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Biomedical subjects

L Bergström

Publications and source records attributed to L Bergström.

At least 55 records · Page 3Linked to original sources
PubMed1995

Leaching of dichlorprop and nitrate in structured soil.

Leaching rates of the herbicide dichlorprop [(+/--2-(2,4-dichlorophenoxy)propanoic acid] and nitrate were measured together in field lysimeters containing undisturbed clay and peat soils. The purpose of the study was to investigate the leaching pattern of the two solutes in structured soils under different precipitation regimes. Spring barley (Hordeum distichum L.) was sown on each monolith and fertilized with 100 kg N ha(-1). Dichlorprop was applied at a rate of 1.6 kg active ingredient (a.i.) ha(-1). Each soil type received supplemental irrigation at two levels ('average' and 'worst-case'), giving total water inputs (irrigation and precipitation) of 664 and 749 mm year(-1), respectively. The larger water input approximately doubled the nitrate loads, from, on average, 11.6 to 21.8 kg N ha(-1) year(-1) in the clay soil and from 37.6 to 65.4 kg N ha(-1) year(-1) in the peat soil. In contrast, dichlorprop leaching was reduced by more than one order of magnitude when the water input was increased, from average amounts of 3.22 to 0.26 g a.i. ha(-1) during an S-month period in the clay and from 28.9 to 2.67 g a.i. ha(-1) in the peat. This leaching pattern of dichlorprop was explained in terms of preferential flow. The dried-out topsoil of 'average' watered monoliths may have allowed water flow in cracks, thus moving some of the herbicide rapidly through the topsoil to the subsoil. Once the compound reached the subsoil, degradation rates would be reduced and the herbicide residues would be stored for later leaching. Nitrate was presumably more evenly distributed in the soil matrix; therefore, water rapidly moving through macropores would not carry significant amounts of nitrate. In contrast, leaching would occur more evenly through the soil matrix, causing larger nitrate loads in the 'worst-case' watered monoliths. These results show that wet years may constitute a worst case scenario in terms of nitrate leaching, but not pesticide leaching, if macropore flow exerts a significant influence on leaching.

Journal Article↗
PubMed1993

Decrease of somatostatin receptor binding in the rat cerebral cortex after ibotenic acid lesion of the nucleus basalis magnocellularis: a quantitative autoradiographic study.

The specific binding of 125I-Tyr11-somatostatin-14 (125I-Tyr11-SS-14) was measured in different cortical regions after unilateral ibotenic acid lesion of the rat nucleus basalis magnocellularis (NBM). A marked loss of acetylcholinesterase-positive fibers was observed in the frontal, parietal, temporal and occipital cortices ipsilateral to the lesion. The loss of cholinergic cell bodies in the NBM was further investigated with choline-acetyltransferase (ChAT) immunohistochemistry which indeed demonstrated a loss of ChAT-positive magnocellular perikarya. Autoradiographic analyses of specific binding of 125I-Tyr11-SS-14 demonstrated a significant reduction in binding density in the denervated parts of the neocortex. The decrease in specific binding was most pronounced (40-50%) in the superficial layers (I-III) of the frontal, parietal and temporal cortices 2 and 4 weeks after lesion. A significant loss in 125I-Tyr11-SS-14 binding in the deeper layers was only observed in the frontal cortex after 2 and 4 weeks. In the occipital cortex a significant decrease was measured in the superficial layers only after 4 weeks. The specific binding in all cortical regions returned to normal after 6 weeks. The results suggested that 125I-Tyr11-SS-14 binding sites are localized on cholinergic afferents in the rat neocortex and that an up-regulation of number of binding sites, alternatively an increased binding affinity occurred with time after lesion.

Animals↗
PubMed1993

Environmental influence on somatostatin levels and gene expression in the rat brain.

