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The Journal of Neuroscience, July 19, 2006, 26(29):7674-7679; doi:10.1523/JNEUROSCI.1285-06.2006

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Neurobiology of Disease
Stereological Analysis of Amygdala Neuron Number in Autism

Cynthia Mills Schumann and David G. Amaral

Department of Psychiatry and Behavioral Sciences and The M.I.N.D. Institute, University of California, Davis, Sacramento, California 95817

Correspondence should be addressed to Dr. David G. Amaral, The M.I.N.D. Institute, University of California, Davis, Medical Center, 2825 50th Street, Sacramento, CA 95817. Email: dgamaral{at}ucdavis.edu

The amygdala is one of several brain regions suspected to be pathological in autism. Previously, we found that young children with autism have a larger amygdala than typically developing children. Past qualitative observations of the autistic brain suggest increased cell density in some nuclei of the postmortem autistic amygdala. In this first, quantitative stereological study of the autistic brain, we counted and measured neurons in several amygdala subdivisions of 9 autism male brains and 10 age-matched male control brains. Cases with comorbid seizure disorder were excluded from the study. The amygdaloid complex was outlined on coronal sections then partitioned into five reliably defined subdivisions: (1) lateral nucleus, (2) basal nucleus, (3) accessory basal nucleus, (4) central nucleus, and (5) remaining nuclei. There is no difference in overall volume of the amygdala or in individual subdivisions. There are also no changes in cell size. However, there are significantly fewer neurons in the autistic amygdala overall and in its lateral nucleus. In conjunction with the findings from previous magnetic resonance imaging studies, the autistic amygdala appears to undergo an abnormal pattern of postnatal development that includes early enlargement and ultimately a reduced number of neurons. It will be important to determine in future studies whether neuron loss in the amygdala is a consistent characteristic of autism and whether cell loss occurs in other brain regions as well.

Key words: autism; neuropathology; stereology; neuronal density; medial temporal lobe; neuroanatomy; amygdaloid complex

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Received July 31, 2005; revised June 6, 2006; accepted June 7, 2006.

Correspondence should be addressed to Dr. David G. Amaral, The M.I.N.D. Institute, University of California, Davis, Medical Center, 2825 50th Street, Sacramento, CA 95817. Email: dgamaral{at}ucdavis.edu

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