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Biomedical subjects

E Fifková

Publications and source records attributed to E Fifková.

At least 19 recordsLinked to original sources
PubMed1997

Fine structure of hippocampal dendrites in the dentate fascia of LS/SS-mice after chronic ethanol treatment.

1. The effect of ethanol and its withdrawal on the dendritic microtubules in the dentate fascia of male mice was studied in the ethanol-sensitive, long-sleep (LS) line and the ethanol-insensitive, short-sleep (SS) line. 2. Both mouse lines were treated with a liquid ethanol diet. Dendrites in the dentate molecular layer (DML) of the right hippocampus were examined. 3. They revealed marked changes in microtubule density as compared with the controls. While the microtubule density in LS mice was significantly reduced by 15% and 18% in the middle and distal third of the DML, respectively, in SS mice the reduction (by 12%) took place in the distal third only. During withdrawal a recovery of the microtubule density has been observed in both lines.

Alcoholism↗
PubMed1994

Changes in GABAergic and non-GABAergic synapses during chronic ethanol exposure and withdrawal in the dentate fascia of LS and SS mice.

Ethanol-sensitive LSIBG and ethanol-insensitive SSIBG mice were exposed to ethanol (23.5% ethanol-derived calories) for 4 months. Half of the animals was sacrificed at this time and the other half was withdrawn from the ethanol diet for 1 month. GABA immunoelectron microscopy was used to study the impact of the treatments on synaptic contacts in the dentate molecular layer. In the LS mice a significant loss of non-GABAergic axospinous synapses (26.7%; p < 0.05) was observed during ethanol exposure which was followed by a loss of GABAergic synapses on dendritic shafts (54.7%; p < 0.01) during withdrawal. In the SS mice there was a significant decrease in the non-GABAergic axospinous synapses (23.5%; p < 0.05) and a significant increase in axodendritic synapses (63.3%; p < 0.05) during ethanol exposure. The observed changes in the GABAergic and non-GABAergic innervation of the dentate fascia induced by ethanol were observed in the projection zone of the perforant path. They could adversely affect the hippocampal physiology with a consequent impairment of mnemonic functions.

Alcohol Withdrawal Delirium↗
PubMed1992

Inhibitory contacts on dendritic spines of the dentate fascia.

GABA-containing axon terminals were observed in the distal two-thirds of the dentate molecular layer to contact spines and dendrites of the granule cells. These contacts have the morphological characteristics of inhibitory synapses: they contain pleomorphic vesicles and have symmetrical junctional specializations. Convergence of an asymmetrical, non-GABAergic and a symmetrical, GABAergic synapse on one spine was often observed.

Animals↗
PubMed1991

Distribution of acetylated alpha-tubulin in brain. In situ localization and biochemical characterization.

We studied the solubility properties of brain acetylated alpha-tubulin, as well as the localization of this tubulin in brain tissue. Endogenous unpolymerized tubulin and cytoskeletal tubulin were fractionated after brain Triton-solubilization. Using the immunoblotting technique, we found that acetylated alpha-tubulin was recovered in the cytoskeletal fraction, and that most (92%) of the acetylated microtubules of this fraction were depolymerized by cold/Ca2+ treatment. In another set of experiments, axonal and soma-dendritic preparations were found to have equivalent amounts of acetylated alpha-tubulin. By immunogold electron microscopy, we established that acetylated microtubules are widely distributed in dendrites of the central nervous system.

Acetylation↗
PubMed1989

In situ localization of myosin and actin in dendritic spines with the immunogold technique.

The in situ detection of macromolecules by means of immunoelectron microscopy provides information about their ultrastructural localization in cellular compartments. With this technique, we have demonstrated that the contractile proteins actin and myosin are both localized in dendritic spines at densities exceeding those of other neuronal compartments. Myosin was associated with actin filaments, with spine plasma membrane, and with membranes of the spine apparatus. Given the dynamic properties of actin and myosin, these data suggest that these proteins may be involved in the mechanism of synaptic plasticity in general and in morphometric change resulting from intense synaptic activation in particular.

