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Biomedical subjects

V Gundersen

Publications and source records attributed to V Gundersen.

14 recordsLinked to original sources
PubMed2001

Comparison of major and trace element concentrations in Danish greenhouse tomatoes (Lycopersicon esculentum Cv. Aromata F1) cultivated in different substrates.

The concentration of major and trace elements was determined for tomato (Lycopersicon esculentumcv. Aromata F1) fruits grown in three different substrate systems. The systems were soil and rockwool irrigated with a normal nutrient solution and rockwool irrigated with a nutrient solution with elevated electrical conductivity (EC). At three harvest times, tomato fruits were analyzed for Ca, Cu, Fe, K, Mg, Mn, Na, P, S, Sr, and Zn by ICP-AES and for Cd, Cr, Mo, Ni, Pb, Sn, and V by HR-ICPMS. The concentrations of Ca, Cd, Fe, Mn, Mo, Na, Ni, Sr, and Zn were significantly different (p < 0.05) for tomato fruits grown on the different substrates. Between the harvest times different levels (p < 0.05) were shown for Ca, Cd, Fe, Mn Na, Ni, Sr, Zn Cu, K, Mg, P, Sn, and V. The concentration of Cd was >15 times higher and the concentration of Ca was 50-115% higher in soil-grown fruits than in rockwool-grown fruits. Principal component analysis applied on each harvest split the data into two groups. One group includes soil-grown fruits, and the other group includes rockwool-grown fruits with the two different nutrient solutions.

Solanum lycopersicum↗
PubMed2001

Redistribution of neuroactive amino acids in hippocampus and striatum during hypoglycemia: a quantitative immunogold study.

Postembedding immunocytochemistry was used to localize aspartate, glutamate, gamma-aminobutyric acid (GABA), and glutamine in hippocampus and striatum during normo- and hypoglycemia in rat. In both brain regions, hypoglycemia caused aspartatelike immunoreactivity to increase. In hippocampus, this increase was evident particularly in the terminals of known excitatory afferents-in GABA-ergic neurons and myelinated axons. Aspartate was enriched along with glutamate in nerve terminals forming asymmetric synapses on spines and with GABA in terminals forming symmetric synapses on granule and pyramidal cell bodies. In both types of terminal, aspartate was associated with clusters of synaptic vesicles. Glutamate and glutamine immunolabeling were markedly reduced in all tissue elements in both brain regions, but less in the terminals than in the dendrosomatic compartments of excitatory neurons. In glial cells, glutamine labeling showed only slight attenuation. The level of GABA immunolabeling did not change significantly during hypoglycemia. The results support the view that glutamate and glutamine are used as energy substrates in hypoglycemia. Under these conditions both excitatory and inhibitory terminals are enriched with aspartate, which may be released from these nerve endings and thus contribute to the pattern of neuronal death characteristic of hypoglycemia.

Amino Acids↗
PubMed2000

Comparative investigation of concentrations of major and trace elements in organic and conventional Danish agricultural crops. 1. Onions (Allium cepa Hysam) and peas (Pisum sativum ping pong).

210 samples of onions (Allium cepa Hysam) from 11 conventionally and 10 organically cultivated sites and 190 samples of peas (Pisum sativum Ping Pong) from 10 conventionally and 9 organically cultivated sites in Denmark were collected and analyzed for 63 and 55 major and trace elements, respectively, by high-resolution inductively coupled plasma mass spectrometry. Sampling, sample preparation, and analysis of the samples were performed under carefully controlled contamination-free conditions. Comparative statistical tests of the element concentration mean values for each site show significantly (p < 0.05) different levels of Ca, Mg, B, Bi, Dy, Eu, Gd, Lu, Rb, Sb, Se, Sr, Ti, U, and Y between the organically and conventionally grown onions and significantly (p < 0.05) different levels of P, Gd, and Ti between the organically and conventionally grown peas. Principal component analysis (PCA) applied to the 63 elements measured in the individual onion samples from the 21 sites split up the sites into two groups according to the cultivation method when the scores of the first and third principal components were plotted against each other. Correspondingly, for peas, a PCA applied to the 55 elements measured as mean values for each site split up the 19 sites into two groups according to the cultivation method when the scores of the third and fourth principal component were plotted against each other. The methodology may be used as authenticity control for organic cultivation after further method development.

