Stress during adolescence is a known risk factor for neuropsychiatric disorders later in life, but how different factors alter the susceptibility to lasting cognitive or affective impairment is only partially understood. Here, we asked whether activin, a member of the TGF-β family, has a role in this process, the rationale being that activin affects the neural underpinnings of cognitive performance and affective behavior in the adult brain. We combined a mouse model of adolescent stress (corticosterone between postnatal days 30-45) with a transgenic mouse line expressing a dominant-negative mutant of activin receptor IB (dnActRIB). Field potential recordings from medial perforant path - granule cell synapses in hippocampal slices from adult control and corticosterone-treated wild-type and transgenic mice yielded the following results: (i) Adolescent stress reduced the input-out (I-O) relationship of the synapse in wt slices in a picrotoxin (i.e. GABAA receptor)-sensitive fashion. (ii) Under control conditions, dnActRIB slices exhibited a smaller I-O relationship than wt slices, which could be rescued by picrotoxin. (iii) Corticosterone pre-treatment did not diminish the I-O relationship in dnActRIB slices. (iv) In slices from unstressed mice, short-term plasticity (STP, in response to 5 stimuli @ 20 Hz) did not differ between genotypes. (v) When re-examined after adolescent corticosterone, both groups showed a significant decrease in STP, which appeared stronger in wt slices. Our preliminary results suggest that adolescent stress entails lasting effects on basic indices of signal transfer between entorhinal cortex and dentate gyrus, the severity of which may be modulated by activin receptor signaling.