Impairment of long-term potentiation and paired-pulse facilitation in rat hippocampal dentate gyrus following developmental lead exposure in vivo

Ruan, Di‐Yun; Chen, Ju-Tao; Zhao, Chen; Xu, Yiming; Wang, Ming; Zhao, Wangfa

doi:10.1016/s0006-8993(98)00739-2

Cited by 70 publications

(24 citation statements)

References 28 publications

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“…Such facilitation also corroborates previous findings (McNaughton 1980;Racine and Milgram 1983;Steffensen and Henriksen 1991). Paired-pulse stimulation of the LPP showed no change at 20 msec ISI and facilitation up to 500 msec ISI, which also confirms previous reports (McNaughton 1980;Ruan et al 1998). FGL did not have any significant effect on these pairedpulse functions for either pathway (LPP-LPP, treatment: F , 1, treatment × ISI interaction: F , 1; MPP-MPP, treatment: F , 1, treatment × ISI interaction: F (2,42) ¼ 2.03, P ¼ 0.14).…”

Section: Fgl Does Not Alter Paired-pulse Functionsupporting

confidence: 92%

The neural cell adhesion molecule-derived peptide FGL facilitates long-term plasticity in the dentate gyrus in vivo

Dallérac¹,

Zerwas²,

Novikova³

et al. 2011

Learn. Mem.

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The neural cell adhesion molecule (NCAM) is known to play a role in developmental and structural processes but also in synaptic plasticity and memory of the adult animal. Recently, FGL, a NCAM mimetic peptide that binds to the Fibroblast Growth Factor Receptor 1 (FGFR-1), has been shown to have a beneficial impact on normal memory functioning, as well as to rescue some pathological cognitive impairments. Whether its facilitating impact may be mediated through promoting neuronal plasticity is not known. The present study was therefore designed to test whether FGL modulates the induction and maintenance of synaptic plasticity in the dentate gyrus (DG) in vivo. For this, we first assessed the effect of the FGL peptide on synaptic functions at perforant path-dentate gyrus synapses in the anesthetized rat. FGL, or its control inactive peptide, was injected locally 60 min before applying high-frequency stimulation (HFS) to the medial perforant path. The results suggest that although FGL did not alter basal synaptic transmission, it facilitated both the induction and maintenance of LTP. Interestingly, FGL also modified the heterosynaptic plasticity observed at the neighboring lateral perforant path synapses. The second series of experiments, using FGL intracerebroventricular infusion in the awake animal, confirmed its facilitating effect on LTP for up to 24 h. Our data also suggest that FGL could alter neurogenesis associated with LTP. In sum, these results show for the first time that enhancing NCAM functions by mimicking its heterophilic interaction with FGFR facilitates hippocampal synaptic plasticity in the awake, freely moving animal.

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Section: Fgl Does Not Alter Paired-pulse Functionsupporting

confidence: 92%

The neural cell adhesion molecule-derived peptide FGL facilitates long-term plasticity in the dentate gyrus in vivo

Dallérac¹,

Zerwas²,

Novikova³

et al. 2011

Learn. Mem.

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“…The hippocampus-dependent spatial learning and memory are correlated closely with hippocampal LTP, impairment of which often leads to memory deficits (Bliss & Collingridge, 1993). Our previous studies have demonstrated chronic lead exposure during development impaired LTP in DG area of hippocampus in rats (Ruan et al, 1998;She, Wang, Zhu, Sun, & Ruan, 2005;Zhu, Wang, She, Yu, & Ruan, 2005).…”

Section: Introductionmentioning

confidence: 94%

Enriched environment restores impaired hippocampal long‐term potentiation and water maze performance induced by developmental lead exposure in rats

Cao

Huang

Ruan

2008

Developmental Psychobiology

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Lead (Pb2+) exposure in children can induce long lasting deficits in cognitive function and has been modeled in experimental animals. Based on previous studies which demonstrated that learning impairments resulting from developmental Pb2+ exposure were reversible if the animals were provided with an enriched environment, here, we asked if environmental enrichment (EE) could also reverse long-term potential (LTP) impairment induced by lead. Rats drank 1,500 ppm lead acetate (PbAc) solution or distilled water throughout gestation and lactation. After weaning at postnatal Day 22, one half of the control and lead-exposed male offspring were given the environmental enrichment treatment through all the experiments until tested. Electrophysiological and Morris water maze test were performed at 8 weeks of age. The result showed that the impaired learning ability induced by lead could be reversed by EE. Furthermore, our results revealed that EPSP LTP and PS LTP impairments induced by lead were also reversible by EE experience.

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“…Deficits in learning have also been observed in rodents exposed to lead (6); these learning deficits have been associated with changes in glutamate receptor binding sites (7). Rats exposed to low levels of lead during the first postnatal month have deficits in memory and long-term potentiation that persist in the adult (8,9). We hypothesize that the persistent detrimental effects of neonatal lead exposure may be due, in part, to deficits in neocortical development.…”

mentioning

confidence: 99%

Neonatal lead exposure impairs development of rodent barrel field cortex

Wilson

Johnston

Goldstein

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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Childhood exposure to low-level lead can permanently reduce intelligence, but the neurobiologic mechanism for this effect is unknown. We examined the impact of lead exposure on the development of cortical columns, using the rodent barrel field as a model. In all areas of mammalian neocortex, cortical columns constitute a fundamental structural unit subserving information processing. Barrel field cortex contains columnar processing units with distinct clusters of layer IV neurons that receive sensory input from individual whiskers. In this study, rat pups were exposed to 0, 0.2, 1, 1.5, or 2 g͞liter lead acetate in their dam's drinking water from birth through postnatal day 10. This treatment, which coincides with the development of segregated columns in the barrel field, produced blood lead concentrations from 1 to 31 g͞dl. On postnatal day 10, the area of the barrel field and of individual barrels was measured. A dose-related reduction in barrel field area was observed (Pearson correlation ‫؍‬ ؊0.740; P < 0.001); mean barrel field area in the highest exposure group was decreased 12% versus controls. Individual barrels in the physiologically more active caudoventral group were affected preferentially. Total cortical area measured in the same sections was not altered significantly by lead exposure. These data support the hypothesis that lead exposure may impair the development of columnar processing units in immature neocortex. We demonstrate that low levels of blood lead, in the range seen in many impoverished inner-city children, cause structural alterations in a neocortical somatosensory map.

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Impairment of long-term potentiation and paired-pulse facilitation in rat hippocampal dentate gyrus following developmental lead exposure in vivo

Cited by 70 publications

References 28 publications

The neural cell adhesion molecule-derived peptide FGL facilitates long-term plasticity in the dentate gyrus in vivo

The neural cell adhesion molecule-derived peptide FGL facilitates long-term plasticity in the dentate gyrus in vivo

Enriched environment restores impaired hippocampal long‐term potentiation and water maze performance induced by developmental lead exposure in rats

Neonatal lead exposure impairs development of rodent barrel field cortex

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