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PubMed1975

Intercellular relationships in the external glial limiting membrane of the neocortex of the cat and rat.

The external glial limiting membrane of the cerebral cortex appears to be a complete astrocytic mantle covering the pial surface of the molecular layer. It consists of flattened cell bodies arranged singly or in small groups spaced about 100 mu apart and multitudes of interdigitating processes arrayed in layers. The glial mantle is thicker in the sulci than on the gyri. It is covered externally by a basal lamina which is associated with collagenous fibrils and cells of the pia mater. The extracellular space in aldehyde-perfused material appears as a regular, electron-lucent interval 150 A wide between adjacent cell membranes. Gap junctions are frequently encountered in the external glial limiting membrane; desmosomes are present between astrocytic processes but are seen much less often.

Animals↗
PubMed1981

Extracellular fluid proteins of goldfish brain: studies of concentration and labeling patterns.

An extraction procedure for the isolation of proteins from the extracellular fluid (ECF) of goldfish brain was developed and applied in an investigation of the time course and pattern of labeling of ECF proteins. The results indicate that two out of the many protein bands present, which migrated at 32,000 and 26,000 daltons on SDS-polyacrylamide electrophoretic gels, could incorporate as much as 50% of the label of the ECF fraction, even though their concentration was only 14%. Measurements of the protein content of the ECF and its volume (24% of the brain) by the inulin method were used to calculate the protein concentration in the extracellular space of goldfish brain. This gave a value of 1.6-2%, i.e., about 50% of the value obtained for the protein concentration of the cytoplasmic fraction devoid of particulate matter. Such a result suggests that the goldfish brain intracellular and extracellular fluids, separated by the neural membranes, contain relatively comparable levels of proteins.

Animals↗
PubMed2004

Relationships between ultrastructural scrapie pathology and patterns of abnormal prion protein accumulation.

On immunohistochemical examination several morphological types of disease-specific prion protein (PrP(d)) accumulation are recognised in the brain of sheep suffering from scrapie. The present study examined the relationship between the type of PrP(d) deposits seen by light microscopy and ultrastructural changes in the olivary nuclei and the dorsal motor nucleus of the vagus (DMNV) in naturally infected sheep with clinical scrapie. The nature and magnitude of sub-cellular morphological changes found in the olivary nuclei differed from the patterns of degeneration previously described in the DMNV. In the olivary nuclei, lamellar bodies in the neuronal perikaryon were found to correlate with marked intraneuronal PrP(d) accumulation. Bizarre, coated, spiral invaginations of the plasmalemma were only found in A(136) homozygous sheep in this nucleus, where few coated pits were usually observed. Neuropil vacuolation in the olivary nuclei was mild and correlated with sparse extracellular PrP(d) deposition. In the DMNV, the magnitude of extracellular immunolabelling in the neuropil was prominent. These extracellular PrP(d )aggregates coincided with intense neuropil vacuolation, increased numbers of coated pits, and with the presence of pre-amyloid changes and infrequent short fibrils in the extracellular space. Scrapie-infected neurons in the two neuroanatomic sites examined, therefore, appear to process and respond to the presence of PrP(d) differently. We hypothesise that vacuolation, coated pits and spiral invaginations of the plasmalemma may be responses to extracellular PrP(d) molecules, and that lamellar bodies are changes associated with the high levels of intraneuronal PrP(d).

Animals↗
PubMed1993

Ischemia-induced accumulation of extracellular amino acids in cerebral cortex, white matter, and cerebrospinal fluid.

In a global model of brain ischemia, accumulation of amino acids was studied in the extracellular space of the auditory cortex and the internal capsule using microdialysis, and in CSF of halothane anesthetized cats. In both brain regions, blood flow determined by hydrogen clearance decreased below 10 ml/100 g/min after extracranial multiple-vessel occlusion, and extracellular potassium activity (Ke) measured in the dialysate increased significantly. A delayed rise in Ke was observed in CSF. In contrast, ischemic amino acid accumulation differed markedly between the two brain regions investigated. In cortex, transmitter amino acids glutamate, aspartate, and gamma-aminobutyric acid (GABA) rose almost immediately after onset of ischemia, and increased 30-, 25-, and 250-fold, respectively, after 2 h of ischemia. The nontransmitter amino acids taurine, alanine, and serine increased 10-, seven-, and fourfold, respectively, whereas glutamine and essential amino acids (valine, phenylalanine, isoleucine, and leucine) increased only 1.5-fold. In the internal capsule, increases in amino acids, if any, were delayed and much smaller than in cortex. The largest alteration was a fivefold elevation of GABA. In CSF, changes in amino acids were small and comparable to those in the internal capsule. Our results demonstrate that ischemia-induced extracellular amino acid accumulation is a well localized phenomenon restricted to gray matter structures that possess release and reuptake systems for these substances. We assume that amino acids diffuse slowly into adjacent while matter structures, and into CSF.

