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Biomedical subjects

B Arvidson

Publications and source records attributed to B Arvidson.

At least 19 recordsLinked to original sources
PubMed1997

Do organic solvents induce changes in the dopaminergic system? Positron emission tomography studies of occupationally exposed subjects.

OBJECTIVES: The objective of this study was to test the hypothesis that long-term occupational exposure to organic solvents may effect the levels and turnover of dopamine in man. METHODS: A study was performed on 17 patients with neuropsychiatric symptoms due to occupational solvent exposure, and 11 healthy non-exposed male volunteers (controls). Positron emission tomography (PET) was used to assess striatal dopaminergic function, using L-[11C]DOPA, [11C]nomifensine and [11C]raclopride as tracers. RESULTS: The rate of dopamine synthesis was significantly increased among subjects with occupational exposure to organic solvents compared with non-exposed controls. After controlling for the difference in age between exposed and controls, the effect of solvent exposure became less apparent and was reduced from +32% (P = 0.009) to +25% (P = 0.07). There were no differences with regard to the binding of [11C]nomifensine. Patients with and without the diagnosis of toxic encephalopathy did not differ with regard to their putaminal uptake of L-[11C]DOPA, [11C]nomifensine and [11C]raclopride. CONCLUSION: The data support the hypothesis that long-term exposure to organic solvents may increase the rate of dopamine synthesis in the brain without affecting the number of presynaptic terminals or postsynaptic dopamine receptors.

Brain↗
PubMed1997

Positron emission tomography studies of healthy volunteers--no effects on the dopamine terminals and synthesis after short-term exposure to toluene.

Despite extensive research, the mechanisms for the effects of organic solvents on the central nervous system are still unknown. One mechanism proposed is that solvents interfere with the synthesis of neurotransmitters. In the present study 11 male healthy volunteers were exposed during 15 min to 100 p.p.m. toluene at light physical exercise, and the dopamine decarboxylase activity and number of terminals in putamen were measured before and after exposure by positron emission tomography. Two different tracers were used [beta-11C]L-DOPA for decarboxylase activity during the in vivo synthesis of dopamine, and [11C]nomifensine to estimate the number of terminals. Although there was a slight increase in the rate of dopamine synthesis in the putamen after the exposure, this difference was not statistically significant (P = 0.4). No effect was observed with regard to the uptake of nomifensine. There was no significant relationship between the dose of toluene and rate of dopamine synthesis, and no significant correlation between the time from end of exposure to start of the PET-camera and DOPA. Our findings indicate that short term exposure to 100 p.p.m. of toluene does not affect the rate of dopamine synthesis or the number of presynaptic terminals.

Adult↗
PubMed1994

A review of axonal transport of metals.

Neurons have efficient mechanisms for the transport of organelles and chemical substances in axons to the nerve terminals and back to the cell bodies. Enzymes involved in transmitter synthesis, peptide transmitters and their precursors are examples of macromolecules that are transported down the axon, anterogradely. For final degradation and possible reuse, many constituents are transported back to the cell body, retrogradely. Retrograde transport is also a pathway by which certain toxins may bypass the blood-brain barrier and accumulate in neurons. In recent years, it has been shown that certain metals may accumulate in neurons following retrograde transport. The metals for which retrograde transport has been demonstrated include lead, cadmium and mercury. In this article recent findings regarding axonal transport of metals are reviewed. The putative mechanisms involved in the uptake of metals into the nerve terminal and the fate of metals in the cell body are outlined. Axonal transport of metals as a possible etiological factor in diseases of the human nervous system is discussed.

Animals↗
PubMed1994

Mercury deposits in neurons of the trigeminal ganglia after insertion of dental amalgam in rats.

An amalgam filling was inserted into the first upper molar of 12 rats and the animals were killed after 3-9 months. Tissue sections from the trigeminal ganglia and the brain stem were then investigated with a sensitive histochemical technique to trace mercury deposits. Within the trigeminal ganglia, nerve cells with mercury deposits were observed in seven out of 12 rats, whereas no mercury was detected in sections from the brain stem. The mechanism responsible for the accumulation of mercury in neurons of the trigeminal ganglia is discussed.

Animals↗
PubMed1992

Inorganic mercury is transported from muscular nerve terminals to spinal and brainstem motoneurons.

The distribution of mercury within the brainstem and spinal cord of mice was investigated with the autometallographic technique after intramuscular administration of a single dose of mercuric mercury (HgCl2). Deposits of mercury were localized to motor neurons of the spinal cord and to brainstem motor nuclei; i.e., neurons with their peripheral projections outside the blood-brain barrier. Unilateral ligation of the hypoglossal nerve prior to the injection of HgCl2 prevented the accumulation of mercury deposits in the ipsilateral hypoglossal nucleus. The selective accumulation of mercury in spinal and brainstem motoneurons is most probably due to a leakage of metal-protein complexes from capillaries in muscle into myoneural junctions, followed by uptake into nerve terminals and retrograde axonal transport. The possible link between this process and the development of motor neuron degeneration in ALS is discussed.

