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At least 181 records · Page 10Linked to original sources
PubMed1968

New evidence supporting the linkage to extracellular space of outer segment saccules of frog cones but not rods.

Previous electron microscopic examinations of outer segments of photoreceptors suggest that many flattened saccules of cones are continuous with the cell membrane and that their lumina connect with the extracellular compartment but that most saccules in rods appear to lack these connections. The saccules probably contain photolabile pigment, and certain potentials appear to result from dipole formation during pigment bleaching. The detection of dipoles from rod saccules may require that the lumina of rod saccules connect with extracellular space, and questions have been raised whether the interpretation of micrographs is correct or the isolation of rod saccules is the result of artifact. Accordingly, lanthanum and barium precipitates were produced near fixed and unfixed frog photoreceptors. Lanthanum precipitates appeared to infiltrate the saccules of fixed cones and the few surviving cones exposed prior to fixation, but no rod saccules were infiltrated except occasional, most basal saccules or saccules within narrow zones of probable damage. Barium precipitates did not infiltrate saccules of either variety of unfixed photoreceptor, but they did occasionally infiltrate around the saccules at points of damage in rod outer segments. The results thus support the view of the patency of saccules of frog cones and are consistent with, but do not prove, the isolation of saccules of frog rods.

Animals↗
PubMed1987

[Relations between the cortical DC potentials and the K+ concentration of the blood and cerebral cortex extracellular space in reversible asphyxia].

The relationship between changes of the cortical DC potential and the K+ concentration gradient across the blood-brain barrier (BBB) was studied in the rat brain during short ventilatory arrest. For this purpose K+ concentrations were measured simultaneously in the extracellular space of the cerebral cortex and in the streaming blood of the carotid artery and the superior sagittal sinus. For measurements ion-selective micro- and macro-electrodes based on the K+ ionophore valinomycin were used. During reversible asphyxia free K+ concentrations in the circulating blood and in the extracellular fluid of the brain tissue increased and re-decreased with different time courses. The resulting difference between the electromotive forces of the ion-selective signals resembled the course of the cortical DC potential during the initial phase of the ventilatory arrest during the post-asphyxiation period. The results suggest that during these events the cortical tissue including the BBB behaves like a K+-selective membrane which is probably located at the blood-brain interface. It is concluded that the capillary-glial complex may principally contribute to the generation of DC shifts associated with the asphyxiation process.

Animals↗
PubMed2001

Inhibition of proteasome activity by the TED4 protein in extracellular space: a novel mechanism for protection of living cells from injury caused by dying cells.

In maturation process of tracheary element (TE) differentiation, many hydrolases are activated to execute programmed cell death of TEs. Such hydrolases are released from maturing TEs into extracellular space. The release of hydrolases should be harmful to surrounding cells. The TED4 protein, a tentative plant non-specific lipid transfer protein that is expressed preferentially in TE-induced culture of zinnia (Zinnia elegans L.), is secreted into the apoplastic space prior to and associated with morphological changes of TEs. Our studies on the interrelationship between the TED4 protein and proteolytic activities using an in vitro TE differentiation system of zinnia revealed the following facts. (1) Active proteasome is released into medium at maturation stage of TE differentiation. (2) The TED4 protein forms a complex with proteasome in culture medium. (3) The TED4 protein inhibits proteasome activity in the medium and crude extracts of zinnia cells. (4) The depletion of the TED4 protein from culture medium results in an increase in mortality of other living cells. These results strongly suggest that the secreted TED4 protein acts as an inhibitor of proteasome to protect other cells from undesirable injury due to proteolytic activities exudated from dying TEs.

Acetylcysteine↗
PubMed2001

Poly[N-(2-hydroxypropyl)methacrylamide] polymers diffuse in brain extracellular space with same tortuosity as small molecules.

