophages in comparison with the percentage of spread macrophages found in the kidney culture supernatants. However, a similar spreading inhibition was caused also by supernatants from the thymus and lymph node cell cultures. In these experiments we confirmed the earlier observations that tumour cells can suppress the activation of macrophages, and we also pointed to the possibility that this effect is not specific only for malignant tissues.

Animals↗
PubMed1997

Integrin-mediated activation of mitogen-activated protein kinase is independent of the activation of protein kinase C epsilon during the spreading of HeLa cells on a gelatin substratum.

Spreading of HeLa cells on a gelatin substratum is initiated by the activation of protein kinase C epsilon (PKC epsilon) upon contact of the cells with the matrix. In this study, we examined the functional role of PKC epsilon in the activation of mitogen-activated protein kinase (MAP kinase) and its relationship to cell spreading. MAP kinase isoforms, Erk-1 and -2, are activated upon attachment of HeLa cells to gelatin. Inhibition of PKC with calphostin C blocked cell spreading without any effect on MAP kinase activation. In contrast, inhibition of MAP kinase kinase blocked adhesion-induced MAP kinase activation, but showed no effect on either translocation of PKC epsilon or cell spreading. Thus, activation of PKC epsilon that occurs upon HeLa cell attachment to gelatin is related to cell spreading but not to the activation of MAP kinase, and MAP kinase is activated upon HeLa cell attachment in the absence of cell spreading.

Calcium-Calmodulin-Dependent Protein Kinases↗
PubMed1998

Perineural spread of head and neck tumors: how accurate is MR imaging?

PURPOSE: Our aim was to determine the precision of MR imaging evaluation of perineural spread of head and neck tumors. METHODS: Nineteen patients had complete extirpation of head and neck tumors (10 squamous cell carcinomas, four adenoid cystic carcinomas, one poorly differentiated carcinoma, one salivary duct carcinoma, one mucoepidermoid carcinoma, one chordoma, and one meningioma) with histologic confirmation of perineural spread. Findings at presurgical contrast-enhanced MR imaging were compared with findings at pathologic examination. RESULTS: The sensitivity of MR imaging for detection of perineural spread was 95%; however, the sensitivity for mapping the entire extent of perineural spread fell to 63%. CONCLUSION: MR imaging may fail to depict microscopic foci of perineural tumor infiltration, leading to underestimation of the extent of perineural spread. Nevertheless, with careful analysis of foraminal architecture and MR enhancement patterns, one can reliably identify the presence if not the extent of perineural spread.

Adult↗
PubMed1991

Phenytoin and retinal spreading depression.

Several studies indicate that spreading depression is fundamentally related to seizure marches and to the aura of classical migraine. Moreover, recent investigations call attention to its possible relevance in clinical disturbances associated with brain ischemia, trauma, and hypoglycemia. The anticonvulsant phenytoin has been shown to protect the nervous tissue from the effects of anoxia and ischemia. These properties suggest that phenytoin should be able to counteract spreading depression. Therefore, we investigated its effect on spreading depression elicited by mechanical or chemical (KCl) stimulation, in isolated chick retinas. The results showed that phenytoin: (1) increases the threshold concentration of KCl to initiate the phenomenon; (2) decreases the velocity of propagation of spreading depression; (3) shortens considerably the duration of the slow potential, ionic (K+, Ca2+, Cl-), and volume changes of the extracellular compartment during spreading depression. Possible mechanisms underlying the observed effects are discussed.

Animals↗
PubMed1992

The oligemic phase of cortical spreading depression is not blocked by tirilazad mesylate (U-74006F).

