Age-related resistance to ?-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid-induced hippocampal lesion

Bernal, Fabián; Andrés, Noemí; Samuel, D.; Goff, Lydia Kerkerian‐Le; Mahy, Nicole

doi:10.1002/1098-1063(2000)10:3<296::aid-hipo10>3.0.co;2-c

Cited by 11 publications

(6 citation statements)

References 56 publications

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“…Moreover, MSG neonatal treatment reduced [ 3 H]‐GABA hippocampal and cortical uptake, reducing the V max and increasing the affinity (Table 2). Thus, although GABAergic neuron susceptibility to excitotoxicity has been evaluated essentially through GABA and GAD immunostaining, it has been demonstrated that intrahippocampal AMPA administration in adult rats induces neuronal death and reduces GABA uptake (Bernal et al, 2000). Similar effects have been observed in retinas lesioned by MSG in vitro treatment, where loss of GABAergic cells is accompanied by significant reductions in GABA uptake (Salceda and Pasantes‐Morales, 1982), and in the hypothalamus, where MSG neonatal treatment diminishes GABAergic cell density and also the GABA uptake of adult mice (Dawson et al, 1982).…”

Section: Discussionmentioning

confidence: 99%

Excitotoxic neonatal damage induced by monosodium glutamate reduces several GABAergic markers in the cerebral cortex and hippocampus in adulthood

Ureña‐Guerrero

Orozco‐Suárez²,

López-Pérez

et al. 2009

Intl J of Devlp Neuroscience

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Monosodium glutamate (MSG) administered to neonatal rats during the first week of life induces a neurodegenerative process, which is represented by several neurochemical alterations of surviving neurons in the brain, where signalling mediated by GABA is essential for excitation threshold maintenance. GABA-positive cells, [(3)H]-GABA uptake, expression of mRNA for GABA transporters GAT-1 and GAT-3, and expression of mRNA and protein for two main GABA synthesizing enzymes, GAD(65) and GAD(67), were measured at postnatal day 60, after MSG neonatal treatment in two critical cerebral regions, cerebral cortex and hippocampus. GABA-positive cells, [(3)H]-GABA uptake, and mRNA for GAT-1, were significantly diminished in both cerebral regions. In the cerebral cortex, MSG neonatal treatment also decreased the mRNA for GAD(67) and protein for GAD(65) without significant changes in its corresponding protein and mRNA, respectively. Moreover in the hippocampus, mRNA and protein for GAD(65) were increased, whilst GAD(67) protein was elevated without significant changes in its mRNA. Clearly these results confirm the GABA cells loss after MSG neonatal treatment in both cerebral regions. As most of the GABAergic markers measured were reduced in the cerebral cortex, this region seems to be more sensitive than hippocampus, where interesting compensatory changes over GAD(65) and GAD(67) proteins were observed. However, it is possible that others neurotransmission systems are also compensating the GABA-positive cells loss in the cerebral cortex, and that elevations in two main forms of GAD in the hippocampus are not sufficient to maintain the neural excitation threshold for this region.

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Section: Discussionmentioning

confidence: 99%

Excitotoxic neonatal damage induced by monosodium glutamate reduces several GABAergic markers in the cerebral cortex and hippocampus in adulthood

Ureña‐Guerrero

Orozco‐Suárez²,

López-Pérez

et al. 2009

Intl J of Devlp Neuroscience

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“…Once all the morphometric data are pooled, and aside from the low number of patients, the diversity of pathologies, ages, and treatments, and the inclusion of data from rat brain calcification, their analysis fits with a power law model with the same numeric constants. This uniformity argues for common synaptic processes whose variability depends on the cellular type (astrocyte or neuron), glutamatergic activity, and energy availability (Robbins et al, 1989; Nitsch and Scotti, 1992; Liévens et al, 1997; Herrmann et al, 1998; Petegnief et al, 1999; Bernal et al, 2000a, b; Liévens et al, 2000; Ramonet et al, 2004). For example, excessive glutamate activity stands out as a critical factor in ischemic (Meldrum and Garthwaite, 1990; Meldrum and Garthwaite, 1990; Obrenovitch and Richards, 1995; Bradford, 1995; Urenjak and Obrenovitch, 1996; Obrenovitch and Urenjak, 1997) or hypoxic (Hagberg et al, 1994; Panigrahy et al, 1995; Rosenblum, 1997; Longo, 1997; De Keyser et al, 1999) injury, including dementia of vascular origin.…”

