Role of nitric oxide in learning and memory and in monoamine metabolism in the rat brain

Yamada, Kiyofumi; Noda, Yukihiro; Nakayama, Shinobu; Komori, Yumiko; Sugihara, Hisayoshi; Hasegawa, Takaaki; Nabeshima, Toshitaka

doi:10.1111/j.1476-5381.1995.tb15011.x

Cited by 143 publications

(61 citation statements)

References 51 publications

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“…It also leads to the degeneration of neurons in hippocampus which plays an important role in learning process (Guo et al 2010). A growing body of evidence suggests that reactive ROS play a crucial role in the development of these impairments as discussed above (Yamada et al 1995;Kucukatay et al 2007). The increased production of oxidants altered neurotransmitter release and increased membrane permeability (Gupta et al 1991).…”

Section: Resultsmentioning

confidence: 99%

Neurobehavioral changes in mice offspring induced by prenatal exposure to acute toxicity of sodium selenite

2011

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Selenium is an essential element with a narrow margin between beneficial and toxic effects. This study was aimed to determine the neurobehavioral changes resulted from the prenatal exposure of mice to high doses of sodium selenite during fetal and early postnatal development. Atomic absorption for monitoring the placental transfer of selenium to offspring was employed. The developmental observations as well as the behavioral tests, such as sensory motor reflexes, and learning and memory test in automatic reflex conditioner (shuttle box) (active avoidance responses) were applied. Adult mice was assigned into three groups: the first group was remained as a control group given phosphate buffered saline; the second and the third groups were orally administrated sodium selenite at doses of 1 mg/kg and 4 mg/kg of the diet, respectively started from the 7 th day to the end of the gestation period. Appearance of body hair and opening of eyes of the pups from treated mothers were delayed in a dose-dependent manner. The body weight gain came significantly lower than those of the control especially at the higher dose. Selenite also inhibited the sensory motor reflexes in all elements of acts and postures in a dose dependent manner. The active avoidance training-test indicated that selenite exposure was associated with learning impairment. Acetylcholine recorded a significant decrease in almost all the period of this study. By using atomic absorption, we found a significant high concentration of selenium in the brain, liver and kidney until the 40 th postnatal day, indicating active transfer of selenium from mothers to embryos.

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Section: Resultsmentioning

confidence: 99%

Neurobehavioral changes in mice offspring induced by prenatal exposure to acute toxicity of sodium selenite

2011

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“…This enzyme produces nitric oxide (NO), a molecule involved in neurosynaptic transmission, and is induced in many pathological conditions. Although the role of NO in learning and memory is still unclear, some studies have reported that systemic NO inhibition had deleterious effects in water maze learning (25)(26)(27). The role of iNOS in the hippocampus, therefore, may go beyond its well established detrimental function in neurological disorders and could contribute to the mechanisms underlying learning and memory.…”

Section: Discussionmentioning

confidence: 99%

Memory-specific temporal profiles of gene expression in the hippocampus

Cavallaro

D’Agata

Manickam

et al. 2002

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

174

146

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Many experiments in the past have demonstrated the requirement of de novo gene expression during the long-term retention of learning and memory. Although previous studies implicated individual genes or genetic pathways in learning and memory, they did not uncover the collective behaviors or patterns of the genes. We have used genome-scale screening to analyze gene expression during spatial learning of rats in the Morris water maze. Our results show distinct temporal gene expression profiles associated with learning and memory. Exogenous administration of one peptide whose sustained increase during memory retention was implicated by microarray analysis, fibroblast growth factor (FGF)-18, improved spatial learning behavior, suggesting that pharmacological modulation of pathways and targets identified may allow new therapeutic approaches for improving learning and memory. Results of this study also suggest that while learning and physical activity involve common groups of genes, the behavior of learning and memory emerges from unique patterns of gene expression across time.

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“…These antagonists have also been found to protect against NMDAinduced neurotoxicity (Haberny et al, 1992;Dawson et al, 1993;Ayata et al, 1997). They also block NMDA-mediated convulsions (Nakamura et al, 1995), and impair learning and memory in several animal models (Ward et al, 1990;Chapman et al, 1992;BoÈ hme et al, 1993;HoÈ lscher & Rose, 1993;HoÈ lscher et al, 1995;Yamada et al, 1995;Harder et al, 1998;Ingram et al, 1998a,b;Meyer et al, 1998;Zou et al, 1998). However, there is also evidence that inhibition of NOS does not impair learning or prevent the induction of long-term potentiation and NMDA-induced convulsions in animals (Buisson et al, 1993;Bannerman et al, 1994a,b).…”

Section: Discussionmentioning

confidence: 99%

Blockade of phencyclidine‐induced effects by a nitric oxide donor

Bujas‐Bobanovic

Bird

Robertson

et al. 2000

British J Pharmacology

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1 Phencyclidine (PCP) is widely used as an animal model of schizophrenia. The aim of this study was to better understand the role of nitric oxide (NO) in the mechanism of action of PCP and to determine whether positive NO modulators may provide a new approach to the treatment of schizophrenia. 2 The eects of the NO donor, sodium nitroprusside (SNP), were studied in PCP-treated rats. Following drug administration, behavioural changes and the expression of c-fos, a metabolic marker of functional pathways in the brain, were simultaneously monitored. 3 Acute PCP (5 mg kg 71 , i.p.) treatment induced a complex behavioural syndrome, consisting of hyperlocomotion, stereotyped behaviours and ataxia. Treatment with SNP (2 ± 6 mg kg 71 , i.p.) by itself produced no eect on any behaviour studied but completely abolished PCP-induced behaviour in a dose-and time-dependent manner. 4 PCP had dierential regional eects on c-fos expression in rat brain, suggesting regionally dierent patterns of neuronal activity. The most prominent immunostaining was observed in the cortical regions. Pre-treatment with SNP blocked PCP-induced c-fos expression at doses similar to those that suppress PCP-induced behavioural eects. 5 These results implicate the NO system in the mechanism of action of PCP. The fact that SNP abolished eects of PCP suggests that drugs targeting the glutamate-NO system may represent a novel approach to the treatment of PCP-induced psychosis and schizophrenia.

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Role of nitric oxide in learning and memory and in monoamine metabolism in the rat brain

Cited by 143 publications

References 51 publications

Neurobehavioral changes in mice offspring induced by prenatal exposure to acute toxicity of sodium selenite

Neurobehavioral changes in mice offspring induced by prenatal exposure to acute toxicity of sodium selenite

Memory-specific temporal profiles of gene expression in the hippocampus

Blockade of phencyclidine‐induced effects by a nitric oxide donor

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