Biomedical subjects

I Dietzel

Publications and source records attributed to I Dietzel.

9 recordsLinked to original sources

PubMed1989

Synaptic potentials in the rat neostriatum in dissociated embryonic cell culture.

Neostriatal cells of embryonic days 19-21 were grown in dissociated cell culture. To test whether the cultures contained predominantly neostriatal cells, a glyoxylic acid staining procedure was used which, after dopamine loading, stained neostriatal cells but not neurons of embryonic neocortical tissue. Whole cell current clamp recording was performed in the neurons after 1-2 weeks in cell culture. Although cells could be driven to discharge by direct depolarization, spontaneous activity was low. All cells responded to gamma-aminobutyric acid (GABA) (0.1-0.5 mM), and the majority of them responded to glutamate (Glu) (0.1 mM). Only about 50% were depolarized by acetylcholine (ACh) (0.1-0.5 mM). Atropine (1-10 microM) did not block this depolarization. Barrages of postsynaptic potentials (PSPs) were induced by applications of Glu or ACh, even if the neuron under observation was not depolarized. All PSPs were depressed by bicuculline (50 microM), indicating their mediation by GABAergic receptors. Exclusively GABAergic PSPs were also observed in cultures raised in the presence of nerve growth factor. The study indicates that neostriatal cells form GABAergic, but not excitatory cholinergic synapses when cultured at this embryonic age under our conditions, resembling the pattern of development observed in slices obtained from neonatal rats.

Acetylcholine↗

PubMed1989

Relations between slow extracellular potential changes, glial potassium buffering, and electrolyte and cellular volume changes during neuronal hyperactivity in cat brain.

The aim of this investigation is to estimate the contribution of spatial glial K+ buffer currents to extracellular K+ homeostasis during enhanced neuronal activity. Neuronal hyperactivity was induced by electrical stimulation of the cortical surface or the ventrobasal thalamic nuclei of cats (5-50 Hz, 0.1-0.2 ms, two to three times threshold stimulation intensity, 5-20 s). The accompanying slow field potential changes were recorded simultaneously across the grey matter with vertical assemblies of eight micropipettes glued 300 microns apart. Using the Poisson equation, the amplitudes of the underlying current sources and sinks were calculated. The current source densities depended on the depth of recording, frequency, strength, and duration of the stimulation. Current sinks, corresponding to a removal of 0.1-0.5 mmoles of monovalent cations per liter of brain tissue and second from the extracellular space, were observed in middle cortical layers, whereas sources appeared at superficial and deeper sites. These sinks and sources might represent K+ moved across glial membranes by spatial buffer currents. The consequences of glial buffer currents of this magnitude were investigated with model calculations. It turned out that measurements of electrolyte and volume changes of the extracellular space (Dietzel et al. Exp. Brain Res. 40:432-439, 1980; Exp. Brain Res. 46:73-84, 1982) could only partially be explained by spatial buffer currents of this magnitude. Comparison of the calculated values with intracellular measurements in neurons and glial cells (Coles et al. Ann. N.Y. Acad. Sci. 481:303-317, 1986; Ballanyi et al. J. Physiol. 382:159-174, 1987) suggests that spatial buffering combines with an approximately equimolar KCl transport and, depending on the preparation, also K+/Na+-exchange across glial membranes.

Action Potentials↗

PubMed1986

Dynamic variations of the brain cell microenvironment in relation to neuronal hyperactivity.

Neuronal hyperactivity has been shown to cause transient changes in ionic concentrations as well as in the volume of the extracellular space (ECS). During enhanced neuronal activity in the sensorimotor cortex of the cat, increases in the extracellular K+ concentration to a ceiling value of 10 mM have been observed concomitant with decreases in the Na+ concentration of similar magnitude. Simultaneously, the Cl- concentration rose steadily during the enhanced neuronal activity, and the extracellular space decreased by about 30%. A mathematical model allowed the interpretation of these concentration and volume changes as results of K+ release by active neurons in exchange for Na+, removal of K+ from the ECS by spatial glial buffering and movements of KCl into glial cells, as well as cell swelling due to metabolically induced transient increases in cellular osmolarity. Similar mechanisms have also been found to operate in gliotic scar tissue, where glial cells appeared to function the same way as in normal cortex, in rat hippocampal slices, and in preparations studied by other investigators.

Animals↗

PubMed1986

Ionic changes and alterations in the size of the extracellular space during epileptic activity.

