Excitatory amino acid receptors in brains of rats with methylazoxymethanol-induced microencephaly

Tamaru, Masao; Yoneda, Yukio; Ogita, Kiyokazu; Shimizu, Jun; Matsutani, Tenhoshimaru; Nagata, Yutaka

doi:10.1016/s0168-0102(05)80003-3

Cited by 12 publications

(8 citation statements)

References 46 publications

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“…Therefore, they also suggested that proliferation of intrinsic neuronal populations including GABAergic and glutamatergic neurons in the cerebral cortex were disturbed by MAM treatment on day 15 of gestation. We also observed that the concentration of excitatory amino acids in these brain regions of MAM-treated rats did not differ from that of controls (Tamaru et al, 1992b), and specific [3H]glutamate (Glu) synaptosomal uptake remained unchanged in the cortex of MAM-treated rats (Johnston and Coyle, 1979). These reports mean that the total number of glutamatergic presynaptic neurons intrinsic to both brain regions is markedly reduced by equivalent values of weight reduction in both brain regions, although the distribution of surviving neurons appears to be normal.…”

Section: Changes Of Monoaminergic Cholinergic Gabaergic and Glutamamentioning

confidence: 50%

“…2). These reductions were well correlated with brain weight reduction, suggesting that the proliferation of postsynaptic neurons bearing Glu receptors intrinsic to both brain regions may be significantly impaired by MAM treatment on day 15 of fetal age (Tamaru et al, 1992a).…”

Section: Excitatory Amino Acid Receptors In Mam-treated Brainsmentioning

confidence: 88%

“…Among these subtypes of Glu receptors, the NMDA receptor complex is known to distribute to the hippocampus and cerebral cortex with a high density (Monaghan and Cotman, 1985). These brain regions are represents the mean of 1G15 determinations (Tamaru et al, 1992a). G/G: Glu/Gly, G/G/S Glu/Gly/spermidine (SPD), KSCN: potassium thiocyanate than 50% of those in controls (Table 1).…”

Section: Excitatory Amino Acid Receptors In Mam-treated Brainsmentioning

confidence: 99%

“…Changes of correct responses and errors on the 8-arm radial maze task of MAM-treated rats(Tamaru et al, 1992a).…”

mentioning

confidence: 98%

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Neurochemical Correlates of Learning Impairment in Microen‐cephalic Rats Induced by Methylazoxymethanol Acetate*

Tamaru

1994

Congenital Anomalies

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Newborn infants with histogenetic brain malformations can be long‐lived with mental retardation, which is considered a major problem in social medicine. Among these infants with mental retardation, many cases are accompanied by microencephaly. Experimentally induced microencephaly in rats presents a useful model for understanding human cerebral disorders. We have studied how neurochemical changes in the brains of microencephalic rats induced by prenatal treatment with methylazoxymethanol acetate (MAM) can affect their learning abilities. We reported that densities of monoaminergic transmitters in the atrophic cerebral hemisphere (CH; consisting of cerebral cortex and hippocampus) of MAM rats was markedly elevated, but that their total quantity per CH unchanged. As for the ability of operant discrimination learning, MAM rats could discriminate tasks. However, excitatory amino acid receptors, in which N‐methyl‐D‐aspartate (NMDA) is well known to be involved in spatial memory, showed decreased total binding in the CH of MAM‐treated rats. Spatial recognition ability evaluated using an 8‐armed radial maze task was impaired. These results suggest that the condensation of monoaminergic terminals in the atrophic CH of MAM rats may compensate for disability in discrimination learning, but the significant reduction of NMDA receptors may impair spatial memory in MAM rats.

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Section: Changes Of Monoaminergic Cholinergic Gabaergic and Glutamamentioning

confidence: 50%

Section: Excitatory Amino Acid Receptors In Mam-treated Brainsmentioning

confidence: 88%

Section: Excitatory Amino Acid Receptors In Mam-treated Brainsmentioning

confidence: 99%

“…Changes of correct responses and errors on the 8-arm radial maze task of MAM-treated rats(Tamaru et al, 1992a).…”

mentioning

confidence: 98%

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Neurochemical Correlates of Learning Impairment in Microen‐cephalic Rats Induced by Methylazoxymethanol Acetate*

Tamaru

1994

Congenital Anomalies

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“…Epileptic attacks are related to a substantial impairment of Ca 2+ ‐homeostasis and an increase of intracellular Ca 2+ ‐precipitation after aberrant activation of excitatory amino acid receptors. This may serve as a fatal defense mechanism in the context of Ca 2+ ‐overload that finally leads to degeneration of affected cells 27,28 . Further, substantial microglial activation has been recently reported in cortical malformations 29 .…”

Section: Discussionmentioning

confidence: 99%

Increased frequency of distinct TSC2 allelic variants in focal cortical dysplasias with balloon cells and mineralization

Schönberger¹,

Niehusmann²,

Urbach

et al. 2009

Neuropathology

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Focal cortical dysplasias with balloon cells (FCD(IIb)) usually present with characteristic imaging and molecular features, that is, a transmantle sign on fluid-attenuated inversion recovery MRI and abundance of allelic variants of the tuberous sclerosis gene 1 (TSC1). Recently, we observed several mineralized lesions (n = 5) lacking this MRI pattern and which surprisingly turned out as FCD(IIb) upon neuropathological examination. These mineralized FCD(IIb) revealed an increased frequency of TSC2 allelic variants but not TSC1 (intron 31: 60% vs. 11% in controls; P = 0.0164, exon 41: 40% vs. 6.5% in controls; P = 0.0441). Mineralized FCD(IIb) have a favorable postsurgical outcome and need consideration in the presurgical differential diagnosis of calcified lesions associated with pharmacoresistant focal epilepsies.

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Evidence of Oxidative Stress in the Brains of Fetuses with CNS Anomalies and Islet Cell Hyperplasia

et al. 2004

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Infants of diabetic mothers have an increased frequency of congenital anomalies, including CNS malformations. Fetal hyperglycemia may promote such damage via oxidative stress. Postmortem studies have shown that fetal hyperglycemia associated with maternal diabetes results in islet cell hyperplasia. Islet cell hyperplasia may correlate with the presence of oxidative stress injury in the CNS because of hyperglycemia and related metabolic derangement. This study examines 3-nitrotyrosine immunoreactivity as a marker of oxidative stress in the brains of fetuses stratified by the presence or absence of islet cell hyperplasia and CNS developmental anomalies. Fetuses with both islet cell hyperplasia and CNS developmental anomalies showed a 1.8-fold increase in semiquantitatively scored 3-nitrotyrosine immunostaining compared to negative controls. Fetuses with islet cell hyperplasia but no CNS anomalies demonstrated a 1.6-fold increase. Comparison between fetuses with islet cell hyperplasia which were stratified by presence or absence of CNS anomalies were not statistically different but did show more intense staining in those with CNS malformations. These results support the contention that hyperglycemia may contribute to CNS malformation via oxidative stress.

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Excitatory amino acid receptors in brains of rats with methylazoxymethanol-induced microencephaly

Cited by 12 publications

References 46 publications

Neurochemical Correlates of Learning Impairment in Microen‐cephalic Rats Induced by Methylazoxymethanol Acetate*

Neurochemical Correlates of Learning Impairment in Microen‐cephalic Rats Induced by Methylazoxymethanol Acetate*

Increased frequency of distinct TSC2 allelic variants in focal cortical dysplasias with balloon cells and mineralization

Evidence of Oxidative Stress in the Brains of Fetuses with CNS Anomalies and Islet Cell Hyperplasia

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