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PubMed1997

The contribution of glial cells to spontaneous and evoked potentials.

The mechanism by which brain cells generate alpha and other rhythms remains obscure, and the possible participation of glial cells in the process continues to be debated. We will present data obtained from freely moving rats in which flashes produced by a light emitting diode implanted under the skin of the scalp evoke retinal and cortical responses recorded through electrodes implanted behind the eye and over visual cortex. In the retina, which is a brain-like structure isolated in the periphery during embryology, the b-wave evoked response is thought to be produced by the Müller glial cells as they maintain potassium ion homeostasis in the extracellular space during the synaptic events initiated by rod and cone activation. We will report on the results of a search in this retinal analogue of the brain for spontaneous activity in the EEG spectrum.

Animals↗
PubMed1992

Anoxia-induced extracellular ionic changes in CNS white matter: the role of glial cells.

The rapid changes in brain extracellular ion concentrations that occur with anoxia are important in understanding the pathophysiology of anoxic-ischemic brain injury. While previous studies have focused on the ionic changes that occur in gray matter areas of the brain, white matter (WM) is also damaged by anoxia. We describe the changes in extracellular K+ concentration ([K+]o) and extracellular pH (pHo) that accompany anoxia in WM, and present new results indicating that glial cells directly contribute to the observed fluctuations of these ions. Anoxia-induced changes in [K+]o and pHo were measured with ion-selective microelectrodes in the isolated rat optic nerve, a typical WM tract. To assess the contribution of glial cells, recordings were also made in optic nerves that contained only glial cells (produced by neonatal enucleation). Anoxia in WM produced less extreme changes in [K+]o and pHo than are known to occur in gray matter; in WM during anoxia, the average maximum [K+]o was 14 +/- 2.9 mM (bath [K+]o = 3 mM) and the average maximum acid shift was 0.31 +/- 0.07 pH unit. These extracellular ionic changes were accompanied by rapid shrinkage of extracellular space volume. The ability of optic nerve axons to conduct action potentials was lost in temporal association with the increase in [K+]o. Increasing bath glucose concentration from 10 to 20 mM resulted in a much larger acid shift during anoxia (0.58 +/- 0.08 pH unit) and a smaller average increase in [K+]o (9.2 +/- 2.6 mM). The increased glucose concentration presumably enhanced anaerobic metabolism, leading to extracellular lactate accumulation and a greater acid shift.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1975

Distribution volumes of [131I]albumin, [14C]sucrose, and 36Cl in sheep lung.

We measured the steady-state volumes of distribution for radioactive chloride, sucrose, and albumin in the lung of six anesthetized, spen-thorax sheep. We allowed 2 days for [131I]albumin to equilibrate throughout the body, 2 h for the 36Cl, and a 40-min constant infusion for [14C]sucrose before killing the animal. Five minutes before death, we gave [125I]albumin to tag lung plasma volume. We killed the animals by clamping both lung hila; we then removed the lungs and homogenized them. We measured residual red cell and plasma volume, total extravascular lung water, and the extravascular content of the three tracers. The distribution volumes expressed as fractions of blood-free lung weight were: 36Cl equals 0.44, sucrose equals 0.28, and albumin equals 0.07. If the sucrose distribution volume is taken as the best estimate of the lung's extravascular extracellular space, then chloride clearly overestimates the interstitial fluid volume, being either bound or partially intracellular. On the other hand, albumin clearly underestimates the interstitial fluid volume.

Animals↗
PubMed1988

Ultrastructural discrimination of lipid droplets and vesicles in atherosclerosis: value of osmium-thiocarbohydrazide-osmium and tannic acid-paraphenylenediamine techniques.

Electron microscopy of atherosclerotic arterial tissue commonly fails to distinguish lipid vesicles from droplets, especially when these are found in the extracellular space. The distinction is important, because vesicular or membranous lipid is composed of phospholipid and unesterified cholesterol, whereas neutral lipid in droplet form implies the presence of cholesteryl ester in atherosclerosis. A new procedure with sequential tannic acid and p-phenylenediamine treatments of osmicated tissue (TA-PDA) allows reliable ultrastructural discrimination of lipid vesicles and droplets. The multilamellar character of many vesicles is revealed. Extracellular droplets are found to possess many surface pits associated with membranous blebs. Pitting of droplets is especially evident after the use of an alternative tissue processing technique, the osmium-thiocarbohydrazide-osmium (OTO) sequence applied en bloc. The two complementary techniques will prove useful for electron microscopic studies of atherosclerotic and other lipid-rich tissues.