Actins↗
PubMed1988

Astrocyte proliferation precedes a decrease in basket cells in the dentate fascia following chronic ethanol treatment in mice.

The effect of chronic ethanol administration on the density of basket cells in the dentate gyrus of mice selectively bred for their sensitivity to acute ethanol exposure (long-sleep, LS and short-sleep, SS) was assessed in two experiments. In addition, the effect of chronic ethanol on the density of dentate granule cells and astrocytes was examined. In the first experiment, mice received 3 weeks of a liquid ethanol diet with 35% of their calories derived from ethanol (EDC). In this experiment, LS mice did not demonstrate a change in the density of granule cells or in the density of basket cells. There was, however, a significant increase in the density of astrocytes as a result of this treatment for the LS mice. The SS mice were unaffected on all measures. In the second experiment, portions of which have been reported previously, mice received a diet with 23% EDC for 3 months. As a result of this exposure, LS mice showed a significant decrease in the density of basket cells, but there was no change in the density of granule cells or astrocytes. There was no difference between controls and experimental mice from the SS group on any of these parameters. These results suggest that at least in the dentate gyrus, chronic ethanol treatment selectively reduces the density of basket cells but only in mice that are more sensitive to the hypnotic effects of acute ethanol exposure. Furthermore, this effect seems to be preceded by an apparent increase in the density of astrocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗
PubMed1987

The effect of chronic ethanol consumption on the fine structure of the CA1 stratum oriens in short-sleep and long-sleep mice: short-term and long-term exposure.

The effect of chronic ethanol administration on the fine structure of the hippocampal CA1 stratum oriens was examined in two lines of mice selectively bred for their differential sensitivity to acute ethanol exposure (long-sleep, LS and short-sleep, SS mice). Two experiments were performed. In the first experiment, mice received a liquid diet for 3 weeks with the final amount of ethanol being 35% ethanol-derived calories. In the second experiment, mice received 23.5% ethanol-derived calories for 3 months. Quantitative electron microscopy of the dendritic spines and synaptic appositions in the stratum oriens of CA1 revealed an interaction between diet and line of mice, but only in the 3-month exposure condition. This difference was due to a significant decrease in the density of spines and synaptic appositions in the LS mice receiving ethanol. Additionally, baseline differences between lines indicate that the lines are differing in the density of spine synapses in the absence of ethanol treatment. The possible interaction between acute sensitivity to ethanol and differences in fine structure are examined.

Animals↗
PubMed1987

Changes in the frequency of basket cells in the dentate fascia following chronic ethanol administration in mice.

The frequency of basket cells in the granule cell layer of the dentate fascia of Short Sleep (SS) and Long Sleep (LS) mice was determined following 3 months of ethanol exposure. These mice were bred for their differential susceptibility to the narcotic effects of acute doses of ethanol. The ethanol-insensitive SS mice were unaffected by the treatment while the ethanol-sensitive LS mice that received ethanol showed a significant decrease in basket cell frequency over their control group counterparts. These basket cells are thought to control the tonic level of activity of the granule cells. Thus, a decrease in basket cell frequency might lead to higher granule cell activity following chronic ethanol exposure. This effect could counteract the assumed stronger depressant effect of ethanol in the relatively ethanol-sensitive LS mice.

Animals↗
PubMed1987

Effect of chronic ethanol consumption on the fine structure of the dentate gyrus in long-sleep and short-sleep mice.

The effect of short- and long-term chronic ethanol consumption on the fine structure of the dentate gyrus was examined in two lines of mice selected for their differential sensitivity to acute ethanol administration. Quantitative electron microscopic analysis of dendritic spines, axon terminals, and synaptic appositions revealed significant differences between the long-sleep and short-sleep mice. In control preparations, long-sleep mice were found to have larger spine areas and perimeters, larger axon terminals, and longer synaptic appositions than short-sleep mice. In addition, the shape of dendritic spines in the long-sleep mice was significantly more complex than those of short-sleep mice. Ethanol tended to increase this complexity in long-sleep mice only. Ethanol had only a limited effect on the other anatomical measures. The results provide evidence for ultrastructural differences between the nervous systems of these lines of mice which may have a role in their differential sensitivity to acute ethanol administration.