Integrative optical imaging was used to show that long-chain synthetic poly[N-(2-hydroxypropyl)methacrylamide] (PHPMA) polymers in a range of molecular weights from 7.8 to 1057 kDa were able to diffuse through the extracellular space in rat neocortical slices. Tortuosity (square root of ratio of diffusion coefficient in aqueous medium to that in brain) measured with such polymers averaged 1.57, a value similar to that obtained previously with tetramethylammonium, a small cation. When PHPMA was conjugated with bovine serum albumin (BSA) to make a bulky polymer with molecular weight 176 kDa, the tortuosity rose to 2.27, a value similar to that obtained previously with BSA alone and with 70-kDa dextran. The method of image analysis was justified with diffusion models involving spherical and nonspherical initial distributions of the molecules.

Animals↗
PubMed1990

Regional variation of extracellular space in the hippocampus.

The factors responsible for the unusual susceptibility of the hippocampus to seizures and ischemic cell damage are not well understood. The CA1 pyramidal subfield of the hippocampus is particularly vulnerable to seizure activity and damage after ischemia. The possibility was examined that regional differences exist in extracellular volume, which might influence neuronal excitability and response to injury in the hippocampus. CA1 stratum pyramidale exhibited an exceptionally low extracellular volume fraction (EVF) of 0.12, whereas the EVFs of CA3 and dentate were considerably higher--0.18 and 0.15, respectively. The EVF of CA1 stratum pyramidale was reversibly reduced by 30 percent when the extracellular potassium concentration was raised from 3.5 to 8.5 mM, a procedure that induced spontaneous electrographic seizures in CA1. Thus there are regional variations in the properties of the extracellular space in the hippocampus that might underlie the propensity of the CA1 region to develop seizures and to suffer damage after ischemia.

Animals↗
PubMed1993

Ethanol inhibits the uptake of exogenous norepinephrine from the extracellular space of the rat cerebellum.

Rapid chronoamperometric recordings using nafion-coated carbon fiber electrodes coupled with pressure-ejection of drugs were used to investigate the effects of ethanol on norepinephrine (NE)-containing nerve terminals in the urethane-anesthetized Fischer 344 rat. Local application of ethanol from a double-barrel micropipette did not produce detectable changes in extracellular levels of NE in the rat cerebellar cortex. However, when ethanol was applied prior to local application of NE, it was seen to inhibit the uptake of NE from the extracellular space. These results were compared to the effects seen from the local application of a known high-affinity uptake inhibitor, nomifensine. Nomifensine was found to inhibit the extracellular uptake of NE in rat cerebeller cortex similar to ethanol. Our results support the hypothesis that one effect of ethanol on the noradrenergic system of the rat cerebellum is an alteration in the uptake of NE into NE-containing nerve endings. In addition, the present data concerning ethanol-induced inhibition of NE clearance or uptake support our previous electrophysiological studies in which we found that ethanol can potentiate the modulatory effects of beta-agonists on GABA responses of cerebellar Purkinje neurons.

Animals↗
PubMed2001

Glutamate, NMDA, and AMPA induced changes in extracellular space volume and tortuosity in the rat spinal cord.

Glutamate release, particularly in pathologic conditions, may result in cellular swelling. The authors studied the effects of glutamate, N-methyl-D-aspartate (NMDA), and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) on extracellular pH (pH(e)), extracellular potassium concentration ([K(+)](e)), and changes in extracellular space (ECS) diffusion parameters (volume fraction alpha, tortuosity lambda) resulting from cellular swelling. In the isolated spinal cord of 4-to 12-day-old rats, the application of glutamate receptor agonists induced an increase in [K(+)](e), alkaline-acid shifts, a substantial decrease in alpha, and an increase in lambda. After washout of the glutamate receptor agonists, alpha either returned to or overshot normal values, whereas lambda remained elevated. Pretreatment with 20 mmol/L Mg(++), MK801, or CNQX blocked the changes in diffusion parameters, [K(+)](e) and pH(e) evoked by NMDA or AMPA. However, the changes in diffusion parameters also were blocked in Ca(2+)-free solution, which had no effect on the [K(+)](e) increase or acid shift. The authors conclude that increased glutamate release may produce a large, sustained and [Ca(2+)](e)-dependent decrease in alpha and increase in lambda. Repetitive stimulation and pathologic states resulting in glutamate release therefore may lead to changes in ECS volume and tortuosity, affecting volume transmission and enhancing glutamate neurotoxicity and neuronal damage.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1971

Uptake of nicotine and extracellular space markers by isolated rat ganglia in relation to receptor activation.

