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Biomedical subjects

F Hefti

Publications and source records attributed to F Hefti.

At least 217 records · Page 12Linked to original sources
PubMed1983

Muscarinic receptors on intact, cultured neurons. Characterization by [3H]quinuclidinylbenzilate binding.

[3H]Quinuclidinylbenzilate (QNB) was used to identify muscarinic cholinergic receptors on intact, cultured neurons from fetal rat brains. Scatchard analysis revealed a single binding site with a dissociation constant Kd = approximately or equal to 170 pM. The rank order of potency of cholinergic drugs to displace [3H]QNB from intact neurons was similar to that observed using isolated membranes of brain homogenates. No difference in the rank order was observed with cultures of neurons from different brain regions which vary in their neuronal composition.

Animals↗
PubMed1983

Chronoamperometry in vivo: does it interfere with spontaneous neuronal activity in the brain?

To test whether chronoamperometry in vivo interferes with spontaneous neuronal activity, chronoamperometric measurements were combined with electrophysiological recordings in the same preparation. Chronoamperometric measurements (0.5--1.0 V applied for 1 s) were taken in the rat corpus striatum and single unit activity was recorded extracellularly in the same area. With potentials of 0.5 V, chronoamperometric measurements did not interfere with spontaneous activity of the striatal neurons, even of those units situated in close proximity (approximately 100 micrometers) to the tip of the electrochemical working electrode. Chronoamperometric measurements at potentials from 0.6 to 1.0 V accelerated or inhibited the firing rates of part of the striatal neurons, even when the electrophysiological circuit was interrupted during the application of the chronoamperometric pulse.

Animals↗
PubMed1982

Effects of oral L-tyrosine administration on CSF tyrosine and homovanillic acid levels in patients with Parkinson's disease.

To determine whether 1-tyrosine administration can enhance dopamine synthesis in humans as it does in rats, we measured levels of tyrosine and the major dopamine metabolite, homovanillic acid, in lumbar spinal fluids of 23 patients with Parkinson's disease before and during ingestion of 100 mg/kg/day of tyrosine. Nine patients took 100 mg/kg/day of probenecid in six divided doses for 24 hours prior to each spinal tap; 14 patients did not receive probenecid. L-tyrosine administration significantly increased CSF tyrosine levels in both groups of patients (p less than .01) and significantly increased homovanillic acid levels in the group of patients pretreated with probenecid (p less than .02). These data indicate that l-tyrosine administration can increase dopamine turnover in patients with disorders in which physicians wish to enhance dopaminergic neurotransmission.

Administration, Oral↗
PubMed1982

Replacement of the anterior cruciate ligament. a comparative study of four different methods of reconstruction.

Eighty-seven patients have been examined 2 years on average after knee ligament reconstruction for a torn anterior cruciate ligament. The patients were divided into four groups according to the type of operation that had been carried out. In the first group an extra-articular lateral repair ("MacIntosh tenodesis") had been performed, in the second group an intra-articular "over-the-top" repair using the quadriceps and the patellar tendon, in the third group a modified "Eriksson" procedure using the patellar tendon, and in the fourth group a combined intra- and extra-articular repair using carbon fibres as a graft. The results of the operations in the different groups are compared. The best results were obtained with the "Eriksson" procedure, closely followed by the "over-the-top" repair. Limited range of motion and retropatellar pain resulting from changes in the alignment of the patella were the main problems. The results after the use of carbon fibres were less good. In two cases the graft tore without further trauma, and there were also problems because of restricted range of motion and retropatellar pain. The worst results were found after extra-articular lateral repair, due to insufficient stability in many cases. However, the best results with regard to the range of motion were found in this group.

Follow-Up Studies↗
PubMed1982

Stimulation of nigrostriatal dopamine neurones by nicotine.

In rats anaesthetized with urethane, firing of neurones of the substantia nigra zona compacta was accelerated after subcutaneous or iontophoretic administration of nicotine or after iontophoretic application of acetylcholine. The excitation was prevented by iontophoretic application of dihydro-beta-erythroidine, but not by atropine. The units were identified by antidromic stimulation as neurones of the nigrostriatal system; their activity was depressed by iontophoretically applied dopamine (DA). Under the same conditions of anaesthesia, a subcutaneous injection of nicotine produced an increase in DA turnover and in homovanillic acid levels in the striatum. The effect of nicotine on striatal DA turnover was comparable to that of electrical stimulation of the nigrostriatal pathway at the average frequency seen in the firing of zona compacta neurones after systemic administration of nicotine. These observations corroborate the idea that nicotine exerts an excitatory action at the level of nigral DA nerve cells. Observations made after electrical stimulation or haloperidol under urethane anaesthesia and after nicotine in unanaesthetized rats suggest that the relatively modest effect of nicotine on striatal DA turnover is due mainly to the short duration of drug action rather than to effects of the anaesthetic on DA metabolism.