Amino Acids↗
PubMed1972

Ca concentration and flux in Ca-deprived arteries.

1. Extracellular Ca and EDTA concentrations in arterial smooth muscle in Ca-free solutions with and without EDTA were estimated from (45)Ca and [(14)C]EDTA washout studies. Ca concentrations were calculated from the measured rate of (45)Ca washout at a given moment, combined with separate determinations of the coefficient of diffusion of Ca in the tissue, while EDTA concentrations were calculated by analysing an exponential phase of [(14)C]EDTA washout and checked by separate determinations of coefficient of diffusion of EDTA in the tissue.2. Extracellular Ca concentrations after 30 min in simple Ca-free saline at 36 degrees C was 0.049 mM at the centre of the tissue and averaged 0.033 mM throughout the tissue; these were well above the value of 0.005 mM-Ca that was found to be the threshold external level for contraction after tissue stores of Ca were removed.3. Extracellular EDTA concentration at the centre of the tissue reached 6.25 mM after 1.9 min in EDTA 12.5 mM at 36 degrees C or after 4.9 min at 5 degrees C. It reached 12.45 mM after 30 min at 5 degrees C, enough to keep free extracellular Ca at this point well below threshold even if all of the Ca in the tissue, determined as 0.42 mumole/g, were suddenly released on warming.4. Ca efflux increased greatly on warming after long periods in cold EDTA, and all measurable Ca left the tissue within 30 min in EDTA 12.5 mM at 36 degrees C although tissue Mg did not fall significantly during this time.5. Contractions elicited by noradrenaline in Ca-free saline, with or without EDTA present, were not associated with any increases in the rate of external loss of Ca greater than 0.001 mumole.g(-1).min(-1).6. Electronmicrographs showed numerous microvesicles that communicated with the extracellular space; also smooth endoplasmic reticulum among other structures that might have contained non-communicating Ca stores.7. The results provide evidence that large responses given by the arteries to noradrenaline in simple Ca-free saline were due to persisting extracellular Ca or to labile Ca stores dependent on this, while small responses obtained after long periods in cold EDTA depended on non-communicating Ca stores whose loss was too temperature-dependent to be limited by diffusion.

Animals↗
PubMed2002

Chondroitin sulfate proteoglycan phosphacan/RPTPbeta in the hypothalamic magnocellular nuclei.

The hypothalamo-neurohypophysial system synthesizes and releases arginine vasopressin (AVP) and oxytocin (OXT) with physiological stimulation. In the present study, we investigated localization of a chondroitin sulfate proteoglycan (CSPG), phosphacan/RPTPbeta, in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of adult rats at both the light and electron microscopic levels. Immunohistochemical analyses demonstrated stronger phosphacan/RPTPbeta immunoreactivity within the SON and PVN compared with adjacent hypothalamic areas. Double labeling experiments showed phosphacan/RPTPbeta immunoreactivity constituting punctate networks to surround the somata and dendrites of AVP- and OXT-secreting magnocellular neurons. Electron microscopic examination further revealed strong phosphacan/RPTPbeta immunoreactivity at extracellular membrane surface of some axons, somata, and dendrites of the SON, but not of synaptic junctions. Interestingly, phosphacan/RPTPbeta immunoreactivity was also observed at extracellular surface membrane between astrocytic processes and neurons rather than between magnocellular neurons. The present results indicate the high expression of the CSPG, phosphacan/RPTPbeta at the extracellular space in the hypothalamic AVP- and OXT-secreting magnocellular neurons.

Animals↗
PubMed2003

Effects of glial toxins on extracellular acidification in the hippocampal CA1 region in vivo.

