Attending to the distractor and old/new discriminations in negative priming

When participants ignore an irrelevant distractor they typically show impaired responding to that item if it becomes the relevant stimulus on a subsequent trial. In Experiment 1 (N = 64), a masked white colour name was presented briefly before a Stroop display. Negative priming in colour naming occurred when the colour of the lettering for the Stroop stimulus matched the colour name displayed in the first display, consistent with the proposal of temporal discrimination theory that negative priming arises because a recurrence of an unattended stimulus cannot readily be classified as old or new. Experiment 2 (N = 32) replicated negative priming in the interleaved-word display where participants had to name the red word from a pair of red and green words. In Experiment 3 (N = 32) and Experiment 4 (N = 28) the participants were required to attend to but not respond to the words in the prime display and name one of two interleaved words in the probe display. Negative priming was observed in this arrangement, consistent with the episodic retrieval theory of negative priming. The temporal discrimination model may need to be extended to situations in which the attended stimuli have different responses attached to them.

Movement trajectories in the presence of a distracting stimulus: Evidence for a response activation model of selective reaching

Consistent with action-based theories of attention, the presence of a nontarget stimulus in the environment has been shown to alter the characteristics of goal-directed movements. Specifically, it has been reported that movement trajectories veer away from (Howard & Tipper, 1997) or towards (Welsh, Elliott, & Weeks, 1999) the location of a nontarget stimulus. The purpose of the experiments reported in this paper was to test a response activation model of selective reaching conceived to account for these variable results. In agreement with the model, the trajectory changes in the movements appear to be determined by the activation levels of each competing response at the moment of response initiation. The results of the present work, as well as those of previous studies, are discussed within the framework of the model of response activation.

Regulation of MAPK activation, AP-1 transcription factor expression and keratinocyte differentiation in wounded fetal skin

Fetal epithelium retains the ability to re-epithelialize a wound in organotypic culture in a manner not dependent on the presence of underlying dermal substrata. This capacity is lost late in the third trimester of gestation or after embryonic day 17 (E-17) in the rat such that embryonic day 19 (E-19) wounds do not re-epithelialize. Moreover, wounds created in E-17 fetuses in utero heal in a regenerative, scar-free fashion. To investigate the molecular events regulating re-epithelialization in fetal skin, the wound-induced expression profile and tissue localization of activator protein 1 (AP-1) transcription factors c-Fos and c-Jun was characterised in E-17 and E-19 skin using organotypic fetal cultures. The involvement of mitogen-activated protein kinase (MAPK) signaling in mediating wound-induced transcription factor expression and wound re-epithelialization was assessed, with the effect of wounding on the expression of keratinocyte differentiation markers determined. Our results show that expression of AP-1 transcription factors was induced immediately by wounding and localized predominantly to the epidermis in E-17 and E-19 skin. c-fos and c-jun induction was transient in E-17 skin with MAPK-dependent c-fos expression necessary for the re-epithelialization of an excisional wound in organotypic culture. In E-19 skin, AP-11 expression persisted beyond 12 h post-wounding, and marked upregulation of the keratinocyte differentiation markers keratin 10 and loricrin was observed. No such changes in the expression of keratin 10 or loricrin occurred in E-17 skin. These findings indicate that re-epithelialization in fetal skin is regulated by wound-induced AP-1 transcription factor expression via MAPK and the differentiation status of keratinocytes.