Long-term potentiation in rat hippocampal slices is impaired following acute lead perfusion

Altmann, L; Sveinsson, Karolina; Wiegand, Herbert

doi:10.1016/0304-3940(91)90771-k

Cited by 53 publications

(9 citation statements)

References 13 publications

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“…The hippocampus is an important target of neurotoxic agents and it accumulates Pb to a greater degree than other parts of the brain (Stoltenburg-Didinger 1994). Behavioral alterations following Pb-exposure have been related to hippocampal dysfunction (Altmann et al 1991). Developmental exposure to Pb seems to alter the development of aminergic neurons mainly in the medulla, cerebral cortex and hippocampus.…”

Section: Discussionmentioning

confidence: 99%

Zinc and Calcium Reduce Lead Induced Perturbations in the Aminergic System of Developing Brain

et al. 2005

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Since alterations in monoamines and monoamine oxidase (MAO) have been postulated to play a role in toxic effects of lead (Pb) on the central nervous system, we have examined the protective effects of calcium (Ca 2+ ) and zinc (Zn 2+ ) supplementation on Pb-induced perturbations in the levels of monoamines and the activity of MAO. Swiss albino mice were lactationally exposed to low (0.2%) and high (1%) levels of Pb-acetate via drinking water of the mother. Pb-exposure commenced on postnatal day (PND) 1, continued up to PND 21 and stopped at weaning. Ca 2+ or Zn 2+ (0.02% in 0.2% Pb-water or 0.1% in 1% Pb-water) was supplemented separately to the mother up to PND 21. The levels of monoamines (epinephrine, norepinephrine, dopamine and serotonin) and the activity of MAO in the brain regions such as hippocampus, cortex, cerebellum and medulla of young (1 month old) and adult (3 month old) mice were determined in the synaptosomal fractions. The synaptosomal monoamines though increased with low level (0.2%) Pb-exposure, significantly decreased with high level (1%) Pb-exposure in all the brain regions in both the age groups. In general, the young mice seem to be more vulnerable to Pb-neurotoxicity. Ca 2+ or Zn 2+ supplementation significantly reversed the Pb-induced perturbations both in the levels of monoamines and in the activity of MAO. However, the recovery in monoamine levels and MAO activity was more pronounced with Ca 2+ supplementation as compared to Zn 2+ . These results provide evidence that dietary Ca 2+ and/or Zn 2+ provide protection against Pb-induced neurotoxic effects.

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Section: Discussionmentioning

confidence: 99%

Zinc and Calcium Reduce Lead Induced Perturbations in the Aminergic System of Developing Brain

et al. 2005

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“…Sections from the contralateral hippocampus were utilized in studies of long-term potentiation (LTP). In previous experiments, LTP was found to be impaired in hippocampal slices following acute lead perfusion (Altmann et al 1991). LTP is generally accepted as an electrophysiological correlate for learning and memory (Alkon et al 1991).…”

Section: Introductionmentioning

confidence: 95%

Glial fibrillary acidic protein and RNA expression in adult rat hippocampus following low-level lead exposure during development

Stoltenburg‐Didinger¹,

Pünder²,

Peters³

et al. 1996

Histochem Cell Biol

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The astroglial cytoskeletal element, glial fibrillary acidic protein (GFAP), is a generally accepted sensitive indicator for neurotoxic effects in the mature brain. We used GFAP as a marker for structural changes in rat hippocampus related to chronic low level lead exposure during different developmental periods. Four groups of rats were investigated: a control group, a perinatal group, which was exposed during brain development (E0-P16), a permanent group, exposed during and after brain development (E0-P100), and a postweaning group, exposed after brain development (P16-P100). Sections were processed for light microscopy (hematoxylin-eosin, Nissl, periodic acid Schiff (PAS) and GFAP-specific immunohistology), for electron microscopy, and for in-situ hybridization (GFAP). Sections were prepared from animals tested for active avoidance learning (AAL) and long-term potentiation (LTP). Chronic lead exposure did not affect glial and neuronal functions, as assessed by LTP and AAL, when lead exposure started after brain development (postweaning group). In this group, astrocytes displayed increased GFAP and GFAP gene transcript levels. However, lead exposure affected neuronal and glial function when the intoxication fell into the developmental period of the brain (perinatal and permanent groups). In these groups, LTP and AAL were impaired, and astrocytes failed to react to the toxic exposure with an adequate increase of GFAP and GFAP gene transcripts. Although GFAP is an accepted marker for neurotoxicity, our data suggest the marker function of GFAP to be restricted to postnatal toxic insult.