Cortical spreading depression is characterised by a wave of depolarization that moves across the cortex leaving in its wake a state of hyperpolarization. Characteristic changes in cerebral blood flow are also seen and these consist of a wave of hyperemia followed by an oligemia, the latter lasting some hours in some experimental animals including the cat. In this study cerebral blood flow was measured using laser Doppler flowmetry in the anesthetised ventilated cat. Spreading depression was initiated with a pin-prick injury prior to or following administration of U74006F (tirilizad mesylate; 3 mg/kg, ivi) or an identical volume of vehicle. Laser Doppler probes were placed bilaterally and in each case studied both the hyperemic and oligemic phases of spreading depression were preserved after administration of either U74006F or its vehicle. These data suggest that free radical mechanisms have no significant role in mediating the blood flow changes of spreading depression and are consistent with data in the literature of a quantitative using single-point measurements that again U74006F does not affect spreading depression.

Animals↗
PubMed1993

Increase of catecholamine content in the extracellular space of the rat's brain cortex during spreading depression wave as determined by voltammetry.

The effect of chemically initiated (KCl) spreading cortical depression on catecholamine content in the extracellular cortical space was examined using voltammetry technique in chloralhydrate-anaesthetized rats. Correlation between alterations in catechol-oxidative current (CA.OC) and the time-course of the slow potential (SP) change (one of the chief features of the spreading depression) showed that spreading depression wave was accompanied by the significant increase in CA.OC content (up to 158 +/- 43%, mean +/- S.D., P < 0.001). The rise of the negative SP preceded significant CA.OC increase by 20 +/- 8 s. This fact provides the evidence that catecholamine overflow cannot participate in triggering spreading depression wave; nevertheless it can be an important link of the spreading depression mechanism.

Animals↗
PubMed1995

The role of extracellular ionic changes in upregulating the mRNA for glial fibrillary acidic protein following spreading depression.

While spreading depression has been shown to be a powerful stimulus in upregulating glial fibrillary acidic protein (GFAP) mRNA expression, the specific physiological signal underlying the upregulation is unknown. During spreading depression, extracellular ionic concentrations are altered markedly. The present study evaluates the role of these changes in extracellular ionic concentrations as potential signals influencing GFAP mRNA expression. Gel foam pledgets saturated with artificial cerebrospinal fluid (CSF) solutions in which [Na+], [Ca2+], [K+] and [H+] were altered one at a time to match concentrations seen in spreading depression were applied to exposed parietal cortex for one hour. Dot and in situ hybridization techniques were used to evaluate GFAP mRNA levels. We found that CSF containing 60 mM KCl produced a dramatic upregulation of GFAP mRNA levels throughout the cerebral cortex of the ipsilateral hemisphere without causing detectable tissue damage. The pattern and time course of the change were similar to those following application of 3 M KCl. Alteration of other ionic species did not affect GFAP mRNA levels. However, the upregulation of GFAP mRNA was not likely due directly to the increased [K+], but rather to the spreading depression that the elevated [K+] induced. This was demonstrated by the finding that the upregulation in GFAP mRNA induced by the potassium exposure was totally blocked by prior administration of MK-801, an NMDA antagonist that blocks spreading depression. These results demonstrate that an upregulation in GFAP mRNA can occur in the absence of degeneration debris and that the initiating events can be related to physiological changes, but that changes in extracellular ionic concentrations are not the likely molecular signals underlying the upregulation.

Animals↗
PubMed2004

Astrocytes contribute to regulation of extracellular calcium and potassium in the rat cerebral cortex during spreading depression.

This study used spreading depression (SD), which is characterized by redistribution of ions, to examine the role of astrocytes in the regulation of extracellular potassium ([K+]o) and calcium ([Ca2+]o) levels. Recurrent spreading depression episodes were induced by application of 3 M potassium chloride to the cortex of adult anesthetized rats while monitoring the extracellular direct current (DC) potential shifts and changes in [K+]o or [Ca2+]o 6-7 mm away. The reversible glial toxins, fluorocitrate (FC) and fluoroacetate (FA), were injected locally into the cortex at doses that are selective for reducing glial function. The peak changes and area under the curve for [K+]o and [Ca2+]o, recovery rate for [K+]o, and interval between spreading depression episodes were measured before and at various times after administration of the toxins. Both fluorocitrate and fluroacetate slowed the recovery of the [K+]o and altered the recovery of the [Ca2+]o. Local injection of glutamate uptake inhibitors or barium had no effect on the peak changes in [K+]o or the rate of recovery of the [K+]o. The slowing of the recovery rate is consistent with the hypothesis that glial cells play a role in the return of [K+]o to baseline after spreading depression in the cortex in vivo. The change in movement of calcium after administration of FC suggests that astrocytes normally extrude calcium during spreading depression, resulting in rapid recovery of the levels of [Ca2+]o with an overshoot. These findings demonstrate that astrocytes contribute to the regulation of both potassium and calcium during and after a stress to the ionic homeostatic mechanisms.

