Increased fearfulness has been associated with adrenocortical activation. Maternal corticosterone (B) treatment increases egg B, and elevated B in ovo enhances chick avoidance of humans. Quail selected for exaggerated (high stress, HS) rather than reduced (low stress, LS) plasma B response to stress are more fearful, and more B is found in HS hen eggs. Thus, we used tonic immobility (TI) and hole-in-the-wall box (HWB) emergence tests to assess fear in chicks hatched from eggs of LS and HS hens implanted with B or no B (CON). The number of inductions required to attain TI, latency to first alert head movement, and duration of TI were determined in one study and the latency until first vocalization (LATVOC), numbers of vocalizations (VOCS), proportions of chicks vocalizing, and the latencies to head (HE) and full-body (FE) emergence from a HWB were assessed in another. The LS chicks required less inductions (P < 0.0005) and had shorter latency to first alert head movement (P < 0.02) than HS chicks, although the duration of TI was unaffected by any of the treatments. During the acclimation period of the HWB tests, more (proportions of chicks vocalizing; P < 0.0001) HS chicks alarm-called sooner (LATVOC; P < 0.0001) and more often (VOCS; P < 0.0001) than did LS chicks, and, although maternal implant treatment did not affect LATVOC, progeny of B-implanted hens showed a tendency toward less (P < 0.07) VOCS than the CON. Chicks hatched from eggs of B-implant mothers also took longer to achieve HE (P < 0.06) and FE (P < 0.05) from the HWB than did their CON counterparts. Stress line, implantation treatment, and their interaction did not alter HE or FE responses. The data suggest that quail stress line genome may or may not be affecting certain fear and alarm responses in chicks via the same mechanism(s) that underlies how elevating maternal B increases egg levels of B that in turn alters the fear behavior of progeny.