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“…Since IL-6 activates the HPA axis, and hippocampus and hypothalamus are critical sites for such activation, the observation that IL-6 in hippocampus stayed elevated longer compared with the other regions at the 6-h time point (data not shown) except in the caudate nucleus emphasizes the importance of IL-6 in the activation of the HPA axis as well as modulation of select brain functions. Children with high Pb body burdens have been reported to have lower IQ levels (McMichael et al, 1994;Pocock et al, 1994), and Pb is known to block hippocampal long-term potentiation (LTP) (Altmann et al, 1991;Lasley et al, 1993) and increase synaptic efficacy, which is a crucial electrophysiological event for memory storage. Interestingly, hippocampal LTP is significantly reduced in transgenic mice with overproduction of brain IL-6; as a result, these transgenic mice have defects in learning (Bellinger et al, 1995).…”

Section: Lps and Lead Effects On Il-6 Production 369mentioning

confidence: 99%

Differential Production of Interleukin-6 in the Brain and Spleen of Mice Treated With Lipopolysaccharide in the Presence and Absence of Lead

Kishikawa

Lawrence²

1998

Journal of Toxicology and Environmental Health, Part A

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The heavy metal lead (Pb) markedly augments the lethality of endotoxin in laboratory animals. Much of the tissue injury produced by endotoxin is thought to be mediated by cytokines. Thus, the effects of Pb on the regulation of interleukin-6 (IL-6), a proinflammatory cytokine that shows high correlation with symptoms of endotoxic shock, and the levels of corticosterone, a hormone produced to prepare the body to cope with stress, upon lipopolysaccharide (LPS; endotoxin) administration were investigated. After intravenous administration of LPS, the kinetics of IL-6 gene expression by Northern blot analysis revealed a rapid increase of IL-6 mRNA, which peaked by 2 h in the spleens and 3 h in the brains of B6C3F1 female mice, with or without Pb exposure. Peak production of IL-6 protein after LPS challenge was observed at 2 h in the spleens and 3 h in the sera regardless of Pb-treatment. However, Pb-exposed mice showed an altered kinetic profile of IL-6 appearance in the brain, in that the levels of IL-6 in the brains peaked at 4 h rather than 3 h, the peak for the control mice. Moreover, at two time points, the amounts of IL-6 were found to be higher in the brains of Pb-treated mice. Increases in IL-6 were detected in multiple areas of the brain, but Pb did not significantly enhance this level in any area. The observation of both IL-6 transcripts and protein in the brains of mice upon peripheral LPS administration is indicative of local de novo synthesis of IL-6 in the brain. IL-6 production in the brain may contribute to the centrally mediated effects of IL-6, since IL-6 in the brain is known to activate the hypothalamus-pituitary-adrenal (HPA) axis. Upon LPS challenge, corticosterone levels peaked at the 2-h time point and stayed elevated for 6 h regardless of Pb exposure. The increases in brain IL-6 and its extended expression by Pb do not appear to have significantly altered the HPA axis on the basis of the corticosterone level, but brain IL-6 is known to affect multiple brain functions such as long-term potentiation.

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Long-term potentiation in rat hippocampal slices is impaired following acute lead perfusion

Cited by 53 publications

References 13 publications

Zinc and Calcium Reduce Lead Induced Perturbations in the Aminergic System of Developing Brain

Zinc and Calcium Reduce Lead Induced Perturbations in the Aminergic System of Developing Brain

Glial fibrillary acidic protein and RNA expression in adult rat hippocampus following low-level lead exposure during development

Differential Production of Interleukin-6 in the Brain and Spleen of Mice Treated With Lipopolysaccharide in the Presence and Absence of Lead

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