Animals↗
PubMed2006

A role for glutamate and glia in the fast network oscillations preceding spreading depression.

The mechanism of the propagation of spreading depression is unclear. Classical theories proposed a self-maintained cycle fed by elevated potassium and/or glutamate in the extracellular space. Earlier we found in vivo a characteristic oscillatory field activity that is synchronous in a strip of tissue ahead of the oncoming wave of neuron depolarization and that occurs before the extracellular potassium level begins to rise [Herreras O, Largo C, Ibarz JM, Somjen GG, Marrín del Río R (1994) Role of neuronal synchronizing mechanisms in the propagation of spreading depression in the in vivo hippocampus. J Neurosci 14:7087-7098]. We investigated here the possible participation of glutamate and the role of glia in the prodromal field oscillations using extra and intracellular recordings and pharmacological manipulations in rat hippocampal slices. As earlier shown in vivo, field oscillations propagated ahead of the negative potential shift covering distances of up to 1 mm. The oscillatory prodromals were initially subthreshold but then each wave became crowned by a population spike. The frequency of the oscillatory prodromals was variable among slices (80-115 Hz), but constant in individual slices. The blockade of ionotropic glutamate receptors decreased the frequency of prodromal oscillations, retarded spreading depression propagation, and shortened the duration of depolarization. Blocking the glutamate membrane transport increased the oscillatory frequency. The selective metabolic poisoning of astrocytes led to gradual disorganization of prodromal oscillations whose frequency first increased and then decreased. Also, the amplitude of the population spikes within the burst diminished as individual cells fired fewer action potentials, although still phase-locked with population spikes. The effects of glial metabolic impairment were observed within the period when neuron electrical properties were still normal, and were blocked by glutamate receptor antagonists. These data suggest that glutamate released from glial cells and possibly also from neurons has a role in the generation of oscillations and neuron firing synchronization that precede the spreading depression-related depolarization, but additional mechanisms are required to fully explain the onset and propagation of spreading depression.

Animals↗
PubMed1994

Photothrombotic infarction triggers multiple episodes of cortical spreading depression in distant brain regions.

The purposes of this study were to determine whether cortical spreading depression occurs outside of the infarct produced by photothrombotic vascular occlusion, and also the direction of spreading. Focal cerebral thrombotic infarction was produced by irradiating the exposed skull of anesthetized rats with green light (560 nm) following systemic injection of rose bengal dye. At proximal sites (approximately 2 mm anterior to the infarct border), transient, severe hyperemic episodes (THEs) lasting 1-2 min were intermittently recorded. THE frequency was greatest in the first hour and declined over a 3-h period. THEs were accompanied (and usually preceded) by a precipitous rise in [K+]0 (from approximately 3 to > 40 mM) and were associated with increases in local tissue oxygen tension (tPO2). Following the rise in [K+]0, clearance of [K+]0 to its pre-THE baseline preceded baseline recovery of CBF. These data indicate that THEs were reactive to physiologic events resembling cortical spreading depression (CSD), which provoked increased demand for oxygen and blood flow, and which spread from proximal sites to areas more distal (approximately 4 mm) from the rim of the evolving infarct. MK-801 (1 mg/kg, i.v.) inhibited subsequent CSD-like episodes. We conclude that photothrombosis-induced ischemia provoked CSD which was triggered either within the infarct core or in the infarct rim and spread to more distal sites. Whether multiple episodes of CSD during infarct generation are responsible for the remote consequences of focal brain injury remains to be determined.

Animals↗