Adult↗
PubMed2004

Glia and volume transmission during physiological and pathological states.

Extrasynaptic communication between neurons or neurons and glia is mediated by the diffusion of neuroactive substances through the extracellular space (ECS). Structural changes and amino acid release occurring under physiological and pathological conditions result in cellular (particularly glial) swelling, leading to dynamic changes in the ECS volume and geometry that in turn affect ECS diffusion. Significant changes in ECS volume and in diffusion barriers occur during development and aging. They are often the result of cell death, astrogliosis, the rearrangement of astrocytic processes and changes in extracellular matrix molecules. Plastic changes in ECS volume, geometry and anisotropy significantly affect the spatial relation of glial processes towards synapses, glutamate or GABA 'spillover', synaptic cross-talk and neuron-glia communication/interaction. In addition, changes occurring during pathological states can be important for diagnosis, drug delivery and treatment.

Aging↗
PubMed2002

A homeostatic mechanism counteracting K(+) -evoked choline release in adult brain.

Choline (Ch) is an essential nutrient as the biosynthetic precursor of acetylcholine (ACh) and phospholipids. Under resting conditions, the intracellular accumulation of Ch (above 10-fold), which is positively charged, is governed by the membrane potential and follows the Nernst equation. Accordingly, in synaptosomes from adult rats during depolarization, we observed a linear relationship between release of free cytoplasmic Ch and KCl concentration (2.7-120 mm). The K(+) -evoked Ch release was Ca(2+) -independent and did not originate from ACh or phospholipid hydrolysis. In superfused brain slices of adult rats, however, a K(+) -induced Ch efflux was absent. Also, under in vivo conditions, 30-60 mm KCl failed to increase the extracellular Ch level as shown by microdialysis in adult rat hippocampus. On the contrary, in brain slices from 1-week-old rats, high K(+) as well as 4-aminopyridine evoked a marked Ch efflux in a concentration-dependent fashion. This phenomenon faded within 1 week. Hemicholinium-3 (HC-3, 1 and 10 microm), a blocker of cellular choline uptake, caused a marked efflux of choline from adult rat slices but no or significantly less release from immature slices. We conclude that depolarization of synaptic endings causes a Ca(2+) -independent release of free cytoplasmic Ch into the extracellular space. In adult rat brain, this elevation of Ch is counteracted by a homeostatic mechanism such as uptake into brain cells.

4-Aminopyridine↗
PubMed1999

Antagonistic effects of 17 beta-estradiol, progesterone, and testosterone on Ca2+ entry mechanisms of coronary vasoconstriction.

The clinical observation that coronary artery disease is more common in men and postmenopausal women than in premenopausal women has suggested cardioprotective effects of female sex hormones including hormone-mediated coronary vasodilation. The purpose of this study was to investigate whether the sex hormone-induced coronary relaxation is caused by inhibition of Ca2+ mobilization into coronary smooth muscle. The effects of 17beta-estradiol, progesterone, and testosterone on vascular reactivity and 45Ca2+ influx were tested in deendothelialized coronary artery strips isolated from castrated male pigs. Prostaglandin F2alpha (PGF2alpha) (10(-5) mol/L) caused significant, maintained contraction of coronary artery strips. Caffeine (25 mmol/L), an activator of Ca2+ release from intracellular stores, caused transient contraction in Ca2+-free solution whereas membrane depolarization by 96 mmol/L KCl, an activator of Ca2+ entry, caused maintained contraction in the presence of external Ca2+. The 3 sex hormones caused significant and concentration-dependent relaxation of PGF2alpha- and 96 mmol/L KCl-induced contractions with 17beta-estradiol being the most effective. The sex hormones did not significantly affect the transient caffeine contraction in Ca2+-free solution. In contrast, the sex hormones significantly inhibited the PGF2alpha- and KCl-induced 45Ca2+ influx. 17beta-Estradiol caused similar inhibition of PGF2alpha- and KCl-induced contractions, suggesting inhibition of the same Ca2+ entry mechanism. However, progesterone and testosterone caused greater relaxation of PGF2alpha-induced contraction than of KCl-induced contraction. We conclude that in coronary arteries of castrated male pigs, sex hormones inhibit Ca2+ entry from extracellular space but not Ca2+ release from intracellular stores. 17beta-Estradiol mainly inhibits Ca2+ entry, whereas progesterone and testosterone cause coronary relaxation by inhibiting other mechanisms in addition to Ca2+ entry.

