S100B infusion into the rat hippocampus facilitates memory for the inhibitory avoidance task but not for the open-field habituation

Souza, Tadéu Mello e; Röhden, Abrahão Bernardo; Meinhardt, Marcus W.; Gonçalves, Carlos Alberto; Quillfeldt, Jorge Alberto

doi:10.1016/s0031-9384(00)00299-7

Cited by 34 publications

(16 citation statements)

References 24 publications

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“…For instance, serum levels of S100B were decreased in anorexia nervosa and normalized with weight gain. These results suggest that nutritional status is an important factor influencing serum levels of S100B [30] .…”

Section: Discussionmentioning

confidence: 72%

“…Animal experiments have demonstrated that intracerebral injection or infusion of S100 could improve cognitive recovery after traumatic brain injury [29] , facilitate memory processing in a dose-dependent way [30] and lead to the consolidation of passive avoidance memory [31] . Recently, histopathological studies demonstrated that mood disorders were characterized by disease-specific glial pathology [32,33] .…”

Section: Discussionmentioning

confidence: 99%

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S100B Serum Levels and Word Memory Processing in Remitted Major Depression as Reflected by Brain Potentials

Zhang

Rothermundt²,

Peters³

et al. 2009

Neuropsychobiology

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Objective: Memory processes, as reflected by ‘old/new’ effects of event-related potentials (ERPs), have been shown to be impaired in depressed patients. This variability might be partly explained by biological factors. S100B is a glial calcium-binding protein with neuroplastic properties; S100B serum levels have been shown to be increased in depressive patients. The pathophysiologic role of S100B in depression, however, is not yet sufficiently understood. Methods: In the present study, ERPs recorded in a visual continuous word recognition paradigm were therefore investigated in patients with remitted major depression in relation to S100B serum levels. Results: Patients with moderately increased S100B serum levels (n = 6) showed a normal old/new effect in contrast to a reduced old/new effect in patients with normal S100B levels (n = 6) compared to aged-matched controls. Conclusions: These findings provide evidence of an association between S100B levels and memory processes in patients with recurrent depression and further suggest a neuroprotective role of moderately increased S100B serum levels in the course of affective disorders.

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Section: Discussionmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 99%

S100B Serum Levels and Word Memory Processing in Remitted Major Depression as Reflected by Brain Potentials

Zhang

Rothermundt²,

Peters³

et al. 2009

Neuropsychobiology

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“…In animal studies, different levels of S100B played different roles in cognitive functioning. Too high levels of S100B have been demonstrated to be harmful [8]; whereas S100B levels that are near normal physiological levels may be protective [10,15,18]. So, the relationship between S100B and cognitive function in patients (with high levels of S100B) and controls (with normal physiological levels of S100B) may be different.…”

Section: Discussionmentioning

confidence: 99%

Risk variants in the S100B gene, associated with elevated S100B levels, are also associated with visuospatial disability of schizophrenia

Zhai

Zhang

Cheng

et al. 2011

Behavioural Brain Research

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a b s t r a c tRs9722 and rs1051169 have been reported as affecting the levels of S100B in the serum or the brain, and haplotypes containing these two SNPs have been associated with schizophrenia. The current study investigated the role of the S100B gene in an endophenotype of schizophrenia-spatial disability. 304 schizophrenia patients and 196 healthy controls were given a block design task and a mental rotation task. Results showed that the two aforementioned SNPs and related haplotypes were associated with the spatial disability of schizophrenia patients. Specifically, risk factors for the elevated S100B levels, including the A allele of rs9722, the G allele of rs1051169, and the AG haplotype, were associated with a poorer performance on both tests of spatial ability, especially the mental rotation task. These results implicate a role for S100B gene polymorphisms in the cognitive functions of schizophrenia patients and encourage further investigation into spatial disability as an endophenotype of schizophrenia.

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“…O'Dowd and colleagues (1997) demonstrated that the application of S100B-antiserum in chicks before or immediately after training on an avoidance task caused amnesia. On the other hand, infusion of S100B to the hippocampus of rats after training in a step-down inhibitory avoidance task facilitated long-term memory in a dose-dependent manner (Mello e Souza et al, 2000). S100B transgenic mice with multiple copies of the human S100B gene (Friend-transgenic-mouse, mainly strains 5 and 8 with 8 and 70 copies of the human S100␤, Friend et al, 1992) showed a range of defects such as female specific hyperactivity, lack of habituation to novelty, and a reduced T-maze spontaneous alternation rate.…”

Section: Functional Studiesmentioning

confidence: 94%

S100B in brain damage and neurodegeneration

Rothermundt

Peters

Prehn³

et al. 2003

Microscopy Res & Technique

537

411

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S100B is a calcium-binding peptide produced mainly by astrocytes that exert paracrine and autocrine effects on neurons and glia. Some knowledge has been acquired from in vitro and in vivo animal experiments to understand S100B's roles in cellular energy metabolism, cytoskeleton modification, cell proliferation, and differentiation. Also, insights have been gained regarding the interaction between S100B and the cerebral immune system, and the regulation of S100B activity through serotonergic transmission. Secreted glial S100B exerts trophic or toxic effects depending on its concentration. At nanomolar concentrations, S100B stimulates neurite outgrowth and enhances survival of neurons during development. In contrast, micromolar levels of extracellular S100B in vitro stimulate the expression of proinflammatory cytokines and induce apoptosis. In animal studies, changes in the cerebral concentration of S100B cause behavioral disturbances and cognitive deficits. In humans, increased S100B has been detected with various clinical conditions. Brain trauma and ischemia is associated with increased S100B concentrations, probably due to the destruction of astrocytes. In neurodegenerative, inflammatory and psychiatric diseases, increased S100B levels may be caused by secreted S100B or release from damaged astrocytes. This review summarizes published findings on S100B regarding human brain damage and neurodegeneration. Findings from in vitro and in vivo animal experiments relevant for human neurodegenerative diseases and brain damage are reviewed together with the results of studies on traumatic, ischemic, and inflammatory brain damage as well as neurodegenerative and psychiatric disorders. Methodological problems are discussed and perspectives for future research are outlined.

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S100B infusion into the rat hippocampus facilitates memory for the inhibitory avoidance task but not for the open-field habituation

Cited by 34 publications

References 24 publications

S100B Serum Levels and Word Memory Processing in Remitted Major Depression as Reflected by Brain Potentials

S100B Serum Levels and Word Memory Processing in Remitted Major Depression as Reflected by Brain Potentials

Risk variants in the S100B gene, associated with elevated S100B levels, are also associated with visuospatial disability of schizophrenia

S100B in brain damage and neurodegeneration

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