In the pyramidal cell layer of the CA1 region of the hippocampus in the urethane-anesthetized adult rat, there is an initial alkalinization followed by an acidification in response to synchronized seizure activity induced by stimulus trains. In this study, the role of astrocytes in these extracellular pH changes during neuronal activity was examined using local injection of two relatively selective glial toxins (fluorocitrate (FC) and fluoroacetate (FA)) into the CA1 cell layer. Both glial toxins reduced the peak level of acidification reached after 20 Hz stimulus trains to the contralateral CA3 region, without changing the lengthening of the afterdischarge, when compared to animals that had received a local injection of vehicle. After administration of either glial toxin, the peak level of acidification still correlated with the total discharge duration, but the levels of acidification were consistently lower than in control animals. Administration of either glial toxin had no effect on the peak alkalinization during the stimulus train, or on the rate of recovery from peak level of acidification. Injection of either vehicle, FA, or FC had no effect on the amplitude or frequency of the neuronal discharge during the afterdischarge. The results suggest that, in normal conditions, astrocytes contribute to the acidification of the extracellular space that occurs in response to intense neuronal activity. This acidification may contribute to feedback regulation of neuronal excitability.

Animals↗
PubMed1999

Role of serotonergic neurons in L-DOPA-derived extracellular dopamine in the striatum of 6-OHDA-lesioned rats.

The effect of L-dihydroxyphenylalanine (L-DOPA) on extracellular dopamine (DA) in the striatum was determined by microdialysis in 6-hydroxydopamine (6-OHDA)-lesioned rats treated with and without the serotonergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT). At the same time the intensity of L-DOPA-induced rotational behavior was assessed. In 6-OHDA-lesioned rats treated with 5,7-DHT, L-DOPA (50 mg/kg, i.p.) increased extracellular DA only to 20% of that measured in animals not treated with 5,7-DHT. Likewise, 6-OHDA-lesioned rats treated with 5,7-DHT exhibited a significantly lower number of L-DOPA-induced rotations. These results suggest that serotonergic terminals in the striatum can convert exogenously administered L-DOPA into DA that can be released into the extracellular space.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2004

Special pharmacokinetics of dipetarudin suggests a potential antitumor activity of this thrombin inhibitor.

Thrombin is a potent mitogen for many tumor cells, suggesting that this enzyme may be involved in tumor genesis and metastasis. Inhibition of thrombin expressed on the surface of tumor cells may improve outcomes in some tumor cases. For this reason, a thrombin inhibitor to be applied in antitumor therapy must have favorable pharmacokinetic attributes to exert its action as long as possible in the extravascular compartment of the extracellular space, with a short action intravascularly, avoiding bleeding and/or other undesirable side-effects. None of the thrombin inhibitors in clinical use has these properties. Here, we report for first time a direct thrombin inhibitor, named dipetarudin that could be very useful in antitumor therapy because of its pharmacokinetic behavior characterized by a rapid distribution in the extravascular space with a slow elimination from this compartment.

Algorithms↗
PubMed1975

Changes in protein levels in perfusates of freely moving cats: relation to behavioral state.

Perfusates from the brains of freely moving cats, obtained by means of a push-pull cannula, contain high concentrations of proteins. The levels vary in a cyclic fashion and are higher during rapid eye movement sleep than during the waking state. The proteins represent a distinctive class of tissue protein and their changing levels appear to reflect an alteration in the protein content of the extracellular space of brain related to behavioral state.

Animals↗
PubMed1977

[Water-electrolyte disorders in the acute period of a stroke].

In 100 patients with different forms of cerebral strokes the author studied the general water content. Its distribution in the organism. Na and K concentration in the plasma and erythrocytes and the general electrolyte content in spaces of the body. It was established that the most frequent syndromes of water-electrolyte disorders in the acute period of strokes is intracellular or general hydratation (81%). In parenchymatous-subarachnoidal hemorrhages the general dehydratation was combined with a hyperhydratation of the extracellular space, while in sichemic strokes there was an anhydridemia up to 10-18 days. A disturbance of the electrolyte metabolism was also expressed in a transmineralization with a drop of the general Na and K content due to intracellular losses. The K deficit was averagely 29% and the Na--15.5% and should be taken into consideration in a substitutive hydro-electrolyte therapy. Solutions with an increased K content should be used in order to compensate its deficit.

Acute Disease↗
PubMed1978

The functional and structural border of the neurohemal region of the median eminence.

