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Biomedical subjects

J Luthman

Publications and source records attributed to J Luthman.

At least 91 records · Page 5Linked to original sources
PubMed1988

Immunohistochemical study of neuronal markers in human gingiva with phenytoin-induced overgrowth.

The immunohistochemical occurrence of several different neuronal markers has been investigated in human gingiva with phenytoin-induced overgrowth. The material was compared to gingival material taken following surgical orthodontic treatment. Gingiva obtained from the phenytoin-treated groups seemed to have a reduced number of neurofilament (NF) immunoreactive nerve fibers in the propria compared to control material. In both phenytoin as well as control gingiva sparsely distributed, thin, calcitonin gene-related peptide (CGRP) and substance P (SP) immunoreactive fibers were found in the propria. No obvious differences between the two groups could be observed for CGRP and SP. Immunoreactive cells for somatostatin (SOM) with a dendritic cell shape were found in the propria in both groups, sometimes in densely packed clusters. A tendency for increase of SOM-immunoreactive cells in the phenytoin-treated gingiva was observed. A few gamma-melanocyte stimulating hormone (gamma-MSH)-immunoreactive cells with a round appearance were found in control as well as phenytoin-affected gingiva. In one instance, however, a heavy gamma-MSH-immunoreactive cell infiltration was seen in the phenytoin sample. No immunoreactivity in either the phenytoin-treated group or in the control group was seen for proctolin or galanin. The results indicated that gingiva with phenytoin-induced overgrowth has a reduced innervation density revealed with NF immunohistochemistry.

Adolescent↗
PubMed1988

Gingival and mucosal reactions after intensive chlorhexidine gel treatment with or without oral hygiene measures.

The aim of this study was to elucidate whether soft tissue reactions during chlorhexidine (CHX) treatment might be associated with meticulous oral hygiene measures. A commercially available 1% chlorhexidine digluconate gel (Hibitane Dental Gel) was applied in a custom tray for the mandibular arch, 10 min daily, for 14 days. A split mouth approach was used to allow evaluation of the effect of oral hygiene measures with toothbrush, toothpaste, and dental floss on one side of the arch. During the treatment period, 8 out of 12 subjects developed gingival and/or mucosal reactions appearing as white patches or ulcerations. Both the gingival reactions on the buccal marginal gingiva and the mucosal reactions near the margin of the custom tray occurred only when the gel treatment was combined with meticulous oral hygiene measures. The white patches, which could easily be detached, leaving ulcerated areas, consisted entirely of stratified squamous epithelium. The findings suggest that intensive treatment with chlorhexidine gel, in individually fitted custom trays, combined with meticulous oral hygiene measures may induce toxic effects on the surface layers of the gingiva and mucosa.

Chlorhexidine↗
PubMed1988

Prenatal methylazoxymethanol treatment potentiates d-amphetamine- and methylphenidate-induced motor activity in male and female rats.

The effects of the stimulant drugs, d-amphetamine and methylphenidate, upon the motor activity of male and female off-spring of pregnant rats, treated on gestation day 15 with the antimitotic agent methylazoxymethanol (MAM, 25 mg/kg) were studied in four experiments. Cortical and striatal hypoplasia induced by prenatal administration of MAM resulted in increased concentrations of catecholamines in those regions. Administration of d-amphetamine and methylphenidate caused significant increases in motor activity; this effect was markedly potentiated in the MAM-treated rats, both the male and female off-spring. Thus, the locomotion and total activity parameters showed similar, but not identical, drastic increases in behaviour induced by the stimulant drugs as a result of the prenatal MAM treatment whereas for the rearing parameter a lesser potentiation by the MAM treatment was observed. This potentiation of the excitatory effects of the stimulant compounds upon the behavioural parameters is interpreted in terms of a relative increase in the density of catecholaminergic terminals in the forebrain regions of the central nervous system. The present results are discussed with regard to the utility of prenatal MAM treatment as a possible animal model for certain neurological disorders.

Animals↗
PubMed1987

Determination of monoamines by use of liquid chromatography with electrochemical detection in the study of selective monoamine neurotoxins.