Food, Organic↗
PubMed1999

Concentrations of 50 major and trace elements in Danish agricultural crops measured by inductively coupled plasma mass spectrometry. 3. Potato (Solanum tuberosum folva).

The multi-element (Ag, Al, Au, Ba, Bi, Ca, Cd, Co, Cr, Cs, Cu, Dy, Er, Fe, Ga, Gd, Ho, In, Ir, La, Lu, Mn, Mo, Nb, Nd, P, Pb, Pd, Pr, Pt, Rb, Re, Rh, Ru, Sb, Sc, Sm, Sn, Sr, Ta, Tb, Th, Ti, Tl, Tm, U, V, Y, Yb, and Zn) concentrations (microg/kg, fresh weight) in potatoes (Solanum tuberosum, Folva) were investigated in this study. The potatoes were grown in two fertilization practices; one with pig slurry and one with calcium ammonium nitrate at three levels of N fertilization (0, 60, and 120 kg of N/ha). The experiment field was located at the Riso National Laboratory Agronomy Farms in Roskilde, Denmark. High-resolution-inductively coupled plasma mass spectrometry (HR-ICPMS) was used for analyses of the samples. The effect of three levels of N fertilization on elemental concentrations of the crop are evaluated by use of discriminant partial least-squares regression (PLS). The results provide useful biological and nutritional information on potatoes.

Crops, Agricultural↗
PubMed1998

Synaptic vesicular localization and exocytosis of L-aspartate in excitatory nerve terminals: a quantitative immunogold analysis in rat hippocampus.

To elucidate the role of aspartate as a signal molecule in the brain, its localization and those of related amino acids were examined by light and electron microscopic quantitative immunocytochemistry using antibodies specifically recognizing the aldehyde-fixed amino acids. Rat hippocampal slices were incubated at physiological and depolarizing [K+] before glutaraldehyde fixation. At normal [K+], aspartate-like and glutamate-like immunoreactivities were colocalized in nerve terminals forming asymmetrical synapses on spines in stratum radiatum of CA1 and the inner molecular layer of fascia dentata (i.e., excitatory afferents from CA3 and hilus, respectively). During K+ depolarization there was a loss of aspartate and glutamate from these terminals. Simultaneously the immunoreactivities strongly increased in glial cells. These changes were Ca2+-dependent and tetanus toxin-sensitive and did not comprise taurine-like immunoreactivity. Adding glutamine at CSF concentration prevented the loss of aspartate and glutamate and revealed an enhancement of aspartate in the terminals at moderate depolarization. In hippocampi from animals perfused with glutaraldehyde during insulin-induced hypoglycemia (to combine a strong aspartate signal with good ultrastructure) aspartate was colocalized with glutamate in excitatory terminals in stratum radiatum of CA1. The synaptic vesicle-to-cytoplasmic matrix ratios of immunogold particle density were similar for aspartate and glutamate, significantly higher than those observed for glutamine or taurine. Similar results were obtained in normoglycemic animals, although the nerve terminal contents of aspartate were lower. The results indicate that aspartate can be concentrated in synaptic vesicles and subject to sustained exocytotic release from the same nerve endings that contain and release glutamate.

Aminooxyacetic Acid↗
PubMed1998

A high affinity glutamate/aspartate transport system in pancreatic islets of Langerhans modulates glucose-stimulated insulin secretion.

