Brain biomarkers based assessment of cognitive workload in pilots under various task demands.

Cognitive workload is an important element of cognitive-motor performance such as that exhibited during the piloting of an aircraft. Namely, an increase in task demands on the pilot can elevate cognitive information processing and, thus, the risk of human error. As such, there is a need to develop methods that reliably assess mental workload in pilots within operational settings. The present study contributes to this research goal by identifying physiological and brain biomarkers of cognitive workload and attentional reserve during a simulated aircraft piloting task under three progressive levels of challenge. A newly developed experimental method was employed by which electroencephalography (EEG) was acquired via a dry (i.e., gel-free sensors) system using few scalp sites. Self-reported responses to surveys and piloting performance indicators were analyzed. The findings revealed that as the challenge (task demands) increased, the perceived mental load increased, attentional reserve was attenuated, and task performance decreased. Such an increase in task demands was also reflected by changes in heart rate variability (HRV), as well as in the amplitude of the P300 component of event-related potentials to auditory probes, and in the spectral power of specific EEG frequency bands. This work provides a first step towards a long-term goal to develop a composite system of biomarkers for real-time cognitive workload assessment and state assessment of pilots in operational settings.

Netrin-1 receptor-deficient mice show enhanced mesocortical dopamine transmission and blunted behavioural responses to amphetamine.

The mesocorticolimbic dopamine (DA) system is implicated in neurodevelopmental psychiatric disorders including schizophrenia but it is unknown how disruptions in brain development modify this system and increase predisposition to cognitive and behavioural abnormalities in adulthood. Netrins are guidance cues involved in the proper organization of neuronal connectivity during development. We have hypothesized that variations in the function of DCC (deleted in colorectal cancer), a netrin-1 receptor highly expressed by DA neurones, may result in altered development and organization of mesocorticolimbic DA circuitry, and influence DA function in the adult. To test this hypothesis, we assessed the effects of reduced DCC on several indicators of DA function. Using in-vivo microdialysis, we showed that adult mice that develop with reduced DCC display increased basal DA levels in the medial prefrontal cortex and exaggerated DA release in response to the indirect DA agonist amphetamine. In contrast, these mice exhibit normal levels of DA in the nucleus accumbens but significantly blunted amphetamine-induced DA release. Concomitantly, using conditioned place preference, locomotor activity and prepulse inhibition paradigms, we found that reduced DCC diminishes the rewarding and behavioural-activating effects of amphetamine and protects against amphetamine-induced deficits in sensorimotor gating. Furthermore, we found that adult DCC-deficient mice exhibit altered dendritic spine density in layer V medial prefrontal cortex pyramidal neurones but not in nucleus accumbens medium spiny neurones. These findings demonstrate that reduced DCC during development results in a behavioural phenotype opposite to that observed in developmental models of schizophrenia and identify DCC as a critical factor in the development of DA function.