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• W1579021687 abstract "Autism is a severe neuropsychiatric disorder characterized by impaired communication, significant reduction in social interaction, and repetitive and stereotyped behaviour. It is highly hereditable (Hoekstra et al., 2007); however, genomic alterations associated to autism have been found only in less than a fifth of the total number of cases. How those alterations ultimately cause the autistic phenotype is still very poorly understood. Besides genomic abnormalities, environmental and epigenetic factors may also increase the risk of developing autism or autistic traits. Prenatal exposure to rubella virus, cytomegalovirus, or to the chemical substances thalidomide and valproate are among the non-genetic causes linked to autism (Persico & Bourgeron, 2006), however causal relationships are not established. Regardless of the origins of autism, neuropathological observations are consistently found in several areas of autistic brains (Bauman & Kemper, 1985; Ritvo et al., 1986), and abnormal patterns of synaptic connectivity are thought to be at the core of the autistic disorder (Belmonte et al., 2004). Indeed, many of the genes associated with high risk for autism and those increasing susceptibility are directly, or indirectly, involved in axon guidance, neuronal signalling, metabolism, cell differentiation and synaptic homeostasis (Weiss et al., 2009; Autism genome project consortium, 2007; Tabuchi et al., 2007; Toro et al., 2010). Therefore, along with an early diagnosis (Limon 2007), the prevention and correction of the abnormal connectivity, and the modulation of the synaptic function are the main goals of current and future treatments of the pathological characteristics of the autistic disorders. Glutamate and GABA are the main excitatory and inhibitory neurotransmitters in the human brain and both have important roles during early development of the nervous system, an ontological stage when the evidence indicates that autism begins. Therefore, it is important to analyse the functional status of glutamatergic and GABAergic neurotransmission in the autistic brain. Cumulative evidence indicates that dysfunctional excitatory and inhibitory synaptic activities underlie several of the characteristics of autism and are, consequently, important targets of pharmacological intervention. In this chapter we describe how glutamate and GABA receptors may participate in the aetiology of autistic disorders and will discuss some of the methods that we have developed to study functional and pharmacological properties of human membrane receptors. We include information demonstrating that functional studies of GABA and glutamate receptors from autistic tissue" @default.
• W1579021687 created "2016-06-24" @default.
• W1579021687 creator A5035781296 @default.
• W1579021687 creator A5084583517 @default.
• W1579021687 creator A5090575202 @default.
• W1579021687 date "2011-08-17" @default.
• W1579021687 modified "2023-10-18" @default.
• W1579021687 title "GABA and Glutamate Receptors of the Autistic Brain" @default.
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• W1579021687 doi "https://doi.org/10.5772/20304" @default.
• W1579021687 hasPublicationYear "2011" @default.
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