Alcoholism↗
PubMed1987

Changes in the nuclear pore complexes of the dentate granule cells in aged rats.

In 3-, 9-, 24-, and 30-month-old male rats (Fischer 344), the nuclear perimeter and the density and diameter of nuclear pore complexes in the granule cells of the dentate fascia were studied. Whereas the nuclear perimeter and the diameter of nuclear pore complexes did not change as a function of age, there was a significant loss of them at 24 months (20%), compared with the third month. This change suggests that the nucleocytoplasmic communication may be impaired with age which would adversely affect protein synthesis, and could explain the loss of the postsynaptic sites of the dentate fascia of aged rats.

Aging↗
PubMed1986

Calcium distribution in dendritic spines of the dentate fascia varies with age.

Calcium distribution in dendritic spines of the dentate fascia was studied as a function of age with the oxalate-pyroantimonate precipitation technique. In postnatal ages P3, P9, P24 and P30 spines were analyzed as to the presence of the spine apparatus (SA) and as to the presence of Ca2+ deposits within the SA and within the spine cytoplasm. The percentage of spines with SA-containing precipitates declined significantly between P3 and P24. Conversely, the percentage of spines with precipitates in the spine cytoplasm was significantly increased by P24. In the absence of an SA loss, this result suggests an age-related decrease in the Ca2+-sequestering capacity by the SA. These parameters were improved by P30 so that they approximated the values of P3. Such a seeming amelioration could be attributed to the fact that the mortality rate in rats sharply increases by P24, so that animals surviving this age represent a selected population in which a compensatory growth of spines has occurred and has secured functionally valid connections.

Aging↗
PubMed1986

Actin filament organization within dendrites and dendritic spines during development.

The myosin S-1 subfragment was used to label actin filaments in the developing rat brain. The results show actin filaments present throughout the dendritic region with highest concentrations within growth cones and regions of spine development. Between 6 and 25 days postnatal, spines became more complex and actin filaments within them increased in number and formed a complex network. The observed organization of actin supports the hypothesis that actin has a role in the protrusion of spines from the dendrite during development.

Actin Cytoskeleton↗
PubMed1985

A possible mechanism of morphometric changes in dendritic spines induced by stimulation.

A number of experimental procedures which induce increased electrical activity (including long-term potentiation) were shown to be accompanied by morphometric changes in dendritic spines. These changes include an enlargement of the spine head, shortening and widening of the spine stalk, and an increase in the length of synaptic apposition. A possible mechanism is suggested which takes into account specific cytological features of the spine and the existence of contractile proteins in neurons. Dendritic spines are defined as special domains of the neuron which have a unique organization of the cytoplasm. Actin filaments form a very dense network in the spine head, and they are longitudinally organized within the spine stalk. Spines were also shown to contain myosin and other actin-regulatory proteins. The high density of the actin network could explain the characteristic absence of the cytoplasmic organelles from dendritic spines. In analogy with other cells, such an actin organization indicates low levels of free cytosolic calcium. Even in the resting state, calcium levels may be unevenly distributed through the neuron, being lowest within the subplasmalemmal region. Due to the high surface-to-volume ratio in spines, the cytoplasm is formed mostly by the subplasmalemmal region. The spine apparatus or the smooth endoplasmic reticulum, which is recognized as a calcium-sequestering site in spines, may also contribute to the low calcium levels there. However, when in the stimulated spine the voltage-dependent calcium channels open, then, given the spine's high surface-to-volume ratio, the concentration of calcium may very quickly attain levels that will activate the actin-regulatory proteins and myosin and thus trigger the chain of events leading to the enlargement of the spine head and to the contraction (i.e., widening and shortening) of the spine stalk. The increased free cytosolic calcium may also activate the protein-producing system localized at the base of the spine, which, under certain conditions, could stabilize the morphometric changes of the spine.

