Mechanisms and functional implications of social buffering in infants: Lessons from animal models

Abstract

Social buffering, which is the attenuation of stress hormone release by a social partner, occurs in many species throughout the lifespan. Social buffering of the infant by the caregiver is particularly robust, and animal models using infant rodents are uncovering the mechanisms and neural circuitry supporting social buffering. At birth, the hypothalamic-pituitary-adrenal (HPA) stress system is functional but is suppressed via extended social buffering by the mother: the profound social buffering effects of the mother can last for 1–2 hours when pups are removed from the mother. At 10 days of age, pups begin to mount a stress response immediately when separated from the mother. The stimuli from the mother supporting social buffering are broad, for tactile stimulation, milk, and an anesthetized mother (no maternal behavior) all sufficiently support social buffering. The mother appears to produce social buffering by blocking norepinephrine (NE) release into the hypothalamic paraventricular nucleus (PVN), which blocks HPA activation. Since the infant amygdala relies on the presence of corticosterone (CORT), this suggests that social buffering of pups by the mother attenuates the neurobehavioral stress response in infancy and prevents pups from learning about threat within mother-infant interactions.

Keywords:

• Social buffering
• Amygdala
• Paraventricular nucleus
• Corticosterone
• Norepinephrine

Additional information

Funding

This work was supported by the NIH under Grants DC009910, MH091451, HD083217 to RS, and by the NSF under Grant BCS-1439258 to MG, RS, MS, and NT.