Experiments with ion-selective microelectrodes revealed that a considerable activity of K ions appears temporarily in the extracellular space (ES) during enhanced neuronal activity and is removed from the ES by diffusion, active uptake, and entry into glial cells. The glial uptake results from the preferential glial K permeability and spatial glial K buffering. The glia responds to the local extracellular accumulation by a depolarization of the exposed part of its membrane. This depolarization will spread along the glial syncytium or extended glial cells. At sites where the extracellular K concentration has not yet increased, the membrane potential will thus be depolarized with respect to the K diffusion potential. Here K will move from the intra- into the extracellular space, in order to restore the electrochemical equilibrium. This induces a current that carries K into glial cells at sites of maximal K accumulation and that transports K out of glial cells at remote areas. In this way K is spatially redistributed. The corresponding current loop in the ES is predominantly carried by Na and Cl, the majority ions. Thus, Na and Ca are transported to the site of K accumulation while Cl moves away. The Cl and K ions are only partially replaced by Na. Hence, a decrease of extracellular osmolarity results, which leads to a water flux from the ES into the cells, inducing a shrinkage of the ES at sites of maximal K accumulation. At remote sites, the opposite effect is expected due to K flow out of glia and Cl transport to these sites. Thus, remote from the area of maximal neuronal activity, an increase of the ES is expected. This mechanism can explain the measured depth profile of the changes in the ES. At sites of maximal neuronal activity, the extracellular space undergoes a reduction by more than 30%. The ionic changes are accompanied by slow negative potential shifts. An increase in intracellular osmolarity due to enhanced metabolic activity and possibly KCl uptake mechanisms contributes to the changes in volume and ionic concentration. Model calculations of the after-effects of the loss of positive charges from the extracellular space and the K-specific glial buffering could predict size and time course of these changes. Experimental tests of this view include observations during epileptiform activity in gliotic scar foci as well as in hippocampal slices with depressed synaptic transmission. The extra- and intracellular ionic changes influence the generation, spread, and termination of seizure activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1984

Light-induced changes in extracellular volume in the retina of the drone, Apis mellifera.

Slices of drone retina were superfused with a Ringer solution containing 1 mM tetraethylammonium (TEA), and the concentration of this ion in the extracellular space [( TEA]0) was measured with ion-sensitive microelectrodes. A train of light flashes for 90 s caused [TEA] to increase by 48 +/- 4% (S.E.), n = 12. Since water crosses cell membranes more readily than TEA does this indicates a volume decrease of at least 32%. Measurements of Ca2+ activity under similar conditions showed an increase of 32 +/- 4% (S.E.), n = 14. Since this is less than the increase in [TEA]0 it suggests that the total amount of Ca2+ in the extracellular space actually decreased.

Animals↗

PubMed1984

Extracellular potassium concentration in chronic alumina cream foci of cats.

Changes in extracellular K+ concentration [( K+]o) were measured with ion-selective microelectrodes in chronic epileptic foci induced by topical application of A1(OH)3 cream on the sensorimotor cortex of cats. The foci were morphologically characterized by a scar surrounded by an area of marked gliosis. Base-line levels of [K+]o in gliotic tissue and its immediate border zone were comparable to those in normal cortical tissue. Peak levels of [K+]o obtained during repetitive electrical stimulation of the cortical surface and thalamic ventrobasal complex were only slightly enhanced with 11.6 mM in chronic foci and 10.8 mM in normal cortex. Iontophoretic K+ application into gliotic tissue was accompanied by slow negative potential shifts comparable to those observed in normal cortex. Passage of constant current through gliotic tissue caused local [K+]o changes in the vicinity of the current-passing electrode. Since these [K+]o changes were similar to those observed in normal tissue, it was concluded that the amount of transcellularly transported K ions was comparable in both tissues. Changes in the size of extracellular space (ES) were investigated by measuring local concentration changes of iontophoretically injected tetramethylammonium and choline ions. During stimulus-induced seizure activity, the ES shrank outside the gliotic area at sites of maximal [K+]o elevation, while it increased at sites within the gliotic tissue where [K+]o rises were smaller. The results suggest that the spatial buffer capacity of gliotic tissue for K+ is not severely impaired. Since the relationship between rises in [K+]o and subsequent undershoots at sites immediately bordering the gliotic tissue is comparable to that in normal cortex, the ability of this epileptic tissue for active K+ uptake appears to be unaffected. This conclusion is further supported by the observation that iontophoretically induced rises in [K+]o during undershoots are reduced to a similar extent as in normal cortex.