In stressed rats the tanycytes of the ventrolateral wall of the third ventricle exhibit by light microscopic immunohistochemistry a positive staining for neurohormones which is distinctly limited to the distal perivascular end of the tanycyte process. Since by electron microscopic immuncytochemistry the tanycyte cytoplasm does not show any reaction product, the light microscopic reaction most likely results from a labeling of the intercellular space in the direct vicinity of the subendothelial cleft. Whether this subendothelial space is permeable to neurohormones was tested by injection of HRP1. In the region of the arcuate nucleus 30 min after intravenous application, the marker is affixed to the membranes of the perivascular tanycyte processes in the subendothelial cleft of capillaries possessing non-fenestrated endothelia. Occasionally, HRP penetrates for a short distance between the tanycytes. Then the labeling of the intercellular cleft ends abruptly. Here, several parallel ridges of tight junctions between the perivascular distal tanycyte processes are found by the freeze-etching technique. Since HRP cannot reach the subendothelial clefts of this region by passing through capillary walls due to the presence of a blood-brain barrier, it is suggested that the marker penetrates from the median eminence this far via the subendothelial extracellular space. It is prevented from spreading further by the tight junctions of the perivascular tanycyte endings. The same way may be taken by the neurohormones. Hence, a border area exists adjacent to the dorsolateral aspect of the neurohemal region of the median eminence where the tanycytes isolate the neuropil from the cerebrospinal fluid not only by their apical tight junctions, but also by basal tight junctions from the subendothelial cleft. This communicates with the perivascular space of the portal vessels.

Animals↗
PubMed1977

Pressure effects on the distribution of extracellular materials in the rhesus monkey outflow apparatus.

An electron-microscopic investigation was conducted to determine the distribution of extracellular materials in the rhesus monkey outflow apparatus at various maintained levels of intraocular pressure. Intraocular pressure was maintained at either 0,8, 15, 22, 30, or 50 mm Hg, by an intracameral needle attached to a reservoir system for a period of 1 h. Thereafter the eyes were fixed either by intracameral perfusion of glutaraldehyde at the appropriate pressure level, or by carotid perfusion of the fixative, or by rapid enucleation and immersion fixation. The electron-dense cationic stains, colloidal thorium and colloidal iron were used to indicate the presence of carbohydrate-rich extracellular materials in the drainage tissues. In the control tissue (15 mm Hg), heavy concentrations of stain were detected within the cores of the trabeculae and in the extracellular spaces of the endothelial meshwork. With pressure elevation there was a progressive decrease in the surface staining on the meshwork cells, an increase in staining intensity within the trabecular cores, and a 'washout' of extracellular materials from the spaces of the endothelial meshwork. The washout was thought to occur via giant vacuoles up to 30 mm Hg, but at 50 mm Hg the process was accelerated by loss of association between the cells of the canal endothelial monolayer. Over the entire pressure range 0 to 50 mm Hg, there was an increase in the staining on the apical surface of the canal endothelium which was associated with a decrease in the incidence of micropinosomes.

Animals↗
PubMed1970

Neuroglia: gliosis and focal epilepsy.

Normal neuroglial cells buffer the extracellular space around neurons and presynaptic terminals against increases in potassium ions. Epileptic foci resulting from brain injury are characterized by areas of intense fibrillary gliosis bordering neuronal tissue. The known pathological changes that occur in gliosis may impair glial control of extracellular potassium ions and lead to excessively excitable neuronal border regions.

Cicatrix↗
PubMed1977

Rate-dependent changes in extracellular potassium in the rabbit atrium.

We measured levels of potassium ion in the extracellular space of isolated superfused rabbit atria continuously with double-barreled microelectrodes of which on barrel was a K+ liquid ion-exchanger microelectrode and the other a potential-sensing micropipette. Increases in heart rate resulted in transient increases in extracellular potassium ([K+]0). When the quiescent atrium was stimulated the maximal increase was 0.4 mM at rates of 60/min, 0.7 mM at 90/min, 0.9 mM at 120/min, 1.3 mM at 200/min, and 1.8 mM at 300/min. The increase was not sustained during continued stimulation but declined toward prestimulation levels. When the stimulus was terminated the extracellular potassium activity decreased below bathing solution values by 0.2 mM after 60/min, 0.5 mM after 90/min, 0.7 mM ater 120/min, 0.9 mM after 200/min, and 1.0 mM after 300/min and subsequently returned to a value equal to that of the bathing solution. The magnitude of the decline in extracellular potassium activity during prolonged stimulation was markedly decreased when the bathing solution contained either zero potassium, ouabain, LiCl, or a decreased Po2 such that an elevation in [K+]0 persisted during stimulation. Moreover, the reduction in [K+]0 that followed the cessation of stimulation also was inhibited. These results support a role of the Na-K pump in maintaining extracellular potassium activity during changes in cardiac rate.