Animals↗
PubMed1997

Interstitial adenosine and serotonin in the feline lumbar spinal cord during short-term ischaemia.

During controlled ischaemia (aortal snare occlusion) of the lumbar spinal cord, microcirculatory (laser-Doppler flowmetry) and segmental neurophysiological parameters (monosynaptic reflexes, polysynaptic reflexes, cord dorsum potential=CDP) as well as interstitial concentrations of adenosine and serotonin (5-HT) were determined in the grey matter using the microdialysis/HPLC method. Ischaemic periods of 1-7 min with a residual blood flow in the lumbar spinal cord of 10-30 % of the preischaemic control blood flow caused a blockade of spinal pathways and an increase of concentrations of interstitial adenosine and 5-HT. This increase started immediately after the initiation of the ischaemic period and reached a maximum at the end or shortly after the end of the ischaemic period during postischaemic hyperaemia. A close correlation between the duration of ischaemia and the interstitial concentration of adenosine and 5-HT was not found. Repetition of ischaemic periods in an experiment did not lead to an extracellular accumulation or an exhaustion of the release of 5-HT, whereas some indication was found for an exhaustion of adenosine release. The course of the increase of interstitial adenosine and 5-HT was partly found to correlate to the loss and recovery of the CDP following ischaemia. The concentrations usually reached control levels before spinal reflexes reappeared. The highly dynamic changes in concentrations of adenosine and 5-HT in the extracellular space of the spinal cord during and after short-term ischaemia revealed some relation to the time course of recovery of segmental spinal functions by reflecting the course of spinal neuronal metabolism.

Adenosine↗
PubMed1985

Light-induced potassium fluxes in the skate retina.

Changes in the extracellular concentration of potassium [K+]0 in response to photic stimulation were studied in the skate retina with the aid of ion-selective electrodes. The results confirm earlier studies in demonstrating that the light-evoked changes originate at three intraretinal sites; an efflux of K+ was recorded in the regions of the two plexiform (synaptic) layers, whereas a decrease in [K+]0 occurred in the extracellular space surrounding the photoreceptors. Prolonged illumination induced long-term alterations in the levels of [K+]0 which, depending upon the retinal depth of the recording electrode, contained contributions from the various sinks and sources of [K+]0. In addition, the marked undershoot of the baseline level of [K+]0 that followed termination of the stimulus suggested the activity of a metabolically driven process for the uptake of extracellular potassium.

Animals↗
PubMed1991

Extracellular alkaline-acid pH shifts evoked by iontophoresis of glutamate and aspartate in turtle cerebellum.

The effect of glutamate and aspartate iontophoresis on extracellular pH was investigated in the turtle cerebellum in vitro. Both amino acids produced a rapid alkaline transient, typically followed by a prolonged acidification. These responses could be evoked in all layers of the cerebellum. Transition from bicarbonate to N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered media amplified the pH shifts. Similar alkaline-acid transients could be evoked in the molecular layer by electrical stimulation of the parallel fibers or the ipsilateral peduncle, or by superfusion of glutamate or aspartate. However, no alkaline shifts were evoked in the granular layer by either parallel fiber or peduncle stimulation. In contrast, the iontophoretically induced alkaline shifts were largest in the granular layer. Compared with the stimulus-evoked alkalinizations, the iontophoretic alkaline shifts were relatively insensitive to Mn2+ or Cd2+. These data suggest that the activity-dependent alkalinization of brain extracellular space is generated by a bicarbonate-independent mechanism related to excitatory synaptic transmission. The results are consistent with a flux of hydrogen ions through cationic channels, but do not support a direct role for voltage-dependent Ca2+ channels. In view of the sensitivity of ion channels to changes in external pH, and the magnitude of the amino acid-induced pH shifts, these results indicate that extracellular pH could play an important modulatory role in excitatory synaptic transmission.

Animals↗
PubMed2006

Vesicular polysaccharide export in Cryptococcus neoformans is a eukaryotic solution to the problem of fungal trans-cell wall transport.

