Records |
Author |
Branchi, I.; Bichler, Z.; Berger-Sweeney, J.; Ricceri, L. |
Title |
Animal models of mental retardation: from gene to cognitive function |
Type |
Journal Article |
Year |
2003 |
Publication |
Neuroscience and Biobehavioral Reviews |
Abbreviated Journal |
Neurosci Biobehav Rev |
Volume |
27 |
Issue |
1-2 |
Pages |
141-153 |
Keywords |
Animals; Animals, Genetically Modified/growth & development; Behavior/physiology; Behavior, Animal; Brain/*growth & development; Cognition/*physiology; *Disease Models, Animal; Environment; Genes; Genetic Diseases, Inborn/physiopathology; Humans; Mental Retardation/classification/*genetics/*physiopathology |
Abstract |
About 2-3% of all children are affected by mental retardation, and genetic conditions rank among the leading causes of mental retardation. Alterations in the information encoded by genes that regulate critical steps of brain development can disrupt the normal course of development, and have profound consequences on mental processes. Genetically modified mouse models have helped to elucidate the contribution of specific gene alterations and gene-environment interactions to the phenotype of several forms of mental retardation. Mouse models of several neurodevelopmental pathologies, such as Down and Rett syndromes and X-linked forms of mental retardation, have been developed. Because behavior is the ultimate output of brain, behavioral phenotyping of these models provides functional information that may not be detectable using molecular, cellular or histological evaluations. In particular, the study of ontogeny of behavior is recommended in mouse models of disorders having a developmental onset. Identifying the role of specific genes in neuropathologies provides a framework in which to understand key stages of human brain development, and provides a target for potential therapeutic intervention. |
Address |
Section of Behavioural Pathophysiology, Laboratorio di Fisiopatologia di Organo e di Sistema, Istituto Superiore di Sanita, Viale Regina Elena 299, 00161 Roma, Italy. branchi@iss.it |
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Place of Publication |
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Language |
English |
Summary Language |
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Original Title |
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Series Editor |
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Series Title |
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Abbreviated Series Title |
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Series Volume |
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Series Issue |
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Edition |
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ISSN |
0149-7634 |
ISBN |
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Expedition |
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Conference |
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Notes |
PMID:12732230 |
Approved |
no |
Call Number |
Equine Behaviour @ team @ |
Serial |
2805 |
Permanent link to this record |
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Author |
Hemelrijk, C.K.; Wantia, J. |
Title |
Individual variation by self-organisation |
Type |
Journal Article |
Year |
2005 |
Publication |
Neuroscience and biobehavioral reviews |
Abbreviated Journal |
Neurosci Biobehav Rev |
Volume |
29 |
Issue |
1 |
Pages |
125-136 |
Keywords |
Aggression; Animals; Behavior, Animal/*physiology; Competitive Behavior/*physiology; Female; Humans; *Individuality; Male; Models, Psychological; Sex Characteristics; *Social Dominance; Time Factors |
Abstract |
In this paper, we show that differences in dominance and spatial centrality of individuals in a group may arise through self-organisation. Our instrument is a model, called DomWorld, that represents two traits that are often found in animals, namely grouping and competing. In this model individual differences grow under the following conditions: (1) when the intensity of aggression increases and grouping becomes denser, (2) when the degree of sexual dimorphism in fighting power increases. In this case the differences among females compared to males grow too, (3) when, upon encountering another individual, the tendency to attack is 'obligate' and not conditional, namely 'sensitive to risks'. Results resemble phenomena described for societies of primates, mice, birds and pigs. |
Address |
Theoretical Biology, University of Groningen, NN Haren, The Netherlands. hemelrij@ifi.unizh.ch |
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Thesis |
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Publisher |
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Place of Publication |
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Editor |
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Language |
English |
Summary Language |
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Original Title |
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Series Editor |
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Series Title |
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Abbreviated Series Title |
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Series Volume |
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Series Issue |
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Edition |
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ISSN |
0149-7634 |
ISBN |
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Medium |
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Area |
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Expedition |
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Conference |
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Notes |
PMID:15652260 |
Approved |
no |
Call Number |
refbase @ user @ |
Serial |
443 |
Permanent link to this record |