1. Uptake of (3)H-nicotine by isolated rat superior cervical sympathetic (SCG) and nodose (NG) ganglia was measured in vitro. Depolarization of the ganglia by nicotine was measured electrically.2. Nicotine depolarized the SCG but not the NG. The mean ED50 for depolarization was 5.3 x 10(-6)M.3. Both ganglia accumulated nicotine when incubated in 3.1 x 10(-5)M(3)H-nicotine: after 30 min incubation the ratios of tissue to medium concentrations were (mean +/- S.E. of mean): SCG, 3.49 +/- 0.13; NG, 2.50 +/- 0.09.4. Total water contents, estimated by drying to constant weight, were: SCG, 83.8 +/- 0.12%; NG, 80.1 +/- 0.21%. Extracellular spaces, measured as (3)H-mannitol space, were: SCG, 38.8 +/- 1.3; NG, 40.3 +/- 0.8% wet weight. These values were not significantly altered by nicotine.5. Correction for tissue fluid spaces indicated that the ratio of the mean intracellular fluid concentration to the extracellular fluid concentration for (3)H-nicotine at 3.1 x 10(-5)M were: SCG, 7.4; NG, 5.6. The ratios were not altered in any consistent manner on varying the nicotine concentration between 3.1 x 10(-7) and 1.6 x 10(-4)M.6. When the nicotine concentration was sufficiently great (6.2 x 10(-6)M or more) to evoke large SCG depolarizations, hexamethonium (2.5 x 10(-3)M) reduced (3)H-nicotine uptake by the SCG by up to 19% without affecting uptake by the NG, and thereby reduced the uptake difference between the two ganglia. With nicotine concentrations <6.2 x 10(-6)M, hexamethonium did not modify uptake by either ganglion.7. It was concluded that nicotine may be concentrated within neurones, and that such intracellular accumulation may be augmented during depolarization induced by nicotine.

Animals↗
PubMed1978

Effect of indomethacin on extracellular space, sodium compartment and sodium excretion in saline loaded rats.

The effects of indomethacin, an inhibitor of prostaglandin synthesis, were studied on the sodium and fluid balance of rats kept on a normal diet and physiologic saline for two weeks. Under the effect of indomethacin the inulin compartment (extracellular space) and Na(24)-compartment expanded from 20.5 plus or minus 4.1 to 25.2 plus or minus 5.1 ml per 100 g, (p.less than 0.001); and from 31.9 plus or minus 2.8 to 37.0 plus or minus 5.6 ml per 100 g, (p less than 0.001), respectively, and the exchanged amount of Na+ increased from 4.33 plus or minus 0.5 to 5.01 plus or minus 1.03 mEq per 100 g, (p less than 0.02). On the other hand, fluid and Na+ uptake and excretion were unaffected. Haematocrit and plasma protein levels decreased (from 42.5 plus or minus 2.98 to 38.6 plus or minus 5.2%, p less than 0.01; and from 5.41 plus or minus 0.67 to 5.01 plus or minus 0.47 g/dl; p less than 0.05, respectively). The experimental findings supported the assumption that (a) under conditions of saline loading the prostaglandins might play a role in the mechanism of natriuresis and their absence might lead to sodium and water retention. (b) The indomethacin induced transient reduction in salt and water excretion could be restored by the combined effect of volume regulating reflex mechanism and physicochemical factors (haemodilution).

Animals↗
PubMed2002

Release of cytochrome c into the extracellular space contributes to neuronal apoptosis induced by staurosporine.

