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Biomedical subjects

L L Iversen

Publications and source records attributed to L L Iversen.

At least 163 records · Page 9Linked to original sources
PubMed1978

Effects of GABA, dopamine, and substance P on the release of newly synthesized 3H-5-hydroxytryptamine from rat substantia nigra in vitro.

The effects of GABA, substance P and dopamine on the release of newly synthesized 3H-5-HT were investigated, using slices of rat substantia nigra superfused with L-3H-tryptophan in vitro. GABA (50 micron) had no inhibitory effect on the potassium-evoked-release of 3H-5-HT. Substance P (50 micron) and eledoisin (50 micron) stimulated the spontaneous release of 3H-5-HT. This effect seems to be indirect and is possibly mediated by dopaminergic neurones, since the dopamine antagonist drug alpha-flupenthixol (1 micron) abolished the substance P-evoked release of 5-HT. Furthermore, it was found that substance P (10 micron) stimulated 3H-dopamine release from nigral slices in vitro and the dopaminergic agonist apomorphine (50 micron) also stimulated 3H-5-HT release. Substance P may, therefore, activate nigral dopaminergic neurones which then release dopamine from their dendrites. The release of dopamine may in turn stimulate 5-HT release from terminals of the raphe-nigral pathway.

Animals↗
PubMed1978

In vitro release of [5-methionine]enkephalin and [5-leucine]-enkephalin from the rat globus pallidus.

Endogenous [5-methionine]enkephalin (Metenkephalin) and [5-leucine]enkephalin (Leu-enkephalin) are released from perfused slices of rat globus pallidus by increased K(+) in a Ca(2+)-dependent manner. Tissue perfused for 40 min contained only 26% of the Met-enkephalin and 44% of the Leu-enkephalin found in the freshly dissected tissue. After perfusion, the mean (+/-SEM) ratio (wt/wt) of Met-enkephalin to Leu-enkephalin was 3.4 +/- 0.2 compared with 5.8 +/- 0.2 in the fresh tissue. The degradation of trace amounts of synthetic [(3)H]enkephalins in the perfusing medium during stimulated release seems to reflect the accelerated degradation of enkephalin released from the tissue: 63% of the Met-enkephalin and 23% of the Leu-enkephalin were degraded in a medium containing bacitracin (30 mug/ml). The mean ratio (wt/wt) of the Met-enkephalin to the Leu-enkephalin recovered after release by exposure of slices to 50 mM K(+) was 2.7 +/- 0.3. When perfusates were corrected for degradation, this ratio increased to about 5.5 which is higher than that found in the perfused tissue. The differences in release, tissue loss, and catabolism of the two enkephalins may be reflecting differences in the metabolic systems operating on the pentapeptides, but this interpretation will have to be validated by in vivo release experiments. In any event these observations strongly suggest that both enkephalins can be considered candidate neurotransmitters in the rat globus pallidus.

Animals↗
PubMed1977

Increased brain dopamine and reduced glutamic acid decarboxylase and choline acetyl transferase activity in schizophrenia and related psychoses.

Dopamine, glutamic acid decarboxylase (G.A.D.) and choline acetyltransferase (C.A.T.) were measured in four regions of post-mortem brains. 41 patients with the hospital diagnosis of schizophrenia (psychotic group) were compared with a control grout normal in the putamen. G.A.D. activity was significantly reduced in the psychotic group, by about 50% in the nucleus accumbens, amygdala and hippocampus, and by about 30% in the putamen. C.A.T. activity was significantly lower in nucleus accumbens from the psychotic group, but normal in other brain regions. From an assessment of case notes, "schizophrenia" was distinguished from "schizophrenia-like psychosis". The biochemical findings for these subgroups were essentially similar, although C.A.T. activity in nucleus accumbens and hippocampus from the schizophrenic group was significantly lower than in controls. It is of brain are associated with schizophrenia and schizophrenia-like psychoses, although whether such neurochemical abnormalities are related to the illness or are a consequence of prolonged treatment with neuroleptic drugs remains unclear.

Adult↗
PubMed1977

Huntington's chorea: selective depletion of activity of angiotensin coverting enzyme in the corpus striatum.

The activity of angiotensin converting enzyme, which transforms the relatively inactive decapeptide angiotensin I to the active octapeptide angiotensin II by removal of an L-histidyl-L-leucine residue, has been assayed in numerous region of the calf brain and of the brains of humans with Huntington's chorea and controls. In calf brain there are pronounced regional variations in enzyme activity, with highest activity in the globus pallidus and area postrema. In human brain, enzyme activity is highest in the corpus striatum, with similar levels in the caudate, putamen, and globus pallidus. Converting enzyme activity is reduced by 83 to 92% in the globus pallidus in Huntington's chorea. The caudate and putamen of choreic patients display 62 to 69% reductions in enzyme activity. Converting enzyme activity in two cerebral cortical regions from choreic brains is not significantly different from control.

Animals↗
PubMed1977

Neurochemical findings in Huntington's chorea.

Huntington's chorea is a dominantly inherited disorder that usually leads to involuntary movements in the third or fourth decade. On gross pathological examination of the post-mortem brain there is a marked atrophy of the caudate nucleus and putamen. Histological examination reveals cell loss in most regions of the brain, although the hippocampus is usually remarkably free of any abnormalities. Studies to detect a biochemical defect in patients with chorea have been largely unrewarding. Since chorea appears to be the clinical counterpart of Parkinson's disease a number of investigations on dopamine metabolism have been carried out by measuring dopamine in the post-mortem choreic brain, and HVA, a metabolite of dopamine, in the CSF of patients. Most studies have found the dopamine concentrations to be normal or sometimes decreased and the activity of the biosynthetic enzyme for dopamine, tyrosine hydroxylase, is normal. The discovery that the inhibitory neurotransmitter, GABA, and the biosynthetic enzyme GAD are greatly decreased in the post-mortem choreic brain provides some rational explanation for the uncontrolled movements in this disorder. The other significant abnormality found in many, but not all, choreic post-mortem brains has been a decrease in the biosynthetic enzyme for acetylcholine, choline acetyl transferase. The evidence that GABA receptors are intact in choreic brain provides an added stimulus for the development of useful GABA-mimetic drugs. For the ultimate eradication of this distressing disorder, however, a search must continue for the primary defect in order that this can be detected before the onset of symptoms, or hopefully in amniotic fluid.

Acetylcholine↗