Selective depletion of caudate nucleus dopamine and serotonin during chronic manganese dioxide administration to squirrel monkeys

Neff, Norton H.; Barrett, Robert E.; Costa, Esther Da

doi:10.1007/bf01900234

Cited by 150 publications

(46 citation statements)

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“…Only 6 papers reported group-average neurochemical endpoints of manganese treatment (Ulrich et al 1979a(Ulrich et al , 1979b(Ulrich et al , 1979cBird et al 1984;Eriksson et al 1992a;Neff et al 1969). Evaluation of motor effects was mostly qualitative with only two studies reporting quantitative tests to evaluate motor response (Eriksson et al 1992a;Newland and Weiss 1992).…”

Section: Parameter Values: Non-human Primate Studiesmentioning

confidence: 99%

“…Internal cumulative manganese doses in inhalation studies were calculated assuming complete absorption (abs =1, as with rodent inhalation studies), and inhalation rates of 490 mL/min/Kg body weight for squirrel monkeys (Ulrich et al 1977) and 420 mL/min/Kg for rhesus monkeys (Bourne 1975). Published reference body weights of the particular monkey species and age were used when weights were not reported (Mella 1924;Neff et al 1969;Pentschew et al 1963).…”

Section: Parameter Values: Non-human Primate Studiesmentioning

confidence: 99%

“…Outcomes to the right of the vertical line were produced by MnO 2 exposure and almost all outcomes to the left by MnCl 2 exposure. Only Bird et al (1984), Eriksson et al 1992a, Neff et al (1969, Ulrich et al (1979aUlrich et al ( , 1979Ulrich et al ( b, 1979c) report average outcomes for more than one animal. Reported outcomes from other studies are from single animals.…”

Section: Figure Captionsmentioning

confidence: 99%

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Adequacy and Consistency of Animal Studies to Evaluate the Neurotoxicity of Chronic Low-Level Manganese Exposure in Humans

Gwiazda

Lucchini

Smith

2007

Journal of Toxicology and Environmental Health, Part A

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The adequacy of existing animal studies to understand the effects of chronic low-level manganese exposures in humans is unclear. Here, a collection of subchronic to chronic rodent and non-human primate studies was evaluated to determine whether there is a consistent dose -response relationship among studies, whether there is a progression of effects with increasing dose, and whether these studies are adequate for evaluating the neurotoxicity of chronic low-level manganese exposures in humans. Neurochemical and behavioral effects were compared along the axis of estimated internal cumulative manganese dose, independent of the route of exposure. In rodents, motor effects emerged at cumulative doses below those where occupationally exposed humans start to show motor deficits. The main neurochemical effects in rodents were an increase in striatal GABA concentration throughout the internal cumulative dose range of 18 to 5300 mg Mn/Kg but a variable effect on striatal dopamine concentration emerging at internal cumulative doses above ~200 mg Mn/Kg. Monkey studies showed motor deficits and effects on the globus pallidus at relatively low doses and consistent harmful effects on both the globus pallidus and the caudate and putamen at higher doses (> 260 mg Mn/Kg). Internal cumulative manganese doses of animal studies extend more than two orders of magnitude (<1 to 5300 mg Mn/Kg) above the doses at which occupationally exposed humans show neurological dysfunction (10-15 mg Mn/Kg). Since the animal data indicate that manganese neurotoxicity may be different at low compared to elevated exposures, most existing animal model studies might be of 3 limited relevance for the risk assessment of chronic low-level manganese exposure to humans. 4

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Section: Parameter Values: Non-human Primate Studiesmentioning

confidence: 99%

Section: Parameter Values: Non-human Primate Studiesmentioning

confidence: 99%

Section: Figure Captionsmentioning

confidence: 99%

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Adequacy and Consistency of Animal Studies to Evaluate the Neurotoxicity of Chronic Low-Level Manganese Exposure in Humans

Gwiazda

Lucchini

Smith

2007

Journal of Toxicology and Environmental Health, Part A

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“…For example, chronic manganese poisoning has been implicated on the development of a Parkinsonian syndrome in humans and monkeys (53). Moreover, cobalt has been shown to induce epilepsy following its cortical implantation in experimental animals (54).…”

Section: Do Environmental Toxicants Influence Central Neurotransmittementioning

confidence: 99%

“…Moreover, cobalt has been shown to induce epilepsy following its cortical implantation in experimental animals (54). Both toxicants have been shown to alter neurotransmitter mechanisms in brain while inducing their degenerative effects (53,54). Excellent reviews on the neurologic effect of mercury (55) and of a variety of other metals (56) have also been published recently.…”

Section: Do Environmental Toxicants Influence Central Neurotransmittementioning

confidence: 99%

Central Neurotransmitter Function and Its Behavioral Correlates in Man

Hanin¹

1978

Environmental Health Perspectives

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The past decade has witnessed a tremendous increase in knowledge towards understanding the function of various brain neurotransmitter substances in behavior. Experimental observations in animals, utilizing specific pharmacological agents, have enabled the development of certain hypotheses regarding neurochemical substrates of behavior. These have led to cautious applications of complementary studies in humans. As a result, several neurotransmitter-related hypotheses have been developed for the explanation of normal behavior, as well as of various abnormal behavior states in psychiatry and neurology. These hypotheses are currently undergoing extensive investigation.Highlights of the above sequence of events are presented, in order to provide as general, yet extensive, an overview of the subject as possible. Examples are provided from both basic laboratory investigations and from clinical findings. Principles of brain neurotransmitter function and interactions are reviewed. Various neurotransmitter-related hypotheses of psychiatric and neurologic interest are introduced. Finally, the role that toxicants may have on behavior via alteration of brain neurotransmitter function is discussed, using the lead intoxicated animal as an illustrative example.

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