Prenatal stress alters the development of socioemotional behavior and amygdala neuron excitability in rats.
Prenatal stress (PS) is a risk factor for neurodevelopmental disorders with diverse ages of onset and socioemotional symptoms.
Some PS-linked disorders involve characteristic social deficits, like autism spectrum disorders and schizophrenia, but PS also promotes anxiety disorders.
We propose the diversity of symptoms following PS arises from perturbations to early brain development. To this end, we characterized the effects of PS on the developmental trajectory of physiology of the amygdala, a late-developing center for socioemotional control.
We found that PS dampened socioemotional behavior and reduced amygdala neuron excitability in offspring during infancy (at postnatal days 10, 14, 17, 21), preadolescence (day 28), and adulthood (day 60).
PS offspring in infancy produced fewer isolation-induced vocalizations and in adulthood exhibited less anxiety-like behavior and deficits in social interaction. PS neurons had a more hyperpolarized resting membrane potential from infancy to adulthood and produced fewer action potentials.
Moreover, adult amygdala neurons from PS animals expressed larger action potential afterhyperpolarizations and H-current relative to controls, further limiting excitability.
Our results suggest PS can suppress socioemotional behavior throughout development and produce age-specific alterations to amygdala physiology.