Amyotrophic Lateral Sclerosis↗
PubMed1992

Accumulation of inorganic mercury in lower motoneurons of mice.

The distribution of mercury within the lower brain stem and spinal cord of mice was investigated at various intervals after a single intramuscular injection of mercuric chloride. The autometallographic technique was used to demonstrate the presence of mercury deposits in tissue sections. Accumulation of mercury was observed in motoneurons of the anterior horns and in motor nuclei of the brainstem. In addition, mercury was present in the neuropil of the area postrema and within renal tubular cells. At the ultrastructural level, mercury was localized to neuronal lysosomes. The preferential accumulation of mercury in motoneurons within the spinal cord and brain stem is most probably due to an uptake of mercury in motor nerve terminals followed by retrograde axonal transport to the cell bodies.

Animals↗
PubMed1990

Retrograde axonal transport of mercury in primary sensory neurons innervating the tooth pulp in the rat.

The pulp cavity of the first upper molar was exposed unilaterally in adult rats with a dental drill and about 1 microliter of mercuric chloride was injected into the coronal pulp. The rats were killed after 1-24 days and frozen sections from the trigeminal ganglia were subjected to silver acetate autometallography for demonstration of mercury. Mercury was found to have accumulated in neurons of the ipsilateral trigeminal ganglion by retrograde axonal transport. The possible implications of this finding are discussed.

Afferent Pathways↗
PubMed1990

Accumulation of mercury in brainstem nuclei of mice after retrograde axonal transport.

Adult mice were injected intramuscularly in the region of the vibrissae muscles on the left side of the nose with a small volume of mercuric chloride dissolved in distilled water. The animals were killed after 1-6 weeks and fixed by whole-body perfusion. Frozen sections were taken from different levels of the brain stem and from the kidney. The sections were subjected to silver acetate autometallography for visualization of mercury. Mercury was found to accumulate in neurones of the facial nerve nuclei, of the motor trigeminal nuclei and of the trigeminal mesencephalic nuclei of the brain stem, after retrograde axonal transport. Mercury was also demonstrated in proximal tubular cells of the kidney. The mechanism for uptake of mercury at the neuromuscular junctions, and the fate of mercury within neurones are analysed. The possible significance of retrograde metal transport for the development of motor neurone disease is discussed.

Administration, Oral↗
PubMed1987

Retrograde axonal transport of mercury.

Female Wistar rats were injected in the tongue with a small volume of 203Hg and were killed 2 weeks later. The lower brain stem with the hypoglossal nuclei was removed and sectioned in a cryostat. Autoradiography of freeze-dried sections showed labeling of both hypoglossal nuclei. The results are regarded as strong evidence of retrograde axonal transport of mercury in the hypoglossal nerve.

Animals↗
PubMed1986

Distribution of 109Cd in the nervous system of rats after intravenous injection.

The distribution of i.v. injected 109Cd within the nervous system was studied in rats 24 h and 1 week after the injection. Measurements by gamma scintillation showed a high uptake of cadmium in peripheral sensory and autonomic ganglia, whereas the uptake was low in the brain, cerebellum, and spinal cord. The accumulation of cadmium in the sciatic nerve was significantly higher than in the brain and spinal nerve roots, but lower than in ganglia. At autoradiography no labeling was seen in the major part of the brain parenchyma, but an accumulation of the metal was observed in structures outside of the blood-brain barrier (BBB), such as the hypophysis, meninges, choroid plexus and pineal gland. Within the peripheral nervous system (PNS), autoradiography showed accumulation of cadmium in the dorsal root ganglia. The results show that the distribution of 109Cd within the nervous system is correlated to regional variations in vascular permeability, blood vessels of different regions permitting penetration of different amounts of the protein-bound cadmium into the nervous tissues. The accumulation of cadmium in certain nervous structures may have relevance for some of the neurotoxicologic effects of this metal that have been demonstrated in animal experiments.

Animals↗
PubMed1986

Autoradiographic localization of cadmium in the rat brain.

Adult rats were injected intravenously with 109CdCl2 and the distribution of the isotope within the brain and neighboring nervous structures was subsequently studied by autoradiography. Cadmium accumulated in regions outside the blood-brain barrier such as the choroid plexus, pineal gland and area postrema, but did not appear in the brain parenchyma. Uptake of cadmium was observed in the trigeminal ganglia close to the nerve cells and in the olfactory bulbs. In addition, cadmium accumulated in the iris, ciliary body and choroid of the eye, but not in the optic nerves. The deposition of cadmium in the olfactory bulbs may be related to the anosmia reported in workers exposed to this metal. The possible harmful effects of accumulation of cadmium in restricted regions of the brain and adjacent nervous structures are discussed.

