Format

Send to

Choose Destination
Dev Neurosci. 2015;37(6):467-75. doi: 10.1159/000434638. Epub 2015 Jul 15.

Interneuron Dysfunction in Syndromic Autism: Recent Advances.

Author information

1
Department of Pediatrics, Shiga University of Medical Science, Otsu, Japan.

Abstract

Autism is an extremely heterogeneous disorder, but its frequent cooccurrence with epilepsy leads to speculation that there may be common mechanisms associated with these disorders. Inhibitory interneurons are considered to be the main cellular elements that control hyperexcitability in the brain, and interneuron dysfunction can cause pathological hyperexcitability linked to seizure susceptibility or epilepsy. This review summarizes some of the recent advances that support the relationship between interneuron dysfunction and cognitive impairment in human syndromic autism, with particular reference to the pathophysiological findings of murine experimental models of autism. Alterations in x03B3;-aminobutyric acid (GABA)ergic circuits include a wide variety of neurobiological dysfunctions and do not simply involve the loss or gain of any given type of inhibitory mechanism. The characteristics of interneuron dysfunction in each murine model of autism differ for each syndrome, and these diversities may be due to differences in genetic backgrounds or some other currently unknown variances. Future studies should give us a greater understanding of the involvement of different classes of GABAergic interneurons and allow us to define the relationship between the precise pathophysiological mechanisms and the corresponding clinical phenotypes in autism.

PMID:
26183392
DOI:
10.1159/000434638
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for S. Karger AG, Basel, Switzerland
Loading ...
Support Center