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Biomedical subjects

L L Iversen

Publications and source records attributed to L L Iversen.

At least 127 records · Page 7Linked to original sources
PubMed1980

Reduced amounts of immunoreactive somatostatin in the temporal cortex in senile dementia of Alzheimer type.

Post-mortem brain tissue from 15 patients dying with a diagnosis of senile dementia of Alzheimer type (SDAT) was compared with tissue obtained from 16 control patients at routine post-mortem. A significant fall in choline acetyltransferase (ChAT) activity was observed in the cortex, hippocampus and amygdala of the SDAT cases and was maximal in the temporal cortex. The fall in ChAT activity observed in the temporal cortex was accompanied by a significant reduction (47%) in immunoreactive somatostatin.

Aged↗
PubMed1980

A new method for the microdissection of the human hypothalamus, with mapping of cholinergic, GABA and catecholamine systems in twelve nuclei and areas.

A new method was developed for the microdissection of the human hypothalamus, based on a local system of co-ordinates, using the fornix as an internal reference curve. Dopamine, noradrenaline, adrenaline, CAT, GAD and GABA were assayed in twelve microdissected nuclei and areas, in nine human post-mortem cases. This neurochemical study was aimed to demonstrate the validity of the dissection method, and its potential usefulness for the controlled study of groups of abnormal human cases.

Adolescent↗
PubMed1980

The present status of benzodiazepines in psychopharmacology.

The benzodiazepines continue to offer many challenging questions for the pharmacologist. For example, do the various different properties exhibited by benzodiazepines, notably the sedative, anxiolytic and anticonvulsant effects, reflect aspects of a single common mechanism of action, or are these properties dissociable? To what extent to chemically unrelated drugs with similar CNS actions, such as the barbiturates, share a common mechanism of action with the benzodiazepines? The development of biochemical techniques for identifying and characterizing CNS benzodiazepine receptors by radioligand binding in vitro and in vivo has been an important recent advance, although the benzodiazepine receptor remains in many ways an enigma. The hypothesis that the anticonvulsant actions of these drugs may be due to their ability to enhance the actions of GABA at CNS synapses is an attractive one, but many questions remain: Do all CNS benzodiazepine receptors interact with GABA sites, and are all GABA receptors linked to benzodiazepine sites? What is the endogenous ligand for the benzodiazepine receptors? Can the anxiolytic and sedative effects of the benzodiazepines be explained by their interaction with GABA mechanisms, or are other interactions more important? Is there more than one sub-type of benzodiazepine receptor in brain? Although these questions cannot be unequivocally answered, the benzodiazepines currently represent one of the most active and exciting areas for basic psychopharmacological research.

Animals↗
PubMed1979

Separation of human brain angiotensin-converting enzyme from enkephalin-degrading activity.

Angiotensin-converting enzyme and enkephalin-degrading enzyme activities were solubilized and purified from a particulate fraction of human diencephalon. Converting enzyme activity and enkephalin-degrading activity elute in different fractions following ion exchange chromatography on DEAE-cellulose, suggesting that they are different enzymes. Both enzymes were purified further by ion exchange chromatography on hydroxylapatite and by gel filtration on Sephadex G-200. The purified enzymes had markedly different sensitivities to known inhibitors of angiotensin-converting enzyme. The data do not support the hypothesis that angiotensin-converting enzyme and enkephalin degrading-enzyme are identical.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1979

Effect of kainic acid injections and other brain lesions on vasoactive intestinal peptide (VIP)-stimulated formation of cAMP in rat brain.

In rat striatal slices, both intrastriatal kainic acid injection, which destroys striatal neurones, and intranigral injection of 6-hydroxydopamine (6-OHDA), which leads to a degeneration of dopamine nerve terminals in the striatum, reduced vasoactive intestinal peptide (VIP)-induced cAMP accumulation by approximately 60%. Cortical ablation, which leads to degeneration of cortico-striatal fibres, had no effect on striatal VIP-induced cAMP formation. Knife cut lesions transecting the stria terminalis, which destroy afferent fibres to the amygdala, decreased the VIP-induced increase in cAMP in amygdala slices by 40%, while kainic acid injection into the amygdala had no effect. Kainic acid injection into several other brain regions, including hippocampus, cortex and hypothalamus also failed to affect the VIP-elicited increase in cAMP in slices, despite reductions in choline acetyl-transferase, glutamate decarboxylase, cyclic nucleotide phosphodiesterase and basal levels of cAMP. The results of a study of the effects of various VIP fragments on cAMP stimulation in striatal and cortical slices suggests that the entire sequence of VIP is necessary for full activity. The results suggest that VIP may be involved in neuromodulation or neurotransmission in the striatum and/or nigrostriatal pathway and also in the stria terminalis from the bed nucleus to the amygdala.

Amygdala↗