Effect of ganglioside on synaptic plasticity of hippocampus in lead-exposed rats in vivo

She, Ji; Wang, Ming; Zhu, Da-Miao; Sun, Liwei; Ruan, Di‐Yun

doi:10.1016/j.brainres.2005.08.044

Cited by 29 publications

(15 citation statements)

References 31 publications

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“…We also observed DP in the DG area with 1 Hz LFS being applied after 15 min post-HFS (data not shown here). These observations are in line with previous studies demonstrating DP could be found in the DG area of anesthetized rats following 1 Hz LFS after 55, 60, or 130 min post-HFS was applied (Kimura and Pavlides, 2000;She et al, 2005;Zhu et al, 2005;Wang et al, 2007). However, DP in the DG area could not be induced by 2 or 5 Hz LFS after 30 min post-HFS in anesthetized rats (Errington et al, 1995).…”

Section: Discussionsupporting

confidence: 92%

Impaired in vivo synaptic plasticity in dentate gyrus and spatial memory in juvenile rats induced by prenatal morphine exposure

et al. 2008

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ABSTRACT:Prenatal morphine exposure induces neurobiological changes, including deficits in learning and memory, in juvenile rat offspring. However the effects of this exposure on hippocampal plasticity, which is critical for learning and memory processes, are not well understood. The present study investigates the alterations of spatial memory and in vivo hippocampal synaptic plasticity in juvenile rats prenatally exposed to morphine. On gestation days 11-18, pregnant rats were randomly chosen to be injected twice daily with morphine or saline. Each juvenile offspring (postnatal day 22-31) performed one two-trial Y-maze task to evaluate spatial memory. Afterwards, the in vivo field excitatory postsynaptic potential (fEPSP) and population spike (PS) were recorded in the perforant path dentate gyrus (DG) pathway in the hippocampus. Prenatal morphine exposure reduced depotentiation (DP), but not longterm potentiation (LTP), of the EPSP slope. However, both LTP and DP of the EPSP slope were depressed in prenatal morphine-exposed juvenile offspring. The morphine group also showed poorer performance for the Y-maze task than the control group. Depressed PS LTP, but not EPSP LTP, in the morphine group suggested that prenatal morphine exposure changed GABAergic inhibition, which mediates EPSP-spike potentiation. Then a loss of GABA-containing neurons in the DG area of the morphine group was observed using immunohistochemistry. Taken together, our results suggest that prenatal morphine exposure impairs the juvenile offspring's dentate synaptic plasticity and spatial memory, and that decreased GABAergic inhibition may play a role in these effects. These findings might contribute to an explanation for the cognitive deficits in children whose mothers abuse opiates during pregnancy. V V C 2008 WileyLiss, Inc.

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Section: Discussionsupporting

confidence: 92%

Impaired in vivo synaptic plasticity in dentate gyrus and spatial memory in juvenile rats induced by prenatal morphine exposure

et al. 2008

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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: 98%

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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“…Then the cholesterol-anandamide complex migrates in the membrane until it reaches a high-affinity receptor for anandamide (e.g., CB1, a GPCR protein with seven transmembrane domains). 59,60 The importance of gangliosides is further demonstrated by the deleterious effects of experimental neuraminidase treatments on neural functions. In this complex, anandamide interacts with the transmembrane domains (e.g., TM6) of the CB1 receptor.…”

Section: Control Of Synaptic Functions By Gangliosidesmentioning

confidence: 99%

A Molecular View of the Synapse

Fantini¹,

Yahi²

2015

Brain Lipids in Synaptic Function and Neurological Disease

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Effect of ganglioside on synaptic plasticity of hippocampus in lead-exposed rats in vivo

Cited by 29 publications

References 31 publications

Impaired in vivo synaptic plasticity in dentate gyrus and spatial memory in juvenile rats induced by prenatal morphine exposure

Impaired in vivo synaptic plasticity in dentate gyrus and spatial memory in juvenile rats induced by prenatal morphine exposure

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

A Molecular View of the Synapse

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