Cortisol circadian rhythms and response to stress in children with autism

Corbett, Blythe A.; Mendoza, Sally P.; Abdullah, Maryam; Wegelin, Jacob A.; Levine, Seymour

doi:10.1016/j.psyneuen.2005.05.011

Cited by 228 publications

(223 citation statements)

References 30 publications

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“…Hirstein et al (2001) suggested that an excessively functioning amygdala may account for the increased autonomic responses in autistic children (Hirstein et al, 2001;Corbett et al, 2006) and the consequent enhanced stress may lead to their withdrawal from an overstimulating world. The present study suggests that enhanced anxiety and fear processing could perhaps further amplify an aversion to complex environmental stimulation typical of social conditions, leading to impaired social interactions and resistance to rehabilitation.…”

Section: Indirect Effects Of Non-amygdala Regionsmentioning

confidence: 99%

Abnormal Fear Conditioning and Amygdala Processing in an Animal Model of Autism

Markram

Rinaldi

Mendola

et al. 2007

Neuropsychopharmacol

337

262

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A core feature of autism spectrum disorders is the impairment in social interactions. Among other brain regions, a deficit in amygdala processing has been suggested to underlie this impairment, but whether the amygdala is processing fear abnormally in autism, is yet not clear. We used the valproic acid (VPA) rat model of autism to (a) screen for autism-like symptoms in rats, (b) test for alterations in amygdala-dependent fear processing, and (c) evaluate neuronal reactivity and synaptic plasticity in the lateral amygdala by means of in vitro single-cell electrophysiological recordings. VPA-treated animals displayed several symptoms common to autism, among them impaired social interactions and increased repetitive behaviors. Furthermore, VPA-treated rats were more anxious and exhibited abnormally high and longer lasting fear memories, which were overgeneralized and harder to extinguish. On the cellular level, the amygdala was hyperreactive to electrical stimulation and displayed boosted synaptic plasticity as well as a deficit in inhibition. We show for the first time enhanced, overgeneralized and resistant conditioned fear memories in an animal model of autism. Such hyperfear could be caused by the hyperreactivity and hyperplasticity found in the lateral amygdala, which may in turn be due to a deficit in the inhibitory system of the amygdala. We hypothesize an 'aversive world' syndrome that could, even if not a primary cause of the disorder itself, underlie some core symptoms in autism, such as impairments in social interactions and resistance to rehabilitation.

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Section: Indirect Effects Of Non-amygdala Regionsmentioning

confidence: 99%

Abnormal Fear Conditioning and Amygdala Processing in an Animal Model of Autism

Markram

Rinaldi

Mendola

et al. 2007

Neuropsychopharmacol

337

262

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“…67 Children with autism demonstrate dysregulation of the HPA and are over-responsive to stress as shown by increases in cortisol. 68 ACTH directly and selectively decreases the expression and secretion of apo B in vitro, 69 hence possibly providing a link between stress and changes of ApoB-100.…”

Section: Apolipoproteinsmentioning

confidence: 99%

“…Some children with autism respond to novel environmental stimuli by marked increases in salivary cortisol 68 that can also be detected in blood. It will be important for future studies to consider alternative explanations such as these when inferring CNS changes based on peripheral samples.…”

Section: Role Of Complement In the Brainmentioning

confidence: 99%

A proteomic study of serum from children with autism showing differential expression of apolipoproteins and complement proteins

Corbett

Kantor²,

Schulman³

et al. 2006

Mol Psychiatry

167

113

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Modern methods that use systematic, quantitative and unbiased approaches are making it possible to discover proteins altered by a disease. To identify proteins that might be differentially expressed in autism, serum proteins from blood were subjected to trypsin digestion followed by liquid chromatography-electrospray ionization-mass spectrometry (LC-ESI-MS) on time-of-flight (TOF) instruments to identify differentially expressed peptides. Children with autism 4-6 years of age (n = 69) were compared to typically developing children (n = 35) with similar age and gender distributions. A total of 6348 peptide components were quantified. Of these, five peptide components corresponding to four known proteins had an effect size > 0.99 with a P < 0.05 and a Mascot identification score of 30 or greater for autism compared to controls. The four proteins were: Apolipoprotein (apo) B-100, Complement Factor H Related Protein (FHR1), Complement C1q and Fibronectin 1 (FN1). In addition, apo B-100 and apo A-IV were higher in children with high compared to low functioning autism. Apos are involved in the transport of lipids, cholesterol and vitamin E. The complement system is involved in the lysis and removal of infectious organisms in blood, and may be involved in cellular apoptosis in brain. Despite limitations of the study, including the low fold changes and variable detection rates for the peptide components, the data support possible differences of circulating proteins in autism, and should help stimulate the continued search for causes and treatments of autism by examining peripheral blood.

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“…This pattern is already well-developed by the third month of infancy (Price et al, 1983;Vermes et al, 1980). It has been suggested that individual differences in cortisol secretion, especially in the morning, may be an important variable for typically developing children (Bartels et al, 2003) as well as children with neuropathology, such as autism (Corbett et al, 2006;Corbett et al, in press). …”

Section: Introductionmentioning

confidence: 97%