[Effect of maternal antepartum psychological therapy upon early infant temperament].

OBJECTIVE: To find out whether there was any change in early infant temperament after mothers had received group psychological therapy on depression and anxiety during pregnancy period. METHODS: A total of 800 subjects meeting the inclusion criteria, without the exclusion criteria and willing to sign the informed consent were recruited randomly from Shanghai International Peace Maternity & Child Health Hospital in their l6th-20th weeks of pregnancy. They were randomized into the therapy group and the control group by the doll randomization table. Women in the therapy group would have a group psychological therapy for 6 times, 1.5 hours each time, while the control group not. The group psychological therapy included therapist introduction and participatory discussion. The therapy concerned the antepartum and postpartum depression, the risk factors concerned with antepartum and postpartum depression, antepartum and postpartum anxiety, psychological defense theory, reflex training and spouse lesson. Mothers reported their babies' infant temperament by filling the early infant temperament questionnaire (EITQ) within 3 months post-delivery. RESULTS: The percent of easy infant temperament type was 87.9% in the psychological therapy group and 81.7% in the hard group. And there was significant difference between two groups (chi2 = 4.530, upsilon=1, P = 0.033). And there were significant differences in the dimensions of approach-withdrawal and threshold of responsiveness in infant temperament between two groups. CONCLUSION: The maternal antepartum psychological therapy can increase the ratio of easy infant temperament. And it has effects upon the temperament dimensions of approach-withdrawal and threshold of responsiveness.

Despair-associated memory requires a slow-onset CA1 long-term potentiation with unique underlying mechanisms.

The emotion of despair that occurs with uncontrollable stressful event is probably retained by memory, termed despair-associated memory, although little is known about the underlying mechanisms. Here, we report that forced swimming (FS) with no hope to escape, but not hopefully escapable swimming (ES), enhances hippocampal α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)-dependent GluA1 Ser831 phosphorylation (S831-P), induces a slow-onset CA1 long-term potentiation (LTP) in freely moving rats and leads to increased test immobility 24-h later. Before FS application of the antagonists to block S831-P or N-methyl-D-aspartic acid receptor (NMDAR) or glucocorticoid receptor (GR) disrupts LTP and reduces test immobility, to levels similar to those of the ES group. Because these mechanisms are specifically linked with the hopeless of escape from FS, we suggest that despair-associated memory occurs with an endogenous CA1 LTP that is intriguingly mediated by a unique combination of rapid S831-P with NMDAR and GR activation to shape subsequent behavioral despair.