Urinary cortisol circadian rhythm in a group of high-functioning children with autism

Richdale, Amanda L.; Prior, Margot

doi:10.1007/bf01048245

Cited by 87 publications

(95 citation statements)

References 23 publications

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“…2 E and F, phases and period lengths of differentiated cells could be well determined, suggesting that the assay system presented in this study has a potential for the screening study (31). These lines of research may contribute to the design of new therapeutic or preventive strategies for human developmental disorders such as autism that are often complicated with circadian rhythm disorders (32,33).…”

Section: Discussionmentioning

confidence: 91%

Development of the circadian oscillator during differentiation of mouse embryonic stem cells in vitro

Yagita

Horie²,

Koinuma³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

206

202

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The molecular oscillations underlying the generation of circadian rhythmicity in mammals develop gradually during ontogenesis. However, the developmental process of mammalian cellular circadian oscillator formation remains unknown. In differentiated somatic cells, the transcriptional-translational feedback loops (TTFL) consisting of clock genes elicit the molecular circadian oscillation. Using a bioluminescence imaging system to monitor clock gene expression, we show here that the circadian bioluminescence rhythm is not detected in the mouse embryonic stem (ES) cells, and that the ES cells likely lack TTFL regulation for clock gene expression. The circadian clock oscillation was induced during the differentiation culture of mouse ES cells without maternal factors. In addition, reprogramming of the differentiated cells by expression of Sox2, Klf4, Oct3/4, and c-Myc genes, which were factors to generate induced pluripotent stem (iPS) cells, resulted in the re-disappearance of circadian oscillation. These results demonstrate that an intrinsic program controls the formation of the circadian oscillator during the differentiation process of ES cells in vitro. The cellular differentiation and reprogramming system using cultured ES cells allows us to observe the circadian clock formation process and may help design new strategies to understand the key mechanisms responsible for the organization of the molecular oscillator in mammals.circadian clock | induced pluripotent stem cells | real-time monitor T he circadian rhythm is a fundamental biological system in mammals involved in the regulation of various physiological functions such as the sleep-wake cycle, energy metabolism, and the endocrine system (1, 2). These physiological rhythms develop gradually in the first year of life in humans (3). It is well known that the human sleep-wake rhythm is generated within a few months after birth. However, a weak circadian rhythm of core body temperature is present immediately after birth, suggesting that the development of the human circadian rhythms starts during fetal life. In fact, recent studies in rodents have suggested the appearance of circadian molecular rhythms in the suprachiasmatic nucleus (SCN) a few days before birth (4). However, little information is available on the development of the mammalian cellular circadian oscillator.In mammals, molecular oscillation of the circadian clock consists of interlocked positive and negative transcription/translation feedback loops (TTFL) involving a set of clock genes and clock-controlled output genes that link the oscillator to the clock-controlled processes (5). CLOCK and BMAL1 are basic-helix-loop-helix (bHLH) PAS transcription factors that heterodimerize and transactivate the core clock genes such as Period (Per1, -2, and -3), Cryptochrome (Cry1 and Cry2), and Rev-Erbα (2, 5, 6). PER and CRY proteins suppress the activity of the CLOCK/BMAL1, whereas REV-ERBα suppresses Bmal1 gene expression.In this study, we focused on the development of the mammalian circadian oscillator du...

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Section: Discussionmentioning

confidence: 91%

Development of the circadian oscillator during differentiation of mouse embryonic stem cells in vitro

Yagita

Horie²,

Koinuma³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

206

202

View full text Add to dashboard Cite

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“…Consistent with this view, a number of studies have appeared to indicate impaired HPA function in children with autism (e.g., Hrdlicka et al 2005), with several studies indicating abnormalities in the HPA-axis's production of hormones such as cortisol (e.g., Corbett et al 2006Corbett et al , 2008Marinović-Ć urin et al 2003;Richdale and Prior 1992). Autism has also been linked with abnormalities in circadian patterns of cortisol (e.g., Marinović-Ć urin et al 2008).…”

Section: Introductionmentioning

confidence: 87%

Comparison of Behavioral Intervention and Sensory-Integration Therapy in the Treatment of Challenging Behavior

Devlin

Healy

Leader

et al. 2010

J Autism Dev Disord

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The objective of the current study was to compare the effects of sensory-integration therapy (SIT) and a behavioral intervention on rates of challenging behavior (including self-injurious behavior) in four children diagnosed with Autism Spectrum Disorder. For each of the participants a functional assessment was conducted to identify the variables maintaining challenging behavior. Results of these assessments were used to design function-based behavioral interventions for each participant. Recommendations for the sensory-integration treatment were designed by an Occupational Therapist, trained in the use of sensory-integration theory and techniques. The sensory-integration techniques were not dependent on the results of the functional assessments. The study was conducted within an alternating treatments design, with initial baseline and final best treatment phase. For each participant, results demonstrated that the behavioral intervention was more effective than the sensory integration therapy in the treatment of challenging behavior. In the best treatment phase, the behavioral intervention alone was implemented and further reduction was observed in the rate of challenging behavior. Analysis of saliva samples revealed relatively low levels of cortisol and very little stress-responsivity across the SIT condition and the behavioral intervention condition, which may be related to the participants' capacity to perceive stress in terms of its social significance.

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“…This study examined changes in salivary cortisol and found that AD children showed elevations in cortisol following exposure to a novel non-social situation, whereas control children did not (p < 0.05). Richdale & Prior (1992) found a tendency in children with high-functioning autism toward cortisol hypersecretion during the daytime hours. This effect was principally found in those children who were integrated into the normal school system, which the authors suggested indicates that the elevated cortisol secretion was a response to environmental stress.…”

Section: Hypersensitivity To Stress: An Important Vulnerability To Ad?mentioning

confidence: 99%

Prenatal stress and risk for autism

Kinney

Münir

Crowley

et al. 2008

Neuroscience & Biobehavioral Reviews

373

251

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This paper reviews several converging lines of research that suggest that prenatal exposure to environmental stress may increase risk for Autistic Disorder (AD). We first discuss studies finding that prenatal exposure to stressful life events is associated with significantly increased risk of AD, as well as other disorders, such as schizophrenia and depression. We then review evidence from animal and human studies that prenatal stress can produce both (a) abnormal postnatal behaviors that resemble the defining symptoms of AD, and (b) other abnormalities that have elevated rates in AD, such as learning deficits, seizure disorders, perinatal complications, immunologic and neuroinflammatory anomalies, and low postnatal tolerance for stress. We explain why an etiologic role for prenatal stress is compatible with genetic factors in AD, and describe how stress can disrupt fetal brain development. Finally, we discuss implications for understanding underlying processes in AD, including potential gene-environment interactions, and developing new therapies and early prevention programs.

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Urinary cortisol circadian rhythm in a group of high-functioning children with autism

Cited by 87 publications

References 23 publications

Development of the circadian oscillator during differentiation of mouse embryonic stem cells in vitro

Development of the circadian oscillator during differentiation of mouse embryonic stem cells in vitro

Comparison of Behavioral Intervention and Sensory-Integration Therapy in the Treatment of Challenging Behavior

Prenatal stress and risk for autism

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