To examine the role of glutamatergic signaling in the function of pancreatic islets, we have characterized a high affinity glutamate/aspartate uptake system in this tissue. The islet [3H]glutamate uptake activity was Na(+)-dependent, and it was blocked by L-trans-pyrrolidine-2,4-dicarboxylic acid, a blocker of neuronal and glial glutamate transporters. Islet glutamate transport activity exhibited a Vmax of 8.48 +/- 1.47 fmol/min/islet (n = 4), which corresponds to 102.2 +/- 17.7 pmol/min/mg islet protein. The apparent Km of islet glutamate transport activity depended on the glucose concentration used in the assay. In the presence of glucose concentrations that do not stimulate insulin secretion (2.8 mM), the apparent Km was 34.7 +/- 7.8 microM (n = 3). However, in high glucose (16.7 mM) the apparent Km increased to 112.7 +/- 16.5 microM (n = 3) with little or no change in Vmax. Like most known plasma membrane glutamate transporters, islet glutamate transporters also transported D-aspartate. Anti-D-aspartate immunoreactivity showed that the islet glutamate/aspartate transport activity was localized to the non-beta cell islet mantle. In perifusion experiments with isolated islets in the absence of exogenous amino acids, L-trans-pyrrolidine-2,4-dicarboxylic acid in the presence of 8.3 mM glucose potentiated insulin secretion 23.3 +/- 2.3% (n = 3) compared with 8.3 mM glucose alone. This effect was abolished in the presence of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione. Furthermore, 6-cyano-7-nitroquinoxaline-2,3-dione alone inhibited glucose-stimulated insulin secretion in isolated islets by 15.9 +/- 5.9% (n = 3). Taken together these data suggest that a high affinity glutamate transport system exists in pancreatic islets and that this system contributes to a glutamatergic signaling pathway that can modulate glucose-inducible insulin secretion.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1996

Selective excitatory amino acid uptake in glutamatergic nerve terminals and in glia in the rat striatum: quantitative electron microscopic immunocytochemistry of exogenous (D)-aspartate and endogenous glutamate and GABA.

To characterize glutamate/aspartate uptake activity in various cellular and subcellular elements in the striatum, rat striatal slices were exposed to 10 and 50 mu M exogenous (D)-aspartate. After fixation with glutaraldehyde/formaldehyde the distribution of (D)-aspartate was analysed by postembedding immunocytochemistry and the ultrastructural distribution was compared with the distributions of endogenous glutamate and GABA. Light microscopically, (D)-aspartate-like immunoreactivity was localized in conspicuous dots along very weakly labelled dendritic profiles and neuron cell bodies. At the electron microscope level gold particles signalling (D)-aspartate occurred at highest density in nerve terminals making asymmetrical contacts with postsynaptic spines (i.e. resembling synapses of cortical afferents). Astrocytic processes also contained gold particles, but at a lower density than nerve endings. In contrast, dendritic spines were only weakly (D)-aspartate-positive. The difference in labelling at 10 and 50 mu M (D)-aspartate was consistent with 'high-affinity' uptake. Neighbouring sections processed with other antibodies showed that the D-aspartate labelling. Occurred in nerve terminals strongly immunoreactive for glutamate, rather than in terminals very weakly glutamate-immunopositive or in nerve endings immunoreactive for GABA. Glutamate labelling of perfusion-fixed striatum confirmed that terminals forming asymmetrical synaptic contacts with spines were enriched with gold particles, suggesting that these terminals use glutamate as a transmitter. This study demonstrates that high-affinity uptake sites for excitatory amino acids in the striatum are most strongly expressed on presumed glutamatergic nerve terminals and on astrocytes.

Animals↗
PubMed1995

Quantification of excitatory amino acid uptake at intact glutamatergic synapses by immunocytochemistry of exogenous D-aspartate.