Animals↗
PubMed1982

Huntington chorea is not associated with hyperactivity of nigrostriatal dopaminergic neurons: studies in postmortem tissues and in rats with kainic acid lesions.

We estimated dopamine release postmortem in the neostriatum of patients with Huntington disease (HD) and in controls. In HD, dopamine levels were unchanged in caudate and elevated in putamen, but homovanillic acid (HVA) and the ratio HVA:dopamine were unaltered in both nuclei. When rats were injected with kainic acid (an experimental model of HD), dopamine levels in striatum remained unchanged 2 to 30 days postoperatively; HVA and 3,4-dihydroxyphenylacetic acid (DOPAC) increased significantly from 2 to 18 days after injections but returned to normal levels later. These findings suggest that the nigrostriatal projection adapts to loss of striatal neurons that normally influence dopamine release and is not hyperactive in HD chorea.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1982

Compensatory mechanisms in the nigrostriatal dopaminergic system in Parkinson's disease: studies in an animal model.

Partial unilateral nigrostriatal lesions of varying severity (from mild to near-total) were produced in rats by intranigral injections of increasing doses of 6-hydroxydopamine. Severity of the lesions was estimated by measurement of striatal tyrosine hydroxylase activity. In such rats, surviving nigrostriatal neurons accelerated their rates of dopamine (DA) synthesis and release (estimated by the ratio of homovanillic acid to tyrosine hydroxylase) only when 60% of more of DA neurons had been destroyed. Striatal DA receptor supersensitivity (estimated by emergence of contraversive rotational behavior induced by apomorphine and L-dopa) developed only when 90% or more of striatal DA nerve terminals had been destroyed. Acceleration of DA turnover by surviving nigrostriatal neurons and the development of striatal DA receptor supersensitivity may represent two compensatory mechanisms through which the nigra adapts to its own destruction and may explain, in part, why clinical signs of parkinsonism emerge only after massive degeneration of DA neurons.

Animals↗
PubMed1981

Dopamine release in rat striatum after administration of L-dope as studied with in vivo electrochemistry.

The time-course of changes in dopamine (DA) release induced by systemic administration of L-DOPA was studied in the rat striatum using electrochemistry in vivo. Recordings were obtained from anesthetized animals in which carbon past microelectrodes were implanted stereotaxically into the striatum. Chronoamperometric measurements were made by applying 0.8 V for 1 sec, with an interval of 5 min between measurements; in some experiments, the potential was scanned every 5 min from 0 to 1.0 V. Administration of L-DOPA (50 mg/kg) after pretreatment with an inhibitor of peripheral aromatic amino acid decarboxylase (AAAD) produced a large rise in chronoamperometric currents, lasting for about 6 h. Different approaches were used to determined whether DOPA, DA or DA metabolites (all of which are oxidized at the potential chosen) were responsible for these DOPA-induced increases. (1) Rats were killed at different times after L-DOPA administration, and their striatal were analyzed biochemically for DOPA, DA, and DA metabolites. Comparison of time-courses indicated that the rise in chronoamperometric responses correlated with elevations in striatal 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) levels rather than with those of DOPA or DA, suggesting that DA metabolites contribute significantly to the increases in chronoamperometric responses observed after administration of L-DOPA. (2) Administration of L-DOPA after pretreatment with an inhibitor of central AAAD, a treatment that results in large increases in striatal DOPA levels but abolishes L-DO DA, suggesting that DA metabolites contribute significantly to the increases in chronoamperometric responses observed after administration of L-DOPA. (2) Administration of L-DOPA after pretreatment with an inhibitor of central AAAD, a treatment that results in large increases in striatal DOPA levels but abolishes L-DO DA, suggesting that DA metabolites contribute significantly to the increases in chronoamperometric responses observed after administration of L-DOPA. (2) Administration of L-DOPA after pretreatment with an inhibitor of central AAAD, a treatment that results in large increases in striatal DOPA levels but abolishes L-DOPA-induced formation of DA and DA metabolites (measured biochemically), failed to increase chronoamperometric responses. This finding indicates that exogenous L-DOPA entering the striatum is not detected with this technique and that it must be decarboxylated to produce the elevations of currents. (3) In animals pretreated with an inhibitor of monoamine oxidase to abolish formation of DOPAC and HVA, L-DOPA administration produced only a small and short lasting increase in chronomaperometric responses, despite sustained and large increases in striatal DA concentrations. By using the potential-scanning technique we showed that these increase in electrochemical responses occur at a potential at which DA but not methylated catechols are oxidized...

4-Butyrolactone↗