Actins↗
PubMed1985

Actin in the nervous system.

Since synaptic plasticity is an important property of the brain, it is timely to try to understand the possible mechanisms underlying this phenomenon. The role of the cytoplasm for neuronal functions has until now been largely overlooked, the main emphases being on the plasma membrane for fast electrical events and on cytoplasmic organelles for the slower metabolic processes. However, recent studies on the cytoplasm of non-muscle cells have stressed the importance of contractile proteins, like actin, on maintaining the cell shape and a number of vital cellular functions, which may be related to the phase transitions in the cytoplasm. The necessary versatility is conferred on the actin networks by actin-associated proteins and by the free cytosolic calcium. In the nervous system, in addition to actin and myosin, a number of actin regulatory proteins was recently isolated, and they were shown to have properties similar to those of other non-muscle cells. Consequently, actin networks in neurons like those in non-muscle cells may be capable of contraction and phase transitions. The phase transitions have a rapid onset, and they may be quickly terminated or they may last over extended periods of time. In this way actin networks may gain control over the state of the cytoplasm and hence over the function of the neuron. Actin may be, therefore, uniquely suited to regulate various plastic reactions. The cytoplasm of growth cones and dendritic spines contains solely actin networks and is devoid of microtubules and neurofilaments. Since both these structures contain myosin and since growth cones are endowed with a considerable motility, dendritic spines also may have a likewise property. The necessary regulation of the levels of free cytosolic calcium may be provided by the spine apparatus in addition to calcium pumps in the plasma membrane and calcium regulatory proteins in the spine cytoplasm. Various types of stimulation which change the level of free cytosolic calcium may induce contraction of the spine actin network which may be responsible for the morphometric changes observed following different experimental interventions and pathological conditions. Although most of the conclusions in this review are rather speculative, they may provide directions for future research in the spine and synaptic plasticity.

Actins↗
PubMed1983

Calcium in the spine apparatus of dendritic spines in the dentate molecular layer.

With a pyroantimonate precipitation technique, we have demonstrated Ca2+ in the sacs of the dendritic spine apparatus in the SER of dendrites and axon terminals, in synaptic vesicles, multivesicular bodies, mitochondria, and glial processes of the dentate molecular layer. It is speculated that the spine apparatus may be a Ca2+ sequestering organelle which may regulate levels of intraspinal and intradendritic Ca2+ during synaptic activity.

Animals↗
PubMed1982

Effect of anisomycin on stimulation-induced changes in dendritic spines of the dentate granule cells.

Tetanic stimulation of the entorhinal area induces significant enlargement of the average dendritic spine area and perimeter in the middle and distal thirds of the dentate molecular layer 4 and 90 min following stimulation. Four minutes after stimulation, the differences between the stimulated and control animals were 20% for the dendritic spine area and 9% for the perimeter in the middle third, and in the distal third 32 and 14%, respectively. Ninety minutes after stimulation the differences were 28 and 11% for the area and perimeter in the middle third, and 33 and 18% in the distal third, respectively. Anisomycin at a dose of 25 mg/kg had no significant effect on the average spine area or perimeter in the various thirds of the dentate molecular layer in the 19 and 105 min post-application intervals. This dose of anisomycin given 15 min prior to the stimulation suppresses the stimulation-induced spine changes in the 4 min interval. In the 90 min interval when the effect of anisomycin on protein synthesis is largely terminated, spine enlargement reappears, being 21% higher than the controls in the middle and distal thirds. The differential effect of anisomycin on dendritic spines in the two post-stimulation intervals is discussed in relation to the effect of anisomycin on protein synthesis. The present experiments thus demonstrate that the stimulation-induced spine enlargement in the dentate fascia can be suppressed by a protein synthesis blocking drug.

Animals↗