The mitochondrial protein cytochrome c has been identified as one of the key signalling molecules of apoptosis. In the present study, we used primary neuronal cultures to investigate whether cytochrome c was released from the mitochondria into the cytosol and subsequently into the culture medium during staurosporine-induced apoptosis and whether extracellular cytochrome c modulates the degree of damage caused by staurosporine. We found the cytochrome c content in the mitochondria decreased 24 h after and increased in the cytosol 8 h after staurosporine was added to the culture medium. The cytochrome c content of the culture medium increased from 8 h up to 24 h after starting the staurosporine treatment. In parallel with the release of cytochrome c into the culture medium, membrane leakage occurred as determined by the release of LDH. Addition of cytochrome c accelerated, whereas the addition of anti-cytochrome c antibodies reduced staurosporine-induced neuronal death suggesting a pro-apoptotic role of cytochrome c released into the culture medium. Under control conditions, extracellularly added cytochrome c (25 ng/ml), which was in the range of the amount of cytochrome c released from staurosporine-treated neurons into the culture medium, increased the percentage of apoptotic neurons to 30% compared with 18% in vehicle-treated controls. Our results suggest that the release of cytochrome c into the extracellular space contributes to neuronal apoptosis induced by staurosporine.

Animals↗
PubMed1996

Intrinsic optical signals in rat neocortical slices measured with near-infrared dark-field microscopy reveal changes in extracellular space.

In the last decade, the measurement of activity-dependent intrinsic optical signals (IOSs) in excitable tissues has become a useful tool for collecting data about spatial patterns of information processing in mammalian brain and spread of excitation. Although the extent of the IOS correlates well with the extent of electrical excitation, its time course is much slower, suggesting that it does not directly monitor the electrical activity. The aim of this study was to investigate the mechanisms responsible for generation of IOSs. Coronal neocortical brain slices of juvenile rats were electrically stimulated at the border of layer VI and the white matter. The induced columnar-shaped IOSs were recorded using dark-field video microscopy. At corresponding locations, alterations in extracellular K+ concentration and extracellular space (ECS) volume were registered using ion-selective microelectrodes. After stimulation, a transient increase of extracellular K+ concentration up to 10 mM and a transient decrease of ECS volume by approximately 4% could be observed. The comparison of the time courses of these parameters yielded considerable differences between extracellular K+ concentration increase and IOS, but obvious similarities between alterations in ECS volume and IOS. To test the hypothesis that changes in IOS reflect changes in ECS, but not extracellular K+ concentration, we recorded under conditions that are known to prevent activity-induced changes in ECS, i.e., in low Cl- solutions and in the presence of furosemide. Both treatments similarly decreased stimulation-induced IOSs and alterations of ECS. However, the effect of these treatments on changes of extracellular K+ was different and did not correspond to the changes of IOS. We conclude that activity-dependent IOSs in rat neocortical slices measured by near-infrared video microscopy reveal changes in ECS. Furthermore, the pharmacological and ion substitutional experiments make it likely that activity-induced IOSs are attributable to cell swelling via a net KCI uptake and a concomitant water influx.

Animals↗
PubMed2002

Water ADC, extracellular space volume, and tortuosity in the rat cortex after traumatic injury.

The diffusion parameters in rat cortex were studied 3-35 days following a cortical stab wound, using diffusion-weighted MR to determine the apparent diffusion coefficient of water (ADC(W)) in the tissue, and the real-time iontophoretic tetramethylammonium (TMA) method to measure the extracellular space (ECS) diffusion parameters: ECS volume fraction alpha and the ADC of TMA(+) (ADC(TMA)). Severe astrogliosis was found close to the wound, and mild astrogliosis was found in the ipsilateral but not the contralateral cortex. Chondroitin sulfate proteoglycan (CSPG) expression was increased throughout the ipsilateral cortex. In the hemisphere contralateral to the wound, alpha, ADC(TMA), and ADC(W) were not significantly different from control values. ECS volume fraction was increased only in the vicinity of the wound, in the region of cell death and severe astrogliosis, at 3 and 7 days after injury. However, both ADC(TMA) and ADC(W) were significantly decreased after lesion in the vicinity of the wound as well as in the rest of the ipsilateral hemisphere distant from the wound. Thus, both ADC(W) and ADC(TMA) decreased in regions wherein alpha did not change but CSPG increased. An increase in extracellular matrix expression may therefore impose diffusion barriers for water as well as for TMA molecules.

Animals↗
PubMed1994

Murine scrapie-infected neurons in vivo release excess prion protein into the extracellular space.