Aluminum Hydroxide↗

PubMed1982

Stimulus-induced changes in extracellular Na+ and Cl- concentration in relation to changes in the size of the extracellular space.

Extracellular Na+ - and Cl- -concentrations ([Na+]o, [Cl-]o) were recorded with ion-selective microelectrodes during repetitive stimulation and stimulus-induced self-sustained neuronal afterdischarges (SAD) in the sensorimotor cortex of cats. In all cortical layers [Na+]o initially decreased by 4-7 mM. In depths of more than 600 micrometer below the cortical surface such decreases usually turned into increases of 2-6 mM during the course of the SADs, whereas in superficial layers [Na+]o never rose above its resting level. [Cl-]o always showed an increase in the course of the SADs often preceded by an initial small decrease. The average increase at a depth of 1,000 micrometers was about 7 mM. [Cl-]o reached peak values at about the end of the ictal period, whereas [Na+]o reached its maximum shortly after the end of the SAD, at times when [K+]o was still elevated above the baseline concentration. These data indicate that the extracellular osmolarity can increase during SAD by up to 30 mM. Such an increase in osmolarity can be explained by an increase in the number of intracellular particles, caused by cleavage of larger molecules during enhanced metabolism. This could lead to cell-swelling due to passive water influx from the extracellular space (ES). However, the resulting reduction of the size of the ES is calculated to be less than 10% for an increase in intracellular osmolarity by 30 mOsm. This value is too small as compared to previously measured ES-reductions under similar conditions (i.e., 30% reduction at 1,000 micrometers; Dietzel et al. 1980). Reductions of the size of the ES that accompany the observed changes in the ionic environment, are quantitatively explained on the basis of the extended glial buffering mechanism described in the preceding paper.

Animals↗

PubMed1980

Transient changes in the size of the extracellular space in the sensorimotor cortex of cats in relation to stimulus-induced changes in potassium concentration.

The time course of local changes of the extracellular space (ES) was investigated by measuring concentration changes of repeatedly injected tetramethylammonium (TMA+) and choline (Ch+) ions for which cell membranes are largely impermeable. After stimulus-induced extracellular [K+] elevations the delta [TMA+] and delta [Ch+] signals recorded with nominally K+-selective liquid ion-exchanger microelectrodes increased by up to 100%, thus indicating a reduction of the ES down to one half of its initial size. The shrinkage was maximal at sites where the K+ release into the ES was also largest. At very superficial and deep layers, however, considerable increases in extracellular K+ concentration were not accompanied by significant reductions in the ES. These findings can be explained as a consequence of K+ movement through spatially extended cell structures. Calculations based on a model combining the spatial buffer mechanism of Kuffler and Nicholls (1966) to osmolarity changes caused by selective K+ transport through primarily K+ permeable membranes support this concept. Following stimulation additional iontophoretically induced [K+]0 rises were reduced in amplitude by up to 35%, even at sites where maximal decreases of the ES were observed. This emphasizes the importance of active uptake for K+ clearance out of the ES.

Animals↗

PubMed1978

Pole cap formation in Escherichia coli following induction of the maltose-binding protein.

After induction with maltose, 30--40% of the total protein in the osmotic shock fluid consist of maltose-binding protein while the induction ratio (maltose versus glycerol grown cells) for the amount of binding protein synthesized as well as for maltose transport is in the order of 10. Induction of maltose transport does not occur during all times of the cell cycle, but only shortly before cell division. Electronmicroscopic analysis of cells grown logarithmically on glycerol or maltose revealed in the latter the formation of large pole caps. These pole caps arise from an enlargement of the periplasmic space. Small cells contain one pole cap, large cells contain two. Pulse label studies with strain BUG-6, a mutant that is temperature sensitive for cell division reveal the following: Growth at the non-permissive temperature prevents maltose-binding protein synthesis and formation of new transport capacity. After shifting to the permissive temperature the cells regain both functions. Simultaneously, the newly formed cells exhibit pole caps. We conclude that the induction of maltose-binding protein is responsible for the formation of pole caps. In addition, beside the presence of inducer, cell cycle events occuring during division are necessary for the synthesis of maltose-binding protein.

Biological Transport, Active↗