Animals↗
PubMed1985

Retrograde axonal transport of cadmium in the rat hypoglossal nerve.

A small volume of radioactively labelled cadmium was injected into the tongue of rats. Two weeks later, the rats were killed and the lower brainstem with the hypoglossal nuclei was dissected out and sectioned in a cryostat. Autoradiography of freeze-dried sections showed accumulation of cadmium in both hypoglossal nuclei. When unilateral nerve section was performed prior to the injection, only the contralateral nucleus was labelled. The results are interpreted as strong evidence for retrograde axonal transport of cadmium in the hypoglossal nerve.

Animals↗
PubMed1984

Evidence for vesicular transport of horseradish peroxidase across endoneurial vessels of the sciatic nerve in normal mice.

The permeability of the endoneurial blood vessels of the sciatic nerve to horseradish peroxidase (HRP) was investigated in mice. The animals were killed 2,5, or 30 min after an i.v. injection of the protein, and the distribution of HRP in the sciatic nerve was studied by light and electron microscopy. HRP was frequently found in endothelial vesicles that were located near both the luminal and the abluminal side of the endothelium. The intercellular junctions appeared to be closed to HRP. The perivascular and interstitial macrophages in the endoneurium accumulated HRP by endocytosis. The results are interpreted as evidence for vesicular transport of HRP across endoneurial vessels to interstitial and perivascular macrophages.

Animals↗
PubMed1984

Oro-facio-digital syndromes I and II: radiological methods for diagnosis and the clinical variations.

In view of the different modes of inheritance and the different prognoses of the two oro-facio-digital syndromes, type 1 (OFD-I) and type 2 (OFD-II), it is important to establish a correct diagnosis in these patients. In this report two new patients with the OFD-I syndrome are presented. One of them (Case 1) had multiple congenital malformations and never made any mental contact. She died at the age of four months and autopsy of the brain revealed abnormalities typical of the syndrome, which are discussed. The other patient (Case 2) has so far had normal mental development. Although these two patients were affected to a very different degree, they both presented the clinical and radiological characteristics of the OFD-I syndrome. These two patients and previously reported cases of the OFD-I and OFD-II syndromes were compared with a patient with the OFD-II syndrome (Case 3), a patient reported earlier who is undergoing follow-up. The radiological features of the skeleton in the two syndromes are presented. The irregular mineralization of the hands and feet characteristic of OFD-I, but not of OFD-II, seems to offer a good opportunity to distinguish between these two syndromes. It is suggested that this finding is pathognomonic for the OFD-I syndrome.

Abnormalities, Multiple↗
PubMed1983

Influence of age on the development of cadmium-induced vascular lesions in rat sensory ganglia.

It is known from previous investigations that parenteral administration of single large doses of cadmium salts causes hemorrhagic lesions in the sensory ganglia of adult rats, whereas the ganglia of immature rats remain unaffected. The present study was undertaken to determine more precisely the age at which vascular lesions occur in the sensory ganglia of rats. At the age of 10 days, thrombocytes accumulated and adhered to the endothelial cells in vessels of the trigeminal ganglion, and at the age of 12 days focal hemorrhages occurred in the vicinity of nerve cells. After the age of 12 days, ultrastructural changes in endothelial cells were present in the trigeminal ganglia, with condensation of the cytoplasm, nuclear pyknosis, and discontinuities of the endothelial lining. Intravascular thrombus formation was also observed. In the dorsal root ganglia, there were no hemorrhages before the age of 22 days. The vascular lesions were then similar to those in the trigeminal ganglia. The possible relation between the structure and permeability of endothelial cells and the development of hemorrhagic lesions is discussed.

Age Factors↗
PubMed1982

Cytofluorescence localization of adriamycin in the nervous system. I. Distribution of the drug in the central nervous system of normal adult mice after intravenous injection.

By a fluorescence-microscopic technique the distribution of the antineoplastic glycoside, adriamycin (doxorubicin), was studied in the CNS of normal adult mice after i.v. injection. Doses comparable to those used in patients for the treatment of malignant diseases were used. The drug did not have access to areas of the brain within the blood-brain barrier but, except for the subcommissural organ, it was consistently localized in the nuclei of neurons and/or glial cells of the circumventricular organs (postremal area, subfornical organ, median eminence, neurohypophysis) as well as in cells of the choroid plexus and lamina cribrosa of the optic nerve. The nuclear fluorescence was accompanied by a less intense extracellular fluorescence when the survival time was shorter than 1 min after the injection. The fluorescence emitted by adriamycin was seen as early as 15 s after injection and showed its highest intensity at 1 and 15 min later. After 24 h fluorescence was no longer observed except for the ependymal zone of the median eminence. Our study thus shows that adriamycin passes from the blood into the nervous parenchyma in those areas of the brain located outside the blood-brain barrier. This finding raises the question whether in such regions there are any neurotoxicologic effects produced by the drug which have not yet been detected.

Animals↗