To study the localization and efficiency of glutamate/aspartate membrane transport in the vicinity of intact glutamatergic synapses, the avascular lamprey spinal cord was incubated with D-aspartate, a metabolically inert transporter substrate. The exogenous D-aspartate was localized by immunocytochemistry after aldehyde fixation. Incubation at 50 or 500 microM D-aspartate for 1 hr caused a prominent D-aspartate labeling of glial processes at glutamatergic synapses, while presynaptic axons and postsynaptic dendrites remained unlabeled. The glial processes surrounding glutamatergic sensory axons with a predominantly tonical firing pattern contained significantly higher levels of D-aspartate than did processes surrounding glutamatergic reticulospinal axons, which fire rarely and in brief bursts. Preparations incubated for 10 hr with 500 microM D-aspartate showed D-aspartate immunolabeling in glia as well as in the two types of glutamatergic axon, but no evidence was obtained for uptake into synaptic vesicles. Nor was such evidence obtained after high-frequency electrical stimulation. The observations suggest that excitatory amino acids delivered diffusely to the extracellular space in the intact CNS are transported almost exclusively into glia. The avid uptake in glial processes, combined with their spatial arrangement around glutamatergic synapses, appears to limit the access of exogenous D-aspartate to the nerve terminal glutamate/aspartate transporter. In physiological conditions, the glial processes are likely to impede the exchange of glutamate between the synaptic cleft and the rest of the extracellular space. The transport was more efficient in glial processes located near tonically active synapses than in ones located near synapses releasing transmitter sporadically. D-Aspartate is not a substrate of vesicular glutamate transport sites at these intact synapses.

Animals↗
PubMed1993

Regulation by the neuropeptide cholecystokinin (CCK-8S) of protein phosphorylation in the neostriatum.

Despite physiological evidence that cholecystokinin (CCK) is an excitatory neurotransmitter in the brain, little is known about its mechanism of action. CCK immunoreactivity in the brain, including projections to the striatum, is primarily attributable to the sulfated octapeptide CCK-8S. We report here that CCK-8S abolishes cAMP-dependent phosphorylation of a dopamine- and cAMP-regulated 32-kDa phosphoprotein (DARPP-32) in striatal neurons. The effect of CCK-8S is prevented by antagonists of CCKB and N-methyl-D-aspartate receptors. Our results support a model in which CCK-8S, originating from CCK or CCK/glutamate corticostriatal neurons, promotes the release of an excitatory neurotransmitter that causes the dephosphorylation and inactivation of DARPP-32, a potent protein phosphatase inhibitor, thereby modulating neuronal excitability.

Animals↗
PubMed1993

Demonstration of glutamate/aspartate uptake activity in nerve endings by use of antibodies recognizing exogenous D-aspartate.

Nerve terminals as well as glial cells are thought to possess high-affinity Na(+)-dependent transport sites for excitatory amino acids. However, recent immunocytochemical results with antibodies against such a transporter isolated from rat brain showed a selective labelling of glial cells [Danbolt et al. (1992) Neuroscience 51, 295-310]. Critical evaluation of the literature indicates that previous evidence for nerve terminal uptake of acidic amino acids might possibly be attributed to glia. To find out whether there is indeed a glutamate transporter in nerve endings, we incubated hippocampal slices with D-aspartate (10 and 50 microM), a metabolically inert substrate for the high-affinity glutamate transport system. After fixation by glutaraldehyde/formaldehyde the slices were processed immunocytochemically with specific polyclonal antibodies raised against D-aspartate coupled to albumin by glutaraldehyde/formaldehyde. The electron-microscopic postembedding immunogold technique demonstrated a large accumulation of gold particles in nerve terminals making asymmetrical synapses, compared to their postsynaptic dendritic spines, as well as in glial cell processes. The labelled terminals include those of the glutamatergic Schaffer collaterals. Axosomatic boutons appeared unlabelled. Comparison with a test conjugate with known concentration of fixed D-aspartate (94 mM) suggests that the concentration attained in the terminals after incubation with 50 microM D-aspartate was in the lower millimolar range. The uptake was totally dependent on Na+, blocked by L-threo-3-hydroxyaspartate, and had a high affinity for D-aspartate (apparent Km about 20 microM). There was no labelling in slices incubated without D-aspartate. Compared to glia, the nerve terminals had a higher D-aspartate density and accounted for a much higher proportion of the total tissue uptake, but this relationship may be different in vivo. At the light-microscopic level the D-aspartate-like immunoreactivity showed a distinct laminar distribution, identical to that shown autoradiographically for D-[3H]aspartate and L-[3H]glutamate uptake sites [Taxt and Storm-Mathisen (1984) Neuroscience 11, 79-100], and corresponding to the terminal fields of the major excitatory fibre systems in the hippocampal formation. The novel approach described here establishes that glutamatergic nerve terminals as well as glia do sustain sodium-dependent high-affinity transport of excitatory amino acids, implying that more than one glutamate transporter must be present in the brain. Immunogold detection of D-aspartate gives a much higher anatomical resolution than electron microscopic autoradiography of D-[3H]aspartate or L-[3H]glutamate uptake, the only method that has been available previously for ultrastructural demonstration of uptake activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

