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Biomedical subjects

L L Iversen

Publications and source records attributed to L L Iversen.

At least 145 records · Page 8Linked to original sources
PubMed1979

Increased dopamine concentration in limbic areas of brain from patients dying with schizophrenia.

Dopamine, noradrenaline, glutamate decarboxylase (GAD) and choline acetyl-transferase (CAT) were measured in post-mortem brain samples from more than 50 patients dying with a hospital diagnosis of schizophrenia and an equal number of controls. GAD was measured in 14 different brain regions, and was significantly lower in both control and schizophrenia patients who died following a protracted illness. If GAD values from patients who died suddenly were compared, no significant differences were observed between the control and schizophrenia groups. There was also no differences between the CAT values measured in 13 different brain regions in the two groups. Noradrenaline values were not different in the two groups in most limbic areas or in the caudate nucleus, but were elevated in the schizophrenic group in nucleus accumbens and in anterior perforated substance. These differences were not, however, statistically significant. On the other hand dopamine concentrations in nucleus accumbens and in anterior perforated substance were significantly elevated (by 34 and 95 per cent, respectively) in the schizophrenia group as compared with controls, although dopamine values were not different in caudate nucleus, putamen, septal nuclei or amygdala. The finding of elevated concentrations of dopamine in certain areas of the limbic forebrain in schizophrenia is discussed in relation to current hypotheses of the involvement of dopamine in this illness, and the difficulties of determining whether the observed changes are related to chronic treatment with antischizophrenic drugs.

Brain Chemistry↗
PubMed1979

[3H]-Quinuclidinyl benzilate binding to muscarinic receptors in rat brain: comparison of results from intact brain slices and homogenates.

1. The binding of [3H]-( +/- )-quinuclidinyl benzilate ([3H]-( +/- )-QNB) to muscarinic sites in rat brain slice and homogenate preparations was compared. 2. Evidence is presented in support of the view that only the (-)-enantiomer of QNB binds with high affinity to muscarinic sites. 3. The Kd value for [3H]-(-)-QNB binding in slices was eight times higher than that measured in homogenates. 4. Similarly, the potencies of various muscarinic ligands as inhibitors of [3H]-(-)-QNB binding were consistently lower in slices than in homogenates. 5. It is proposed that the results may reflect differences in the binding properties of muscarinic receptors in intact tissue slice and homogenate preparations.

Animals↗
PubMed1978

Angiotensin-converting enzyme: presence of high activity in choroid plexus of mammalian brain.

The activity of angiotensin-converting enzyme in rat choroid plexus was higher than that of any other organ, being 6--7 times higher than that in lung and more than 50 times higher than in any other region of brain. Rabbit choroid plexus also had high activity of enzyme while that of human choroid plexus was relatively low. The enzyme in rat choroid plexus showed similar biochemical properties to that in other tissues; it was inhibited by the nonapeptide SQ 20,881, by (Sar1-Ala8)-angiotensin II and by EDTA, and required chloride ions for activity. As in other tissues, the choroid plexus enzyme was associated with particulate fractions after differential centrifugation. The corpus striatum and substantia nigra had the highest activities in the various brain regions examined.

Animals↗
PubMed1978

Naloxone as a GABA antagonist: evidence from iontophoretic, receptor binding and convulsant studies.

From the following three lines of evidence, it is proposed that at least part of the convulsant activity of naloxone is a result of GABA receptor blockade. Firstly, iontophoretic naloxone reversibly antagonized GABA-evoked depression of firing rate in 21 of 27 neurons tested in the rat olfactory tubercle-nucleus accumbens region, without blocking inhibition evoked in the same cells by glycine (15 cells) or morphine (6 cells). Secondly, i.p. naloxone in high doses caused convulsions in mice, and potentiated the convulsant activity of bicuculline, but not that of strychnine. Diazepam, which protected mice against convulsions elicited by bicuculline, but not by strychnine, also protected mice against naloxone. Thirdly, naloxone, morphine, levorphanol and its non-analgesic enantiomer dextrorphan displaced 3H-GABA from GABA receptor sites in homogenates of human cerebellum, all with comparable low potencies (IC50 = 250--400 micron). There was no correlation with affinities at the stereospecific receptor sites that mediate opiate-induced analgesia, since the potent opiates etorphine and diprenorphine were relatively inactive (IC50 greater than 3 mM). In addition naloxone displaced 3H-GABA from receptor sites in rate forebrain and cerebellum, with similar low potency.

Action Potentials↗
PubMed1978

Subsensitivity of the rat striatal dopaminergic system after treatment with bromocriptine: effects on [3H]spiperone binding and dopamine-stimulated cyclic AMP formation.

Repeated daily administration of the dopamine (DA) agonist bromocriptine (15 mg/kg; s.cut.) to rats led to a time dependent decrease in the in vitro binding of [3H]spiperone to striatal membranes. Kinetic analysis of [3H]spiperone binding after 2 and 7 days of bromocriptine treatment showed a 25-50% reduction in the total number of binding sites with no changein their affinity for spiperone. There was also a decreased accumulation of cyclic AMP (cAMP) in striatal slices in response to DA after bromocriptine treatment. The DA-sensitive adenylate cyclase in striatal homogenates, however, remained unchanged in bromocriptine treated rats. There was also no change in cyclic nucleotide phosphodiesterase activity in striatal tissue after bromocriptine treatment. Furthermore, incubation of striatal slices in the presence of the phosphodiesterase inhibitor isobutylmethylxanthine did not alter the decreased cAMP response to DA after 2 days of bromocriptine treatment. These results suggest that a decreased number of DA receptor sites may be responsible for the reduced cAMP response to DA in striatal slices after bromocriptine treatment.

3',5'-Cyclic-AMP Phosphodiesterases↗