In the present study we have quantified preprosomatostatin-mRNA and somatostatin levels in rat brain following environmental stimulation. Animals were housed for 30 days in an enriched or impoverished environment prior to analysis. After 30 days of housing half of the rats from each environment were behaviourally tested for 3 days. Housing in enriched environment improved performance in a spatial learning situation. The open-field behaviour of these animals was characterized by initially higher rearing scores and a more rapid habituation to novel environment as measured by spontaneous locomotor activity. We found significantly elevated somatostatin levels in the cortex following enriched environment, compared with impoverished environment. Exposure to behavioural testing of impoverished animals led to increased cortical somatostatin levels. Hypothalamic somatostatin levels increased significantly after housing in enriched environment, while the testing procedure had no influence. Our data shows that the somatostatin system in the rat brain was activated in association with cognitive changes, that were induced by housing in an enriched environment.

Animals↗
PubMed1993

Effects of nucleus basalis lesion on muscarinic receptor subtypes.

The cholinergic system in the central nervous system is an important component of the neural circuitry of learning, memory and cognition. A decline of cholinergic innervation in the human brain is a characteristic feature of dementia of Alzheimer's type. In this study, changes in cholinergic markers were studied after a unilateral lesion of the nucleus basalis magnocellularis (nbM). Acetylcholinesterase (AChE) histochemistry showed a loss of cortical AChE-containing neurons, and choline acetyltransferase (ChAT) immunohistochemistry demonstrated a loss of cholinergic cells in nbM. The localizations of muscarinic M1 and M2 receptors using [3H]pirenzepine ([3H]PZ) and [3H]AF-DX 384, respectively, were studied by quantitative autoradiography 1, 2, 4 and 6 weeks following unilateral ibotenic acid lesion of nbM. A significant decrease in [3H]PZ binding sites was observed at postlesion week 1 in the parietal and temporal cortices. The decrease in [3H]AF-DX 384 binding sites on the lesioned side was observed throughout frontal, parietal and temporal cortices after postlesion week 1, with a significant increase after 6 weeks, possibly as result of loss of presynaptic receptors and upregulation of postsynaptic ones. Moreover, laminar distribution after nbM lesion shows that M1 and M2 receptor binding sites are more affected in superficial layers (I,II,III) than in the deep layers (IV,V,VI), depending on ligand, postlesion period and cortical region. Furthermore, nbM lesion causes a higher deficit of M2 receptors than of M1 receptors. These data suggest the existence of a presynaptic population as well as a postsynaptic population of M1 and M2 receptors which are differently affected after unilateral nbM lesion.

Acetylcholinesterase↗
PubMed1991

Regional distribution of somatostatin receptor binding and modulation of adenylyl cyclase activity in Alzheimer's disease brain.

We have previously reported a reduction in the inhibitory effect of somatostatin on adenylyl cyclase activity in the superior temporal cortex of a group of Alzheimer's disease cases, compared to a group of matched controls. In the present study, the levels of high affinity 125I-Tyr11-somatostatin-14 binding, its modulation by guanine nucleotides and the effects of somatostatin on adenylyl cyclase activity have been measured in preparations of frontal cortex, hippocampus, caudate nucleus and cerebellum from the same patient and control groups. A significant reduction in 125I-Tyr11-somatostatin-14 binding was observed in the frontal cortex, but not other regions, of the Alzheimer's disease group, compared with control values. The profiles of inhibition of specific 125I-Tyr11-somatostatin-14 binding by Gpp(NH)p were similar in all regions in both groups. No significant differences in basal, forskolin-stimulated, or somatostatin and neuropeptide Y inhibitions of adenylyl cyclase activity were found between the two groups. The pattern of change of somatostatin binding in the Alzheimer's disease cases observed in the present study differs from the reported pattern of loss of somatostatin neurons and may be secondary to the degeneration of somatostatin receptor-bearing cholinergic afferents arising from the nucleus basalis. The results of this study indicate that impaired somatostatin modulation of adenylyl cyclase is not a global phenomenon in Alzheimer's disease brain and also that there are no major disruptions of somatostatin receptor-G-protein coupling or of adenylyl cyclase catalytic activity in this disorder.

Adenylyl Cyclases↗