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Cognitive-attentional test anxiety theory posits that test-anxious individuals direct attention internally, thus interfering with task-relevant information processing. Nevertheless, working-memory deficits are often obscured by compensatory exertion of increased effort by anxious subjects on cognitive tasks. Failure to identify anxietyspecific performance decrements has led some authors to replace the test anxiety construct with one emphasizing skill deficiencies. This investigation examined whether information-processing deficits are inherent sequelae of test anxiety or merely reflect lowered exam-taking ability in test-anxious persons.

Past studies have shown that ontogenetic treatment of quinpirole (QNP) produces a number of behavioral effects that can be alleviated by administration of antipsychotics such as haloperidol, providing a useful behavioral screen for disorders such as schizophrenia. In this study, 16 female Sprague-dawley rats were used, with 8 rats injected with QNP(1 mg/kg) and 8 rats injected with saline once daily from postnatal days (PD) 1-11. All rats were behaviorally tested as adults on several tasks: The reference and working memory versions of the Morris water task (MWT), the radial arm maze (RAM), the Whishaw reaching task, and locomotor activity. Results showed that on the MWT, QNP-treated rats demonstrated significant enhancement on acquisition latency of both versions, but a deficit on the probe trial of the reference memory version. The acquisition enhancement was due to hyperlocomotion observed in QNP-treated rats, because these animals demonstrated increased locomotion in an activity chamber compared to controls. On the RAM, QNP-treated rats demonstrated a deficit in reference memory but not working memory, congruent with MWT findings. Interestingly, QNP-treated rats demonstrated a significant enhancement in reaching accuracy on the Whishaw reaching task, which may due to an overactive dopaminergic system. Future studies will analyze underlying mechanisms.

Debate continues on the merits of strictly limiting alcohol consumption during all of pregnancy, and whether “safe” consumption levels and/or times exist. Only a relatively few experimental studies have been conducted that limit the timing of exposure to specific events during development and the exposure level to one that might model sporadic, incidental drinking during pregnancy. In the present study, the effects of two acute gavage exposures to low and moderate levels of ethanol (peak blood ethanol concentrations (BEC) of 104 and 177 mg/dl, respectively) either during gastrulation on gestational day (GD) 7 (at GD7:0 h and GD7:4 h) or during neurulation on GD8 (at GD8:6 h and GD8:10 h) on the spatial learning and memory abilities of adult mice in the radial arm maze (RAM) were examined. Mice were selected from a prenatal ethanol exposure (PAE) cohort that had been tested as neonates for their sensorimotor development (Schambra et al., 2015) and as juveniles and young adults for open field activity levels and emotionality (Schambra et al., 2016). Mice exposed on either of the two gestational days to acute, low or moderate levels of ethanol were deficient in overall performance in the RAM in adulthood. Importantly, mice in ethanol exposed groups took longer to reach criterion in the RAM, and many mice in these groups failed to do so after 48 trials when testing was terminated. Exposure to a low level of ethanol on either GD7 or GD8, or a moderate level on GD7, resulted in significant impairment in spatial reference (long-term) memory, while only mice exposed on GD7 to the low level of ethanol were significantly impaired in spatial working (short-term) memory. Mice exposed to the low ethanol level on either day had significantly shorter response latencies, which may reflect impairment of processes related to response inhibition or executive attention in these mice. For all measures, distributions of individual scores revealed a relatively small subset of mice in each PAE group who scored well outside the range of the control group, which skewed the population distributions to varying degrees in the direction of worse performance for the PAE groups. Overall the data suggest that after acute, low level ethanol exposure early in gestation, the likelihood that an individual mouse embryo experienced measureable ill-effects due to the exposure was rather low, but in a few of the embryos, damage occurred that resulted in significant deficits in later performance. The overall characteristics of our cohort of PAE mice, including delayed sensorimotor development, mild hypoactivity and increased emotionality, as shown in previous studies, together with deficits in spatial learning and memory as shown here, resemble those in a subset of human Fetal Alcohol Spectrum Disorder (FASD) diagnoses, specifically ADHD-Inattentive type (ADHD-I) and/or Sluggish Cognitive Tempo (SCT). Although possible correspondences between mechanisms underlying PAE-induced deficits in mice and those operating in humans remain undefined, further study with this mouse PAE model may ultimately help advance understanding of the causes of these conditions in affected children. This study highlights the possibility of risk associated with low to moderate sporadic alcohol consumption during the first month of human pregnancy.

This study examined the impact of working memory deficits (WMD) on the academic achievement of adolescents with ADHD. Adolescents (n=79) aged 13 to 17 years with a clinical diagnosis of ADHD were subtyped into those with and without WMD based on impairment in at least two measures, and then compared on their academic achievement and clinical profile. Results indicated that adolescents with ADHD plus WMD (23%) manifest significantly lower academic achievement than those with adequate WM. By contrast, there were no group differences in psychiatric comorbidity, severity of ADHD symptoms and psychological adjustment. We also found a unique contribution of WM to academic achievement over and above that of other clinical features. These findings suggest that WMD compromise the educational attainment of a subgroup of individuals with ADHD. Individuals with ADHD should be screened for WMD to prevent academic failure and WM should be considered as a treatment target.

This study examined the impact of working memory deficits (WMD) on the academic achievement of adolescents with ADHD. Adolescents (n=79) aged 13 to 17 years with a clinical diagnosis of ADHD were subtyped into those with and without WMD based on impairment in at least two measures, and then compared on their academic achievement and clinical profile. Results indicated that adolescents with ADHD plus WMD (23%) manifest significantly lower academic achievement than those with adequate WM. By contrast, there were no group differences in psychiatric comorbidity, severity of ADHD symptoms and psychological adjustment. We also found a unique contribution of WM to academic achievement over and above that of other clinical features. These findings suggest that WMD compromise the educational attainment of a subgroup of individuals with ADHD. Individuals with ADHD should be screened for WMD to prevent academic failure and WM should be considered as a treatment target.

Despite the interest in the neuroimaging of working memory, little is still known about the neurobiology of complex working memory in tasks that require simultaneous manipulation and storage of information. In addition to the central executive network, we assumed that the recently described salience network [involving the anterior insular cortex (AIC) and the anterior cingulate cortex (ACC)] might be of particular importance to working memory tasks that require complex, effortful processing. Method: Healthy participants (n = 26) and participants suffering from working memory problems related to the Kleine–Levin syndrome (KLS) (a specific form of periodic idiopathic hypersomnia; n = 18) participated in the study. Participants were further divided into a high- and low-capacity group, according to performance on a working memory task (listening span). In a functional magnetic resonance imaging (fMRI) study, participants were administered the reading span complex working memory task tapping cognitive effort. Principal findings: The fMRI-derived blood oxygen level dependent (BOLD) signal was modulated by (1) effort in both the central executive and the salience network and (2) capacity in the salience network in that high performers evidenced a weaker BOLD signal than low performers. In the salience network there was a dichotomy between the left and the right hemisphere; the right hemisphere elicited a steeper increase of the BOLD signal as a function of increasing effort. There was also a stronger functional connectivity within the central executive network because of increased task difficulty. Conclusion: The ability to allocate cognitive effort in complex working memory is contingent upon focused resources in the executive and in particular the salience network. Individual capacity during the complex working memory task is related to activity in the salience (but not the executive) network so that high-capacity participants evidence a lower signal and possibly hence a larger dynamic response.

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