Action Potentials↗
PubMed1996

Reductive activation markedly increases the stability of cathepsins B and L to extracellular ionic conditions.

Cathepsins B and L are thought to function extracellularly in pathological conditions. pH-Activity profiles of cathepsin B, measured in phosphate and acetate-Mes-Tris buffers of constant ionic strength, indicated that cathepsin B is sensitive to specific buffer ions, as previously reported for cathepsin L. In assessing the activity of these enzymes in vitro the influence of the buffer must therefore be taken into account. In Hank's balanced salt solution, a buffer modeling the extracellular fluid, the half-life of activated human liver cathepsin B at 37 degrees C is 245 +/- 11.3 s, at pH 7.2, and 857 +/- 50.1 s, at pH 6.8 (the peritumor pH), indicating that cathepsin B is markedly stable under these conditions. The stability was increased by the additional presence of proteins. Without immediate activation, however, the stabilities of both cathepsins B and L were markedly decreased, a large proportion of their activity being lost before it could be measured. Enzymes injected into the extracellular space in the unactivated state would therefore survive for only a very short time in their native conformation. It is proposed that the active site thiolate-imidazolium ion pair contributes substantially to the stability of cathepsins B and L to extracellular ionic conditions.

Buffers↗
PubMed1988

[The effect of phenytoin on free fatty acid liberation and mononucleotide metabolism in transient ischemia].

Ischemia gives rise to severe energy depletion and influx of Ca from the extracellular space, and it is suggested that increased intracellular Ca leads to the activation of phospholipase C and A, and to liberation of free fatty acids (FFA) in particular arachidonic acid. Phenytoin has been reported not only to maintain the intra- and extracellular cation balance but blockade the Ca channel. The purpose of the present study is to investigate the effect of phenytoin on the liberation of FFA, energy metabolism and mononucleotide metabolism in ischemic brain. Male Wistar rats were subjected to global cerebral ischemia induced by the occlusion of basilar and bilateral common carotid arteries. The brains were frozen in situ by the funnel technique after 5 or 30 min of ischemia or after 10, 30, or 60 min of recirculation following 30 min of ischemia. Purine and pyrimidine nucleotides, FFA, and glycolytic intermediates were measured by HPLC, GLC, and fluoro-enzymatic method. In non-treated rats, ATP reached a nadir after 5 and 30 min of ischemia. Phenytoin significantly attenuated ATP depletion after 5 and 30 min of ischemia. And also E.C. is higher in phenytoin treated rats than in non-treated rats in ischemia. After 60 min of recirculation, ATP recovered to 1.93 +/- 0.02 mumol (72.3% of pre-ischemia) in treated rats but 1.60 +/- 0.07 mumol/g (60% of pre-ischemia) in non treated rats. In E.C., there are significant differences between non-treated and treated rats after 10 and 30 min of recirculation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

The structure, distribution, and quantitative relationships of the glia in the abdominal ganglia of the horse leech, Haemopis sanguisuga.

The glial cells in abdominal ganglia of the horse leech Haemopis sanguisuga were studied by electron microscopy and analysed quantitatively to evaluate the suitability of this easily obtainable carnivorous species for physiological studies. Each abdominal ganglion contains eight giant glial cells, 12,000-14,000 small glial cells, and approximately 300 neurons. The giant glial cells constituted 44.6% and the small glial cells 6.4% of the ganglion's volume. The giant glial cells contain glycogen and bundles of filaments that are chiefly located in their periphery, close to the neurons into which they send processes. The small glial cells are frequently surrounded by the giant glial cells but also occur around neuronal perikarya and axon tracts, as well as against the basal lamina and connective tissue layers. The small glial cells contain lysosomes and sometimes form a trophospongium with the neurons. A system of extracellular channels, which is continuous with the basal lamina, indents the giant glial cells and extends around parts of the neurons. The extracellular channels contain a matrix that appears very similar to the basal lamina and to the cytoplasm in the processes of the small glial cells. Some of the extracellular channels contain collagen fibrils. Hemidesmosomes join the matrix-filled extracellular channels to both the neurons and the giant glial cells. Ionic lanthanum has a free access to the neurons and glial cells via the extracellular spaces and matrix-filled channels. Areas of synaptic intermingling rarely contain glial cell processes.

Abdomen↗