The Power of an Infant\u27s Smile: Maternal Physiological Responses to Infant Emotional Expressions

Infant emotional expressions, such as distress cries, evoke maternal physiological reactions. Most of which involve accelerated sympathetic nervous activity. Comparatively little is known about effects of positive infant expressions, such as happy smiles, on maternal physiological responses. This study investigated how physiological and psychological maternal states change in response to infants\u27 emotional expressions. Thirty first-time mothers viewed films of their own 6- to 7-month-old infants\u27 affective behavior. Each observed a video of a distress cry followed by a video showing one of two expressions (randomly assigned): a happy smiling face (smile condition) or a calm neutral face (neutral condition). Both before and after the session, participants completed a self-report inventory assessing their emotional states. The results of the self-report inventory revealed no effects of exposure to the infant videos. However, the mothers in the smile condition, but not in the neutral condition, showed deceleration of skin conductance. These findings demonstrate that the mothers who observed their infants smiling showed decreased sympathetic activity. We propose that an infant\u27s positive emotional expression may affect the branch of the maternal stress-response system that modulates the homeostatic balance of the sympathetic and parasympathetic nervous systems

Means and SEMs for skin conductance change from baseline for each condition and phase.

<p>Means with an asterisk are significantly different, <i>p</i> < .05. Means with two asterisks are significantly different, <i>p</i> < .001.</p

Schematic illustration of experimental procedure for each condition.

<p>Schematic illustration of experimental procedure for each condition.</p

Study of the mechanisms involved in the vasorelaxation induced by (−)-epigallocatechin-3-gallate in rat aorta

1. This study investigated several mechanisms involved in the vasorelaxant effects of (−)-epigallocatechin-3-gallate (EGCG). 2. EGCG (1 μM–1 mM) concentration dependently relaxed, after a transient increase in tension, contractions induced by noradrenaline (NA, 1 μM), high extracellular KCl (60 mM), or phorbol 12-myristate 13-acetate (PMA, 1 μM) in intact rat aortic rings. In a Ca(2+)-free solution, EGCG (1 μM–1 mM) relaxed 1 μM PMA-induced contractions, without previous transient contraction. However, EGCG (1 μM–1 mM) did not affect the 1 μM okadaic acid-induced contractions. Removal of endothelium and/or pretreatment with glibenclamide (10 μM), tetraethylammonium (2 mM) or charybdotoxin (100 nM) plus apamin (500 nM) did not modify the vasorelaxant effects of EGCG. In addition, EGCG noncompetitively antagonized the contractions induced by NA (in 1.5 mM Ca(2+)-containing solution) and Ca(2+) (in depolarizing Ca(2+)-free high KCl 60 mM solution). 3. In rat aortic smooth muscle cells (RASMC), EGCG (100 μM) reduced increases in cytosolic free Ca(2+) concentration ([Ca(2+)](i)) induced by angiotensin II (ANG II, 100 nM) and KCl (60 mM) in 1.5 mM CaCl(2)-containing solution and by ANG II (100 nM) in the absence of extracellular Ca(2+). 4. In RASMC, EGCG (100 μM) did not modify basal generation of cAMP or cGMP, but significantly reversed the inhibitory effects of NA (1 μM) and high KCl (60 mM) on cAMP and cGMP production. 5. EGCG inhibited the enzymatic activity of all the cyclic nucleotide PDE isoenzymes present in vascular tissue, being more effective on PDE2 (IC(50)∼17) and on PDE1 (IC(50)∼25). 6. Our results suggest that the vasorelaxant effects of EGCG in rat aorta are mediated, at least in part, by an inhibition of PDE activity, and the subsequent increase in cyclic nucleotide levels in RASMC, which, in turn, can reduce agonist- or high KCl concentration-induced increases in [Ca(2+)](i)