The mechanisms by which macromolecules are transported through the cell wall of fungi are not known. A central question in the biology of Cryptococcus neoformans, the causative agent of cryptococcosis, is the mechanism by which capsular polysaccharide synthesized inside the cell is exported to the extracellular environment for capsule assembly and release. We demonstrate that C. neoformans produces extracellular vesicles during in vitro growth and animal infection. Vesicular compartments, which are transferred to the extracellular space by cell wall passage, contain glucuronoxylomannan (GXM), a component of the cryptococcal capsule, and key lipids, such as glucosylceramide and sterols. A correlation between GXM-containing vesicles and capsule expression was observed. The results imply a novel mechanism for the release of the major virulence factor of C. neoformans whereby polysaccharide packaged in lipid vesicles crosses the cell wall and the capsule network to reach the extracellular environment.

Animals↗
PubMed1998

Degeneration in vivo of rat hippocampal neurons by wild-type Alzheimer amyloid precursor protein overexpressed by adenovirus-mediated gene transfer.

In an attempt to elucidate the pathological implications of intracellular accumulation of the amyloid precursor protein (APP) in postmitotic neurons in vivo, we transferred APP695 cDNA into rat hippocampal neurons by using a replication-defective adenovirus vector. We first improved the efficiency of adenovirus-mediated gene transfer into neurons in vivo by using hypertonic mannitol. When a beta-galactosidase-expressing recombinant adenovirus suspended in 1 M mannitol was injected into a dorsal hippocampal region, a number of neurons in remote areas were positively stained, presumably owing to increased retrograde transport of the virus. When an APP695-expressing adenovirus was injected into the same site, part of the infected neurons in the hippocampal formation underwent severe degeneration in a few days, whereas astrocytes near the injection site showed no apparent degeneration. These degenerating neurons accumulated different epitopes of APP, and beta/A4 protein (Abeta)-immunoreactive materials were undetected in the extracellular space. A small number of degenerating neurons showed nuclear DNA fragmentation. Electron microscopic examinations demonstrated that degenerating neurons had shrunken perikarya along with synaptic abnormalities. Microglial cells/macrophages were often found in close proximity to degenerating neurons, and in some cases they phagocytosed these neurons. These results suggest that intracellular accumulation of wild-type APP695 causes a specific type of neuronal degeneration in vivo in the absence of extracellular Abeta deposition.

Adenoviridae↗
PubMed1976

Human ecchordosis physaliphora and chick embryonic notochord. A comparative electron microscopic study.

The ecchordosis physaliphora, a small gelatinous mass attached to the midline of the clivus, is characterized ultrastructurally by glycogen-laden intracytoplasmic vacuoles, focally distended endoplasmic reticulum and perinuclear cisterns with cytoplasmic invaginations, large clusters of granular endoplasmic reticulum interdigitating with mitochondria, and an abundant extracellular space. These morphologic features are also present in the 9-day embryonal chick notochord and the human chordoma and serve to reaffirm the derivation of the ecchordosis and chordoma from notochordal rests.

Animals↗
PubMed1995

Elevated extracellular glutamate levels increased the formation of hydroxyl radical in the striatum of anesthetized rat.

Results from various in vitro experiments have indicated that excitotoxicity and oxidative stress are two interrelated major mechanisms in causing neuronal damage in brain disorders such as cerebral ischemia/reperfusion. Thus, we have conducted experiments to investigate whether in the striatum of anesthetized rats the elevated brain extracellular concentrations of glutamate could increase the formation of hydroxyl radical. Elevation of glutamate levels and trapping of hydroxyl radical were accomplished by perfusing Ringer solutions containing both glutamate and salicylic acid through microdialysis probes implanted in rat striatum. The formation of hydroxyl radical was quantitated as the increased amounts of 2,3 and 2,5 dihydroxybenzoic acid (DHBA) which were the hydroxylative products of salicylic acid. Eluted microdialysates were directly injected onto high performance liquid chromatography (HPLC) with electrochemical detector via an on-line automatic injector. This method was authenticated by in vitro studies employing Fenton-type hydroxyl radicals generation system. Our results indicated that elevated glutamate concentrations (15 mM, 1.5 mM, and 150 microM glutamate in perfusing solutions) would significantly increased both the concentrations of 2,3 and 2,5 DHBA. In conclusion, we have obtained direct evidence showing that the elevated glutamate concentrations in brain extracellular space would increase the formation of hydroxyl radical, and these results implied that oxidative stress occurring in brain disorders might be induced by excitotoxicity.

