Biomedical subjects
F Boon
Publications and source records attributed to F Boon.
Involvement of multiple opiate receptors in opioid kindling.
D-Tyr-Ser-Gly-Phe-Leu-Thr (DSLET), beta-endorphin, morphiceptin and morphine were microinjected at 48-h intervals into the amygdala or hippocampus of awake rats in an attempt to identify the opiate receptor types involved in opioid kindling. DSLET, beta-endorphin, morphiceptin and morphine were injected into the lateral ventricle to assess the possibility of kindling seizures by this route. The delta-receptor agonist DSLET effectively kindled convulsions when microinjected into amygdala or ventral hippocampus. The convulsions were suppressed or strongly attenuated by ICI 174,864, a specific antagonist of the delta-receptor, microinjected into the same brain site, but were not affected by ICI 174,864 administered peripherally. When microinjected into amygdala or hippocampus, beta-endorphin and morphiceptin also kindled convulsions, which were antagonized by naloxone but not by ICI 174,864. Morphine evoked EEG epileptiform activity but did not kindle convulsions from limbic brain sites. DSLET occasionally evoked epileptiform spiking and submaximal convulsions when injected into ventricle, and morphiceptin evoked epileptiform spiking only, but tolerance to these effects occurred after repetition of the injections. Thus, convulsions can be kindled by activation of either mu-, delta- or epsilon-receptors when opioids are injected directly into limbic tissue. However, the ability of these compounds to kindle seizures is markedly reduced when they are administered into ventricle. The striking differences between the present results and previous results obtained by peripheral or intraventricular administration of opioid peptides suggest that the route of administration, among other variables, is a crucial factor in assessing the epileptogenic properties of opioid peptides.
Failure of aspartame to affect seizure susceptibility in kindled rats.
The effect of aspartame administered by gavage to rats on amygdala and hippocampal kindled seizures was assessed. Despite the administration of a wide range of doses (25-2000 mg/kg) no evidence for an effect of aspartame on afterdischarge threshold or seizure strength was obtained when testing was done at a time when serum and brain levels of neutral amino acids are known to be significantly elevated as a result of this treatment. There is controversy whether dietary aspartame (N-L-aspartyl-L-phenylalanine 1-methyl ester), a food additive sweetner, can lead to seizures in susceptible humans and in laboratory animals. A proseizure effect of high consumption of aspartame has been alleged (Wurtman, 1985; Walton, 1986) and denied (Gaull, 1985). Recent studies using mice have yielded mixed results. Thus, Kim and Kim (1986) and Pinto and Maher (1988) observed potentiating effects of high loads of aspartame on chemically induced seizures, but Nevins, Arnolde and Haigler (1986) observed no effect on chemical and ECS seizures. We used the electrical kindling model of epilepsy to assess whether aspartame can alter seizure threshold or strength in rats. The kindled response is highly repeatable and stable and has been shown to be sensitive to a large variety of pharmacological treatments (Racine, 1978) and to dietary manipulation (McCann, Cain and Philbrick, 1983).
Paroxetine for self-injurious behavior.
Explore the source record for details and available documents.