Section: Discussionmentioning

confidence: 99%

Similar calcification process in acute and chronic human brain pathologies

et al. 2006

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Cellular microcalcification observed in a diversity of human pathologies, such as vascular dementia, Alzheimer's disease, Parkinson's disease, astrogliomas, and posttraumatic epilepsy, also develops in rodent experimental models of central nervous system (CNS) neurodegeneration. Central to the neurodegenerative process is the inability of neurons to regulate intracellular calcium levels properly, and this is extensible to fine regulation of the CNS. This study provides evidence of a common pattern of brain calcification taking place in several human pathologies, and in the rat with glutamate-derived CNS lesions, regarding the chemical composition, physical characteristics, and histological environment of the precipitates. Furthermore, a common physical mechanism of deposit formation through nucleation, lineal growth, and aggregation is presented, under the modulation of protein deposition and elemental composition factors. Insofar as calcium precipitation reduces activity signals at no energy expense, the presence in human and rodent cerebral brain lesions of a common pattern of calcification may reflect an imbalance between cellular signals of activity and energy availability for its execution. If this is true, this new step of calcium homeostasis can be viewed as a general cellular adaptative mechanism to reduce further brain damage.

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“…Forty‐two rats were divided into two groups: (1) hippocampus‐injected rats that received a unilateral injection of either 50 mM PBS ( n = 5; sham), 6.4 nmol α‐AA ( n = 5; α‐AA), 2.7 nmol AMPA ( n = 4; AMPA), or 6.4 nmol α‐AA + 2.7 nmol AMPA ( n = 5; α‐AA + AMPA); or (2) MS‐injected rats that similarly received an injection of either PBS ( n = 5), α‐AA ( n = 6), AMPA ( n = 6), or α‐AA + AMPA ( n = 6). The AMPA dose was selected according to previous studies (Petegnief et al, 1999; Bernal et al, 2000a). Due to area differences in vulnerability to the excitotoxic lesion (Rodríguez et al, 2000), post‐lesion times were 60 days for MS‐lesioned rats and 15 days for hippocampus‐lesioned animals.…”

Section: Methodsmentioning

confidence: 99%

Heterogeneity between hippocampal and septal astroglia as a contributing factor to differential in vivo AMPA excitotoxicity

Rodrı́guez

Martinez-Sanchez

Bernal

et al. 2004

J of Neuroscience Research

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Astroglial participation in the regional differences of vulnerability to alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-induced neurodegeneration was investigated in the rat hippocampus and medial septum using L-alpha-aminoadipate (alpha-AA) as a specific astroglial toxin. alpha-AA was microinjected in the hippocampus and the medial septum and a time-course study was carried out between 2 hr and 3 days. When compared to controls, microinjection of alpha-AA in the hippocampus induced within 3 days a reversible loss of glial fibrillary acidic protein (GFAP) immunostaining and a microglial reaction without any neuronal loss, whereas in the medial septum it caused no effects on astroglial, microglial, or neuronal populations. Differences in hippocampus and medial septum vulnerability were also evidenced when alpha-AA was co-injected with AMPA and neurodegeneration was assessed in terms of neuronal loss, glial reactions, calcification, and atrophy of the area. In the hippocampus, alpha-AA increased AMPA excitotoxicity with marked disorganization of all hippocampal subfields, increased neuronal loss, a more important astroglial reaction, a larger area of microgliosis, and a greater abundance of calcium deposits. By contrast, in the medial septum alpha-AA did not modify any parameter of the AMPA-induced lesion. In conclusion, the presence of different astroglial populations in hippocampus and medial septum results in a different participation to AMPA excitotoxicity that may determine, at least in part, the specific regional vulnerability to neurodegeneration.

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Age-related resistance to ?-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid-induced hippocampal lesion

Cited by 11 publications

References 56 publications

Excitotoxic neonatal damage induced by monosodium glutamate reduces several GABAergic markers in the cerebral cortex and hippocampus in adulthood

Excitotoxic neonatal damage induced by monosodium glutamate reduces several GABAergic markers in the cerebral cortex and hippocampus in adulthood

Similar calcification process in acute and chronic human brain pathologies

Heterogeneity between hippocampal and septal astroglia as a contributing factor to differential in vivo AMPA excitotoxicity

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