Determination of regional monoamine levels in the CNS in the study of the effects of selective monoaminergic neurotoxins is a reliable method with which to study the morphological changes in denervated as well as re- or hyperinnervated regions as evidenced by comparisons with several other methods. In the acute stage, the changes in monoamine levels reflect both the beginning of the degeneration and the acute pharmacological effects exerted by several monoaminergic neurotoxins. The only exception to this seems to be the MPTP-induced chronic decrease of DA in the nucleus accumbens and the tuberculum olfactorium where no morphologic changes have been found so far.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1987

Sprouting of striatal serotonin nerve terminals following selective lesions of nigro-striatal dopamine neurons in neonatal rat.

The effects of neonatal intracisternal 6-hydroxydopamine (6-OHDA; 50 micrograms) treatment on striatal serotonin (5-HT) nerve terminals in rat have been characterized using histo- and neurochemical methods. The 6-OHDA lesion caused a 60% reduction of striatal dopamine (DA) concentration when analyzed in the adult stage, while 5-HT levels were increased by about 40% and 3H-5-HT uptake in vitro was increased by about 60%. Using computerized image analysis, a marked increase in 5-HT-like immunoreactive terminal density was found in both rostral (+200%) and caudal (+50%) striatum. Pretreatment with the DA uptake blocker amfolenic acid completely counteracted the 6-OHDA-induced alterations in both DA and 5-HT neurons in the striatum, while pretreatment with the noradrenaline uptake blocker desipramine had no significant effects. Regional analysis of 5-HT levels in the CNS after neonatal 6-OHDA treatment or the combined desipramine + 6-OHDA treatment showed no significant effect in any of the brain areas analyzed, apart from the observed 5-HT increase in striatum. It was furthermore observed that the striatal 5-hydroxyindoleacetic acid (5-HIAA)/5-HT ratio was decreased, while the 3,4-dihydroxyphenylacetic acid (DOPAC)/DA ratio was increased following the 6-OHDA lesion, indicating compensatory mechanisms in turnover of transmitters. These alterations were completely reversed after pretreatment with amfolenic acid. The present results support the view that the 5-HT hyperinnervation following neonatal 6-OHDA treatment is a collateral sprouting response induced by lesioning of the striatal DA neurons.

Animals↗
PubMed1986

Penetration of oxytetracycline into tissue-cages in calves.

Concentrations of oxytetracycline (OTC) in serum and tissue-cage fluid (TCF) from subcutaneous tissue-cages were determined after single and repeated intravenous and intramuscular doses of 10 mg/kg to calves. Intravenous administration resulted in higher levels, and greater area under curve (AUC) in TCF, than did intramuscular administration. However, the penetration measured as the ratio of AUC in TCF to AUC in serum was equal, and therefore independent of the route of administration. A linear relationship between AUC in serum and AUC in TCF could be demonstrated. Half-lives of OTC in serum were 4.9 +/- 3.1 h after intravenous, and 6.1 +/- 2.0 h after intramuscular administration. In TCF the half-lives were 21.5 +/- 4.4 h and 24.5 +/- 11.5 h after intravenous and intramuscular administration, respectively. Repeated dosing resulted in accumulation of OTC in TCF. Lesser accumulation in older cages indicated altered characteristics of the cages with the passage of time. In serum, no substantial accumulation was seen after repeated i.v. dosing until the dosing interval was shortened to 6 h.

Animals↗
PubMed1986

Effects of 1% chlorhexidine gel treatment on sympathetic adrenergic nerves in human buccal mucosa.

The effect of treatment with a commercially available 1% chlorhexidine gel (Hibitane Dental) in custom trays for 14 days (10 min daily) on the sympathetic adrenergic nerves in biopsies from human buccal mucosa was investigated. Chemical assay of endogenous noradrenaline concentration and immunocytochemical demonstration of tyrosine hydroxylase served as markers for structural and functional integrity of the adrenergic nerves. The mean concentration of noradrenaline in chlorhexidine treated tissues did not differ from the mean concentration in control. No morphologic or fluorescence intensity differences of the tyrosine hydroxylase immunoreactivity were found in the chlorhexidine treated tissues when compared to controls. These findings indicate that a relatively intense treatment with a commercially available 1% chlorhexidine gel does not affect the adrenergic innervation of human buccal mucosa.

