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Autism: Neuropathology, Alterations of the GABAergic System, and Animal Models
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- معلومة اضافية
- Publisher Information:
Elsevier 2005
- نبذة مختصرة :
This chapter discusses autism neuropathology, the role of GABAergic system, the system in which neurons produce gamma-aminobutyric acid (GABA) as their output, in this disorder, and the relevance of rodent models with autistic features. With respect to the neuropathology of autism, consistent findings have emerged for the limbic system, cerebellum, and cerebral cortex. The neuropathologic data of the limbic system show increased cell packing density and smaller neurons. These observations might be explained by an arrest of normal development. As with the cholinergic system, several studies have reported a reduction in GABA function, availability, and activity in autism. A decrease in GABA receptor binding has also been shown in autism. Evidence indicates that GABA plays a role in several developmental processes, including cell migration, proliferation, and differentiation. Although the neuropathologic results in autistic subjects are revealing, animal models are essential for a better understanding of the pathophysiology, cause, and treatment of autism. The recent linkages of neuroligin (NLGN), DLX, and engrailed 2 (En2) to autism offer possibilities for animal models, particularly if introducing the relevant, specific mutations (as opposed to simple knockouts [Kos]) and can cause interesting pathology and behavior.
- الموضوع:
- Availability:
Open access content. Open access content
- Note:
Autism: Neuropathology, Alterations of the GABAergic System, and Animal Models
- Other Numbers:
CIT oai:authors.library.caltech.edu:63265
van Kooten, Imke A. J. and Hof, Patrick R. and van Engeland, Herman and Steinbusch, Harry W. M. and Patterson, Paul H. and Schmitz, Christoph (2005) Autism: Neuropathology, Alterations of the GABAergic System, and Animal Models. In: GABA in Autism and Related Disorders. International Review of Neurobiology. No.71. Elsevier , New York, NY, pp. 1-26. ISBN 9780123668721. https://resolver.caltech.edu/CaltechAUTHORS:20151229-234715148
1017651066
- Contributing Source:
CALIFORNIA INST OF TECH
From OAIster®, provided by the OCLC Cooperative.
- الرقم المعرف:
edsoai.on1017651066
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