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Biomedical subjects

F Fonnum

Publications and source records attributed to F Fonnum.

At least 181 records · Page 10Linked to original sources

The effect of parenteral glutamate treatment on the localization of neurotransmitters in the mediobasal hypothalamus.

The localization of cholinergic, aminergic and amino acid-ergic neurones in the mediobasal hypothalamus has been studied in normal rat brain and in brains where neurones in nucleus arcuatus were destroyed by repeated administration of 2 mg/g body weight monosodium glutamate to newborn animals. In normal animals acetylcholinesterase staining, choline acetyltransferase and aromatic L-amino acid decarboxylase were concentrated in the median eminence and the arcuate nucleus. Glutamate decarboxylase was concentrated at the boundary between the ventromedial and the arcuate nuclei, with lower activity in the arcuate nucleus and very low activity in the median eminence. Nucleus arcuatus contained an intermediate level of high affinity glutamate uptake. In the lesioned animals, there were significant decreases in choline acetyltransferase, acetylcholinesterase staining and glutamate decarboxylase in the median eminence, whereas choline acetyltransferase activity and acetylcholinesterase staining, but not glutamate decarboxylase activity, were decreased in nucleus arcuatus. Aromatic L-amino acid decarboxylase was unchanged in all regions studied. The high affinity uptakes of glutamate, dopamine and noradrenaline, and the endogenous amino acid levels were also unchanged in the treated animals. The results indicate the existence of acetylcholine- and GABA-containing elements in the tuberoinfundibular tract. They further indicate that the dopamine cells in the arcuate nucleus are less sensitive to the toxic effect of glutamate than other cell types, possibly because they contain less glutamate receptors.

Acetylcholinesterase↗

Evidence for glutamate as a neurotransmitter in the corticofugal fibres to the dorsal lateral geniculate body and the superior colliculus in rats.

The high-affinity uptake of L-glutamate, D-aspartate and GABA were examined in homogenates from the dorsal lateral geniculate body and the superior colliculus after removal of the right visual cortex of adult rats. The high-affinity uptake of D-aspartate and L-glutamate were reduced by 53 to 75% respectively in the dorsal lateral geniculate body and by 46 and 53% respectively in the superior colliculus ipsilateral to the lesion. The uptake on the contralateral side was unaffected. The reductions were detected 3 days after the lesion and were maximally developed after 7 days. Subcellular fractionation showed that the main part of the uptake was confined to the synaptosomal fraction of both regions and that the reductions were most prominent in this fraction. The lesion was not accompanied by significant changes in high-affinity uptake of GABA nor in changes of choline acetyltransferase and glutamate decarboxylase activities. The high-affinity L-glutamate uptake on the contralateral visual cortex was unchanged from control values. After ablation of the visual cortex the level of L-glutamate was reduced by 32 and 17% in the ipsilateral dorsal lateral geniculate body and superior colliculus, respectively. The levels of the other amino acids examined, including L-aspartate, were unchanged. Enucleation had no effect on the uptake of L-glutamate and of GABA in the dorsal lateral geniculate body or in the superior colliculus.

Animals↗

The inhibition of choline acetyltransferase in guinea-pig cornea.

The effects of different compounds on the inhibition of choline acetyltransferase in guinea pig cornea have been studied. N-hydroxyethyl-4(naphthylvinyl)pyridinium bromide inhibited the enzyme in the cornea when a 0.5% solution was applied topically to the eye. The inhibition could not be explained by redistribution of the inhibitor after homogenization of the tissue. Inhibition of the enzyme was slowly reversed and nearly full enzyme activity was obtained when the eye was left intact for 48 hrs. N-methyl-4(naphthylvinyl)pyridinium bromide was a less efficient inhibitor in vivo and no inhibition was found with bromo acetonyl trimethylammonium bromide or acryloylcholine. Corneal ChAT was inhibited by the application of 3-methyl-5-methoxyphenyl pyridinium bromide, but the mechanism was obscured by the compound causing corneal oedema. The investigation shows that epithelium of the cornea can be used to test the in vivo effect of choline acetyltransferase inhibitors.

Acetone↗