Adrenergic Fibers↗
PubMed1986

Quantitation of noradrenaline nerve density in mouse iris by computer-assisted image analysis.

The density of noradrenaline (NA)-containing nerve fibres in mouse iris was measured with computer-assisted image analysis techniques both under normal conditions and during regeneration. Noradrenaline nerves were visualized by Falck-Hillarp formaldehyde condensation technique in whole-mount spread preparations of mouse irides. The samples were analysed in a fluorescence microscope connected to a commercially available image analysis system (IBAS/Kontron). A software program was developed for specific detection of fluorescence and the nerve density was determined by calculating the area covered by fluorescence in percentage of total measuring field. The method showed good reproducibility as observed both when repeated measurements were performed in the same measuring field or when consecutive measurements on the same set of irides were performed. Also the inter-assay variation between control values in the different experiments was low. Loading of the adrenergic nerves by incubation in alpha-methyl-NA or conditions leading to partial diffusion of the fluorophore had minor effects on the nerve density values. The regeneration of the NA nerve fibres after a selective toxic sympathectomy with 6-hydroxydopamine was also studied. The nerve fibre density values measured by image analysis correlated well with the uptake of [3H]NA; the endogenous NA levels recovered much more slowly, however. It thus seems that endogenous transmitter levels might be a somewhat insensitive index of nerve terminal regrowth, at least in early stages of regeneration. The results indicate that image analysis is a powerful tool to quantitate a transmitter-identified nerve terminal network in a histological preparation.

Adrenergic Fibers↗
PubMed1986

Effect of MPTP and its pyridinium metabolites on monoamine uptake and on central catecholamine neurons in mice.

The effect of MPTP and its pyridinium metabolites MPDP+ and MPP+ on the in vitro [3H]monoamine uptake in synaptosomal preparations from mouse striatum and cerebral cortex was investigated. All compounds inhibited [3H]monoamine uptake in a dose-dependent manner in both regions analysed. MPP+ had the highest affinity to dopamine and noradrenaline uptake sites, while MPTP had the highest affinity to serotonin uptake sites. The results indicate that the affinity of MPP+ to different monoamine uptake sites appears to be better correlated to MPTP neurotoxicity as expressed in vivo than MPTP and MPDP+. Intracerebral injection of MPP+ into substantia nigra produced an almost complete disappearance of dopamine in striatum and noradrenaline in cerebral cortex, while injection of MPTP or MPDP+ had no or only moderate catecholamine-depleting effects. The MPP+-induced catecholamine depletion could be partially reversed by pretreatment with the catecholamine uptake blocker nomifensine. Histological analysis disclosed that MPP+ was a potent generally cytotoxic agent, while MPDP+ less and MPTP least so. The present results are compatible with the view that an interaction with the catecholamine uptake mechanism, probably through an uptake and accumulation of extraneuronally formed MPP+, is most likely the explanation for neuron-specific neurotoxic action on catecholamine neurons following MPTP administration.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1986

Effects of the parkinsonism-inducing neurotoxin MPTP and its metabolite MPP+ on sympathetic adrenergic nerves in mouse iris and atrium.

The effect of systemic administration of the parkinsonism-inducing neurotoxin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and its metabolite MPP+ (1-methyl-4-phenylpyridine) on sympathetic adrenergic nerves in mouse iris and atrium has been investigated employing histo- and neurochemical techniques. The results indicate that MPTP does not have any potent neurotoxic effects on sympathetic adrenergic nerves. The effects of MPTP noted appear mainly to be restricted to a noradrenaline (NA) -depleting action and an acutely transient impairment of the NA uptake mechanism. This latter effect could be counteracted by monoamine oxidase inhibition. MPP+ was found to have more potent neurotoxic actions than MPTP as reflected i.e. by a patchy loss of histochemically demonstrable adrenergic nerves in iris which persisted for at least 7 days. Pretreatment with the NA uptake blocker desipramine antagonised the effects of MPP+, indicating that neurotoxicity is mediated via the NA uptake mechanism. The difference in neurotoxic potency of MPTP between sympathetic adrenergic nerves and central catecholamine neurons might be related to differences in metabolism of MPTP in the CNS and the periphery and/or due to the sympathetic adrenergic nerves being more resistant towards the cytotoxic actions following MPTP administration.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