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As stated previously the integration of cognitive
As stated previously, the integration of cognitive flexibility and emotion regulation is hypothesized to be bi-directional (Zelazo and Cunningham, 2007). Although it is clear that emotion regulation develops rapidly during the preschool years (Eisenberg, 2000), evidence of how specific emotion regulation strategies emerge has been lacking. Many scholars contend that young children may utilize cognitive flexibility as an early emotion regulation strategy, but this hypothesized phenomenon has been under-researched (Cole et al., 2004; Gross, 1998; Kopp, 1989; Ochsner and Gross, 2008). Perlman et al. (2014) were the first to show that irritable yet non-impaired preschool children showed a greater DLPFC response to frustration than their less irritable peers. The association between irritability and DLPFC activation during a cognitive flexibility task suggests that relatively more irritable preschoolers may use well-developed cognitive flexibility, and underlying neural circuitry, to manage daily salient frustration. Shifting attention between competing demands may be one way irritable yet adaptively functional preschoolers manage emotional challenges.
As opposed to previous work on the neural correlates of childhood executive functions (see Moriguchi and Hiraki, 2011; Perlman et al., 2015a; Wood et al., 2009), our study is limited in that we did not find any age-related effects. This is perhaps because our Pet Store Stroop Task was specifically designed to be challenging, but easily attainable in order to investigate neural variation related to irritability rather than neural dissociations between those who could vs. could not complete the task. A second limitation of the study may be that fNIRS methodology is only able to detect hemoglobin changes in the outer cortex and is, thus, best suited for specific hypothesis testing rather than an investigation of widely distributed circuitry. In this study, we used a probe that focused on the DLPFC as a region of interest based on previous localization studies. Thus, other areas of the transketolase that underlie cognitive flexibility or contribute to irritability, such as the parietal cortex (Gottlieb, 2007; Gurd et al., 2002), anterior cingulate (Bush et al., 2000) or amygdala (Deveney et al., 2013; Leibenluft et al., 2003), could not be measured in the current study. A final limitation of this study that is poised to become a prime avenue for future direction concerns the specificity of our findings to a single dimension of negative affect (irritability). It is possible that DLPFC activation in relation to cognitive flexibility might correlate negatively with another dimension of negative affect, such as anxiety, or not at all, or that a relationship between this other dimensions might have a different neural substrate. Future studies employing fMRI will be better poised to examine these questions while investigating a more diffuse circuitry.
Conflict of interest statement
Author note
This work was supported by National Institutes of Health (K01 MH094467 PI: Susan Perlman, R21 MH100189 PI: Susan Perlman, and R01 MH107540 PI: Susan Perlman). Yanwei Li was sponsored by the China Scholarship Council. Adam S. Grabell received support from the National Institutes of Health (T32MH018951; PI: David Brent).
We thank Lisa Bemis, Caroline MacGillivray, Meghan Murphy, and Brianna Jones for their help in subject recruitment and data collection. FNIRS analytical methodology included in this manuscript is developed by Theodore Huppert and Jeffrey Barker and is made publicly available through the following link: https://bitbucket.org/huppertt/nirs-toolbox/wiki/Home. Please address correspondence to Susan B. Perlman, University of Pittsburgh, Department of Psychiatry, 121 Meyran Ave, Pittsburgh, PA, 15213, Phone: 412-624-4139, Fax: 412 383 8336,
Introduction
We have known for half a century that the brain and behavior of altricial species, including humans and rodents, continues to develop after birth, and that genetics and experience interact to guide the intricate process of constructing the brain (Andersen and Teicher, 2008; De Bellis and Thomas, 2003; Fisher, 1955; Landers and Sullivan, 2012; Levine, 1957, 2005; Mainardi et al., 1965). This open system enables early-life experiences to sculpt the brain and optimize behaviors to more closely fit diverse environments to enhance survival (Bock et al., 2014). However, this same open system can permit developmental perturbations to produce vulnerability to psychiatric disorders and maladaptive behaviors that reduce access to resources, especially during critical periods for programming complex cognition and behavior (Andersen and Teicher, 2008; Opendak and Sullivan, 2016). In particular, trauma experienced from a caregiver during a sensitive window in early life can produce life-long deficits in threat processing and social behavior across many species (Amaral, 2003; Callaghan et al., 2014; McEwen, 2003; Moriceau et al., 2006; Tang et al., 2014; Tzanoulinou and Sandi, 2017; Zeanah et al., 2003). Modeling this in rodents suggests that repeated pairing of cues associated with the caregiver and with trauma can disrupt the typical developmental trajectory of brain areas important for both forming attachments and learning about threat (Opendak and Sullivan, 2016; Raineki et al., 2012). In particular, we have observed that trauma experienced in the presence of the caregiver has similar neurobehavioral consequences as trauma experienced directly from an abusive caregiver; these socially anchored traumas produce unique and profound effects that go beyond those of trauma alone.