Friday, May 21, 2010
Franklin Hall B Level 4 (Philadelphia Marriott Downtown)
1:00 PM
S. Y. Ma
,
Developmental Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY
I. Kuchna
,
Developmental Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY
K. Nowicki
,
Developmental Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY
J. Wegiel
,
Developmental Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY
H. Imaki
,
Developmental Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY
I. Cohen
,
Psychology, NYS Institute for Basic Research in Developmental Disabilities, Staten Island, NY
E. London
,
Psychology, NYS Institute for Basic Research in Developmental Disabilities, Staten Island, NY
M. Flory
,
Research Design, NYS Institute for Basic Research in Developmental Disabilities, Staten Island, NY
W. T. Brown
,
Human Genetics, NYS Institute for Basic Research, Staten Island, NY
T. Wisniewski
,
Developmental Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY
J. Wegiel
,
Developmental Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY
Background: The claustrum ontogeny and morphology indicate a pallial and subpallial origin and explains why the claustrum receives inputs from multiple cortical areas, integrates the multiple inputs into a new signal, and redirects sensory information throughout the striatum and thalamus. Involvement in sensorimotor integration and cognition suggests that the claustrum plays a role in higher order functionality enabling the organism to rapidly adapt to the subtleties and nuances of an ever changing environment (Edelstein and Denaro 2004). The severely compromised ability to adapt characteristic of autism suggests that these high order functions are not processed properly and that developmental alterations of the claustrum may contribute to the autistic phenotype.
Objectives: The aim of this study was to test the hypothesis that claustrum development is modified and to characterize the type of structural changes employing unbiased morphometric methods.
Methods: Brain hemispheres of 13 autistic and 14 control subjects 4 to 64 years of age were fixed in 10% formalin, dehydrated and embedded in celloidin. The fractionator method was used to determine the number of neurons, the Cavalieri method to estimate the volume of the claustrum, and Nucleator method to determine the volume of neurons and neuronal nuclei.
Results: In subjects 4 to 23 years of age both the claustrum and the prepiriform claustrum were characterized by developmental delays. Volume of the claustrum was reduced by 30% on average, and the total number of neurons by 29% whereas the numerical density was not modified. The volume of neurons in this younger group of autistic subjects was reduced by 32% and the volume of neuronal nuclei was proportionally less (by 31%).
Conclusions: The claustrum showed a similar range of developmental delay to the structures interacting with the claustrum including the entorhinal cortex, several striatal subdivisions and the thalamus as shown in our other studies. These results support the hypothesis that developmental delay of the claustrum may contribute to the rigidity of behaviors and the lack of ability to adapt to a changing environment seen in autism.
