Coincident development and synchronization of sleep-dependent delta in the cortex and medulla.

In early development, active sleep is the predominant sleep state before it is supplanted by quiet sleep. In rats, the developmental increase in quiet sleep is accompanied by the sudden emergence of the cortical delta rhythm (0.5-4 Hz) around postnatal day 12 (P12). We sought to explain the emergence of the cortical delta by assessing developmental changes in the activity of the parafacial zone (PZ), a medullary structure thought to regulate quiet sleep in adults. We recorded from the PZ in P10 and P12 rats and predicted an age-related increase in neural activity during increasing periods of delta-rich cortical activity. Instead, during quiet sleep, we discovered sleep-dependent rhythmic spiking activity-with intervening periods of total silence-phase locked to a local delta rhythm. Moreover, PZ and cortical delta were coherent at P12 but not at P10. PZ delta was also phase locked to respiration, suggesting sleep-dependent modulation of PZ activity by respiratory pacemakers in the ventral medulla. Disconnecting the main olfactory bulbs from the cortex did not diminish cortical delta, indicating that the influence of respiration on delta at this age is not mediated indirectly through nasal breathing. Finally, we observed an increase in parvalbumin-expressing terminals in the PZ across these ages, supporting a role for local GABAergic inhibition in the PZ's rhythmicity. The unexpected discovery of delta-rhythmic neural activity in the medulla-when cortical delta is also emerging-provides a new perspective on the brainstem's role in regulating sleep and promoting long-range functional connectivity in early development.

DELTA-RHYTHMIC ACTIVITY IN THE MEDULLA DEVELOPS COINCIDENT WITH CORTICAL DELTA IN SLEEPING INFANT RATS.

In early development, active sleep is the predominant sleep state before it is supplanted by quiet sleep. In rats, the developmental increase in quiet sleep is accompanied by the sudden emergence of the cortical delta rhythm (0.5-4 Hz) around postnatal day 12 (P12). We sought to explain the emergence of cortical delta by assessing developmental changes in the activity of the parafacial zone (PZ), a medullary structure thought to regulate quiet sleep in adults. We recorded from PZ in P10 and P12 rats and predicted an age-related increase in neural activity during increasing periods of delta-rich cortical activity. Instead, during quiet sleep we discovered sleep-dependent rhythmic spiking activity-with intervening periods of total silence-phase-locked to a local delta rhythm. Moreover, PZ and cortical delta were coherent at P12, but not at P10. PZ delta was also phase-locked to respiration, suggesting sleep-dependent modulation of PZ activity by respiratory pacemakers in the ventral medulla. Disconnecting the main olfactory bulbs from the cortex did not diminish cortical delta, indicating that the influence of respiration on delta at this age is not mediated indirectly through nasal breathing. Finally, we observed an increase in parvalbumin-expressing terminals in PZ across these ages, supporting a role for GABAergic inhibition in PZ's rhythmicity. The discovery of delta-rhythmic neural activity in the medulla-when cortical delta is also emerging-opens a new path to understanding the brainstem's role in regulating sleep and synchronizing rhythmic activity throughout the brain.

Trait neuroticism does not relate to cardiovascular reactivity or habituation to repeated acute psychosocial stress.

Neuroticism has been associated with adverse cardiovascular health. Adverse cardiovascular health outcomes have also been linked to cardiovascular reactivity and cardiovascular reactivity habituation to acute psychosocial stress. As such, cardiovascular stress reactivity and habituation may be a factor in the association between neuroticism and disease risk. However, studies of the relationship between neuroticism and cardiovascular reactivity have produced mixed results. Moreover, the relationships between neuroticism, cardiovascular reactivity habituation, and general affect across a repeated stress paradigm have not been examined. The present study aimed to assess the relationships between neuroticism, positive and negative affect, and cardiovascular reactivity and habituation to acute psychosocial stress in a large, demographically diverse sample. Participants (N = 426) completed two 4-min mental arithmetic stressors, each with a separate baseline, in a single laboratory session while having discrete blood pressure and heart rate measurements taken. State positive and negative affect were measured immediately following informed consent, after receiving task instructions, and after each stress task. Trait neuroticism was measured using the Big Five Inventory. Each stress task elicited significant cardiovascular changes. Trait neuroticism was not significantly associated with cardiovascular reactivity or cardiovascular reactivity habituation, within or across stress tasks (all p's > 0.12). Across the entire study protocol, neuroticism was significantly related to lower positive affect and higher negative affect (both p's < 0.001). Trait neuroticism did not relate to stress-related cardiovascular adjustments but might confer a predisposition toward high negative affect.