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"Behavior genetics"
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Genesis : the deep origin of societies
Discusses how \"the only way for us to fully understand human behavior is to study the evolutionary histories of nonhuman species\"-- Provided by publisher.
Book
Dysfunction in GABA signalling mediates autism-like stereotypies and Rett syndrome phenotypes
Mutations in the X-linked
MECP2
gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality. Rett syndrome is characterized by apparently normal early development followed by regression, motor abnormalities, seizures and features of autism, especially stereotyped behaviours. The mechanisms mediating these features are poorly understood. Here we show that mice lacking
Mecp2
from GABA (γ-aminobutyric acid)-releasing neurons recapitulate numerous Rett syndrome and autistic features, including repetitive behaviours. Loss of MeCP2 from a subset of forebrain GABAergic neurons also recapitulates many features of Rett syndrome. MeCP2-deficient GABAergic neurons show reduced inhibitory quantal size, consistent with a presynaptic reduction in glutamic acid decarboxylase 1 (
Gad1
) and glutamic acid decarboxylase 2 (
Gad2
) levels, and GABA immunoreactivity. These data demonstrate that MeCP2 is critical for normal function of GABA-releasing neurons and that subtle dysfunction of GABAergic neurons contributes to numerous neuropsychiatric phenotypes.
The GABAergic system in Rett syndrome
Rett syndrome, a neurodevelopmental disorder with autistic features, is caused by mutations in the methyl-CpG-binding protein 2 gene (
MECP2
). A number of mouse models with full and cell-type specific deletions of
Mecp2
have been generated, but show only a subset of the signs of Rett syndrome. Now Huda Zoghbi and colleagues report that mice with selective deletion of MeCP2 in GABAergic neurons show not only impaired GABAergic function, but capitulate many of the key features of Rett syndrome. The finding that disturbance of inhibitory neurons causes a variety of neuropsychiatric phenotypes suggests that the GABAergic system may be a promising target for therapeutic intervention.
Mutations in the methyl-CpG-binding protein 2 (MeCP2) gene cause Rett syndrome, a neurodevelopmental disorder with features of autism. Multiple mouse models of MeCP2 have been generated, but show only a subset of the symptoms of Rett syndrome. These authors find that mice with selective deletion of MeCP2 in GABA-mediated neurons show not only impaired GABA-mediated function, but capitulate multiple key features of Rett, further suggesting a role of inhibitory function in neuropsychiatric disease.
Journal Article
The selfish gene
Dawkins articulates a gene's eye view of evolution--a view giving center stage to these persistent units of information, and in which organisms can be seen as vehicles for their replication. This work not only brought the insights of Neo-Darwinism to a wide audience, but galvanized the biology community, generating much debate and stimulating new areas of research. Forty years later, its insights remain as relevant today as on the day it was published.
Book
New developments in human neurocognition: clinical, genetic, and brain imaging correlates of impulsivity and compulsivity
Impulsivity and compulsivity represent useful conceptualizations that involve dissociable cognitive functions, which are mediated by neuroanatomically and neurochemically distinct components of cortico-subcortical circuitry. The constructs were historically viewed as diametrically opposed, with impulsivity being associated with risk-seeking and compulsivity with harm-avoidance. However, they are increasingly recognized to be linked by shared neuropsychological mechanisms involving dysfunctional inhibition of thoughts and behaviors. In this article, we selectively review new developments in the investigation of the neurocognition of impulsivity and compulsivity in humans, in order to advance our understanding of the pathophysiology of impulsive, compulsive, and addictive disorders and indicate new directions for research.
Journal Article
Social behaviour : genes, ecology and evolution
\"Humans live in large and extensive societies and spend much of their time interacting socially. Likewise, most other animals also interact socially. Social behaviour is of constant fascination to biologists and psychologists of many disciplines, from behavioural ecology to comparative biology and sociobiology. The two major approaches used to study social behaviour involve either the mechanism of behaviour - where it has come from and how it has evolved, or the function of the behaviour studied. With guest articles from leaders in the field, theoretical foundations along with recent advances are presented to give a truly multidisciplinary overview of social behaviour, for advanced undergraduate and graduate students. Topics include aggression, communication, group living, sexual behaviour and co-operative breeding. With examples ranging from bacteria to social mammals and humans, a variety of research tools are used, including candidate gene approaches, quantitative genetics, neuro-endocrine studies, cost-benefit and phylogenetic analyses and evolutionary game theory\"--Provided by publisher.
Book
Shank3 mutant mice display autistic-like behaviours and striatal dysfunction
Autism spectrum disorders (ASDs) comprise a range of disorders that share a core of neurobehavioural deficits characterized by widespread abnormalities in social interactions, deficits in communication as well as restricted interests and repetitive behaviours. The neurological basis and circuitry mechanisms underlying these abnormal behaviours are poorly understood. SHANK3 is a postsynaptic protein, whose disruption at the genetic level is thought to be responsible for the development of 22q13 deletion syndrome (Phelan–McDermid syndrome) and other non-syndromic ASDs. Here we show that mice with
Shank3
gene deletions exhibit self-injurious repetitive grooming and deficits in social interaction. Cellular, electrophysiological and biochemical analyses uncovered defects at striatal synapses and cortico-striatal circuits in
Shank3
mutant mice. Our findings demonstrate a critical role for SHANK3 in the normal development of neuronal connectivity and establish causality between a disruption in the
Shank3
gene and the genesis of autistic-like behaviours in mice.
Protein link to autism
Genomic studies have identified numerous candidate genes for autism spectrum disorders, many of which encode synaptic proteins. One of the most promising is
Shank3
, which codes for a key post-synaptic density protein at glutamatergic synapses. Peça
et al
. show that mice with
Shank3
deletions display several features of autism, including social deficits, as well as abnormal striatal synapses and cortico-striatal circuitry. The findings demonstrate a crucial role for
Shank3
in neuronal connectivity and provide a mechanism for its possible function in autistic-like behaviours.
Journal Article
