Person:

Bosquet Enlow, Michelle

Respiratory sinus arrhythmia (RSA) is related to cardiac vagal outflow and the respiratory pattern. Prior infant studies have not systematically examined respiration rate and tidal volume influences on infant RSA or the extent to which infants' breathing is too fast to extract a valid RSA. We therefore monitored cardiac activity, respiration, and physical activity in 23 six-month old infants during a standardized laboratory stressor protocol. On average, 12.6% (range 0–58.2%) of analyzed breaths were too short for RSA extraction. Higher respiration rate was associated with lower RSA amplitude in most infants, and lower tidal volume was associated with lower RSA amplitude in some infants. RSA amplitude corrected for respiration rate and tidal volume influences showed theoretically expected strong reductions during stress, whereas performance of uncorrected RSA was less consistent. We conclude that stress-induced changes of peak-valley RSA and effects of variations in breathing patterns on RSA can be determined for a representative percentage of infant breaths. As expected, breathing substantially affects infant RSA and needs to be considered in studies of infant psychophysiology.

Highly penetrant mutations leading to schizophrenia are enriched for genes coding for N-methyl-D-aspartate receptor signaling complex (NMDAR-SC), implicating plasticity defects in the disease's pathogenesis. The importance of plasticity in neurodevelopment implies a role for therapies that target these mechanisms in early life to prevent schizophrenia. Testing such therapies requires noninvasive methods that can assess engagement of target mechanisms. The auditory N100 is an obligatory cortical response whose amplitude decreases with tone repetition. This adaptation may index the health of plasticity mechanisms required for normal development. We exposed participants aged 5 to 17 years with psychosis (n = 22), at clinical high risk (CHR) for psychosis (n = 29), and healthy controls (n = 17) to an auditory tone repeated 450 times and measured N100 adaptation (mean amplitude during first 150 tones − mean amplitude during last 150 tones). N100 adaptation was reduced in CHR and psychosis, particularly among participants <13 years old. Initial N100 blunting partially accounted for differences. Decreased change in the N100 amplitude with tone repetition may be a useful marker of defects in neuroplastic mechanisms measurable early in life.

Infants from an early age have a bias to attend more to faces than non-faces and after 5 months are particularly attentive to fearful faces. We examined the specificity of this “fear bias” in 5-, 7-, and 12-month-old infants (N = 269) and 36-month-old children (N = 191) and whether its development is associated with features of the early rearing environment, specifically maternal anxiety and depression symptoms. Attention dwell times were assessed by measuring the latencies of gaze shifts from a stimulus at fixation to a new stimulus in the visual periphery. In infancy, dwell times were shorter for non-face control stimuli vs. happy faces at all ages, and happy vs. fearful, but not angry, faces at 7 and 12 months. At 36 months, dwell times were shorter for non-faces and happy faces compared to fearful and angry faces. Individual variations in attention dwell times were not associated with mothers’ self-reported depression or anxiety symptoms at either age. The results suggest that sensitivity to fearful faces precedes a more general bias for threat-alerting stimuli in early development. We did not find evidence that the initial manifestation of these biases is related to moderate variations in maternal depression or anxiety symptoms.