Anesthesia↗
PubMed1978

[Ultrastructural features of the kidney following administration of antidiuretic hormone].

In the course of antidiuresis induced in rats by the antidiuretic hormone injection on the background of moderate water load (in difference from the hormone injection without the water load) the expansion of the extracellular spaces and of the basal labyrinth in the epithelium of the collecting tubules and of the thin descending limb of Henle's loop was revealed; this was apparently associated with the presence of intratubular pressure gradient under the given conditions. In both the experimental versions there occurred cytoplasmic vacuolization and expansion of the interstitial cells perinuclear space in the kidney medulla. These data confirm the hypothesis on the role of the intercellular contact in the transepithelium water reabsorption path in the kidney during the urine concentration process, and indicate the participation of the interstitial cells in this process.

Animals↗
PubMed1977

[Electron microscopic study of the small intestine in intestinal lymphangiectasia and constrictive pericarditis (author's transl)].

Electron microscopic study of the small intestine in cases of intestinal lymphangiectasia and in cases of constrictive pericarditis was performed. This study revealed that numerous chylomicron-like particles are present in the lymphatic lumina, in the extracellular spaces of the lamina propria, and within the interepithelial spaces between the absorptive cells. Presence of chylomicron-like particles in the intestinal lumen suggested possibility of passage of these substances into the intestinal tract through the interepithelial spaces. Similar findings to those as seen in intestinal lymphangiectasia were observed in constrictive pericarditis. A few pseudopode-like cytoplasmic projections of the undifferentiated crypt cells were noted. Other mechanisms of enteric protein loss are postulated.

Chylomicrons↗
PubMed1998

Multiple interactions between insect lipoproteins and fat body cells: extracellular trapping and endocytic trafficking.

The binding and internalization of a circulating insect lipoprotein, high density lipophorin (HDLp), by insect fat body cells was studied at the electron-microscopic level using ultrasmall gold-labeled HDLp and DiI-labeled HDLp, which were visualized by silver enhancement and diaminobenzidine photoconversion, respectively. Internalization of HDLp seems to conflict with the selective process by which the lipids are transported between HDLp and fat body cells. The pathway followed by the internalized lipoproteins was investigated. In addition, the localizations of HDLp in fat body cells of young and older adult locusts were compared because of the previously reported age-related differences in distribution of cell-associated and internalized HDLp. In the present study, internalized labeled HDLp was observed in early endosomes, late endosomes, and putative lysosomes. In older adults, these labeled structures were much less abundant than in young adults. Moreover, in these animals, the labeled endosomal/lysosomal vesicles were located close to the plasma membranes. A more intense labeling was observed in the extracellular matrix in older adults compared to young adults. In both developmental stages, an apparent accumulation of labeled HDLp was found in extracellular spaces. We propose that this entrapment of HDLp may be essential for selective lipid transport between HDLp and fat body cells.

Affinity Labels↗
PubMed2001

Novel structures in secreting the androgenic gland hormone.

The secretory granules in the androgenic gland of the terrestrial isopod Armadillidium vulgare, which have been indistinct for long time because of vulnerable structures, were revealed by using the rapid-freezing and freeze-substitution method. The fine structure of the androgenic gland is conspicuous by the distribution of numerous particular organelles in the cytoplasm consisting of the endoplasmic reticulum and the Golgi complex, and by having a number of highly organized structures developed between the androgenic gland cells. The structures connect to the intercellular space, which is seen as intercellular canaliculi for exporting the androgenic gland hormone. The plasma membranes near the particular structure of the intercellular canaliculi in the androgenic gland are often specialized to form cellular junctions. The secretory granules including the electron-dense materials, which are supposed to be peptides of androgenic gland hormone, are distributed beside the particular structure of the intercellular canaliculi. Some of the granules are seen to fuse with the plasma membranes. This observation suggests that, in the Armadillidium vulgare, the secretory granules containing androgenic gland hormone are transferred to the extracellular space through the intercellular canaliculi particularly developed for exporting the peptide hormone. This is the first evidence to show the secretory mechanism of the androgenic gland hormone in the Isopoda.

Animals↗