An originally heretical proposition that the transmissible spongiform encephalopathies are caused by a host-coded protein (the prion hypothesis) is now current dogma. Indeed these disorders are commonly called prion diseases but the prion hypothesis provides no readily acceptable explanation for the source of the informational component of the agent necessary to code for the diversity of strains of scrapie. Ultrastructural immunolocalisation of prion protein (PrP) in murine scrapie shows that PrP accumulates in association with the plasmalemma of neurones, diffusing from the neuronal cell surface into the extracellular space around small neurites prior to aggregation and fibril assembly. These events occur without the involvement of other cell types. The area of neuropil infiltrated with extracellular PrP around infected neurons and neurites indicates that the form of PrP initially produced is not immediately amyloidogenic.

Animals↗
PubMed1984

Reduction of the sucrose-saline interdiffusion in the sucrose gap technique by controlled compression of the extracellular space in myocardial preparations.

The time course and the extent of the sucrose-saline interdiffusion in the sucrose gap technique was investigated experimentally. 14C-sucrose diffusion and voltage clamp experiments were performed with designs of the sucrose apparatus allowing accurate control of the size of the holes in the rubber partitions defining the sucrose gap. Experiments with frog ventricular strips demonstrated that compression of the extracellular space to around 15% of its undisturbed value was possible without disturbance of the intracellular conduction pathway. The procedure reduced the sucrose-saline diffusion significantly and proved indispensible for obtaining reliable voltage-current relations in voltage clamp experiments.

Action Potentials↗
PubMed2002

CLV3 is localized to the extracellular space, where it activates the Arabidopsis CLAVATA stem cell signaling pathway.

Plant growth and development depends on the activity of a continuously replenished pool of stem cells within the shoot apical meristem to supply cells for organogenesis. In Arabidopsis, the stem cell-specific protein CLAVATA3 (CLV3) acts cell nonautonomously to restrict the size of the stem cell population, but the hypothesis that CLV3 acts as an extracellular signaling molecule has not been tested. We used genetic and immunological assays to show that CLV3 localizes to the apoplast and that export to the extracellular space is required for its function in activating the CLV1/CLV2 receptor complex. Apoplastic localization allows CLV3 to signal from the stem cell population to the organizing center in the underlying cells.

Arabidopsis↗
PubMed1983

Application of an automatic electronic image analyzer to the measurement of myocardial extracellular space.

The volume of the rat myocardial extracellular compartment was determined by electronic image analysis (Zeiss Micro-Videomat) and compared with values obtained by point-counting on the same histological micrographs. The data suggest that the results obtained by the two methods may be expected to be approximately within 10% of each other. The subjective component of the morphometry was not entirely eliminated due to some heterogeneity in the staining of the histological sections. Until the deficiencies in staining homogeneity are eliminated, the main advantage of the image analysis compared to point-counting will be limited to a greater labor efficiency.

Animals↗
PubMed2005

Carbonic anhydrase IV and XIV knockout mice: roles of the respective carbonic anhydrases in buffering the extracellular space in brain.

Previous studies have implicated extracellular carbonic anhydrases (CAs) in buffering the alkaline pH shifts that accompany neuronal activity in the rat and mouse hippocampus. CAs IV and XIV both have been proposed to mediate this extracellular buffering. To examine the relative importance of these two isozymes in this and other physiological functions attributed to extracellular CAs, we produced CA IV and CA XIV knockout (KO) mice by targeted mutagenesis and the doubly deficient CA IV/XIV KO mice by intercrossing the individual null mice. Although CA IV and CA XIV null mice both are viable, the CA IV nulls are produced in smaller numbers than predicted, indicating either fetal or postnatal losses, which preferentially affect females. CA IV/XIV double KO mice are also produced in fewer numbers than predicted and are smaller than WT mice, and many females die prematurely before and after weaning. Electrophysiological studies on hippocampal slices on these KO mice showed that either CA can mediate buffering after synaptic transmission in hippocampal slices in the absence of the other, but that eliminating both is nearly as effective as the CA inhibitor, benzolamide, in blocking the buffering seen in the WT mice. Thus, both CA IV and CA XIV contribute to extracellular buffering in the central nervous system, although CA IV appears to be more important in the hippocampus. These individual and double KO mice should be valuable tools in clarifying the relative contributions of each CA to other physiological functions where extracellular CAs have been implicated.

Animals↗