A quantitative electron microscopic immunocytochemical study of the distribution and synaptic handling of glutamate in rat hippocampus.

One of the major problems in glutamate immunocytochemistry has been the difficulty involved in separating immunocytochemical labelling due to metabolic glutamate from the labelling caused by transmitter glutamate. Another problem appears to be the accessibility of antigenic sites in conventional light microscopic preparations. In the present report, we have applied the primary glutamate antiserum onto ultrathin tissue sections, followed by the use of a colloidal gold detection system. The use of this postembedding immunogold procedure allows equal access of antibodies to all cellular compartments exposed at the section surface, allows quantitative assessment of the immunoreactivity, and affords a high resolution compatible with studies at the organelle level. When applied to slice preparations the immunogold procedure can be used to identify releasable pools of glutamate. These methodological advances have greatly increased the usefulness of glutamate immunocytochemistry as a tool to study putative glutamatergic terminals in the CNS.

Animals↗
PubMed1986

Metabolism and transport of amino acids studied by immunocytochemistry.

The immunocytochemical method for demonstrating amino acids makes it possible to study accumulation and depletion of amino acids in individual tissue compartments resulting from experimental manipulations. We have incubated hippocampal slices in oxygenated Krebs solution, containing various additives, under basal conditions and during synaptic release of transmitters evoked by elevated K+ concentrations or by veratrine. Immunoreactivities for glutamate (Glu-LI), aspartate (Asp-LI), glutamine (Gln-LI), gamma-amino-butyrate (GABA-LI) and taurine (Tau-LI) have been demonstrated by specific antibodies after fixation of the slices in glutaraldehyde. Prolonged depolarisation depleted Glu-LI, Asp-LI and Gln-LI from nerve-ending-like structures. GABA-LI was less affected and Tau-LI not affected at all. The depletion of immunoreactivities could be prevented by metabolic precursors of transmitter amino acids, notably glutamine. This effect of glutamine was abolished by inhibiting glutaminase with diazooxonorleucine. Glu-LI, Asp-LI, GABA-LI and Gln-LI accumulated in astroglial cells during conditions of prolonged depolarization-induced release. The accumulation of GABA-LI in glia was strongly increased by inhibition of aminotransferases by aminooxyacetic acid. The described changes in Glu-LI were prevented by low Ca2+/high Mg2+, and promoted when the glial enzyme glutamine synthetase was inhibited by methionine sulfoximine. D-Aspartate, a metabolically inert competitive inhibitor/substrate for high affinity uptake of glutamate, inhibited the accumulation of Glu-LI in glia. The results confirm the biochemically derived theories on metabolic compartmentation in nervous tissue, and add knowledge on the dynamics of the cellular distribution of amino acids. They also indicate the possibilities offered by the present approach for studying metabolism and pharmacology at the cellular level.

Amino Acids↗