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Studies have applied single-reference-point or safety margin hypotheses to examine how advanced traveler information affects travel behaviors. However, these theories may fail to fully capture the trade-offs among origin departure time, airport access time, and terminal processing time in terms of airport ground access behaviors. In this study, we developed a tri-reference-point hypothesis and assumed that the rate of change of utility may change at the air passenger’s preferred (PAT), earliest acceptable (EAT), and latest acceptable (LAT) airport arrival times. With an empirical data set collected from 304 passengers at Taipei Songshan Airport, the study examined the tri-reference-point hypothesis by analyzing airport ground access mode choice behaviors with a pooled framework that combined revealed and stated preferences. Moreover, the study developed four alternative specifications for schedule delay variables, assuming that air passengers used different reference points to determine relative gains and losses of the expected airport arrival time. The specifications included selecting both EAT and LAT as the zero-utility points (an indifference-band specification) and either one of PAT, EAT, and LAT as the single zero-utility point. Regardless of which specification was employed for schedule delay variables, the tri-reference-point hypothesis was generally supported. In particular, a significant difference of the rate of change of utility around PAT, EAT, and LAT was identified in the analysis results. When managing increasing road travel times and increasingly congested terminals, air passengers were more willing to retime their origin departure time to an earlier time than to switch their ground access mode. The implications of the analysis results for airport ground access management are discussed in the study.

Acupuncture has been used for treating drug addiction since the 1970s, but little is known about the mechanisms by which acupuncture affects drug cue-induced relapse. The transcription factor delta-FosB (ΔFosB) plays a critical role in behavior and pathology after chronic use of cocaine. ΔFosB regulates glutamate receptor signaling and dendritic spine morphology in animal models. This experimental study compared the effects of electroacupuncture (EA) at acupoints LI4 and LI11 with those of another potentially beneficial intervention, gabapentin (GBP), alone or in combination, on reinstatement of cocaine-induced conditioned place preference (CPP) and levels of ΔFosB and glutamate receptor subunit 2 (GluR2) expression in the nucleus accumbens (NAc). EA at LI4 and LI11 significantly prevented cue-induced cocaine CPP reinstatement, whereas needle insertion without electrical stimulation at these acupoints had no such effect. EA also significantly attenuated cocaine-induced increases in ΔFosB and GluR2 expression in the NAc. Unexpectedly, these effects were reversed when GBP was combined with EA. Treatment with EA at LI4 and LI11 prevented cocaine-induced increases in dendritic spine density in the NAc core and shell. Our results suggest that EA at LI4 and LI11 may prevent cocaine relapse by modulating ΔFosB and GluR2 expression, as well as dendritic spine density.

Dendritic arbor architecture profoundly impacts neuronal connectivity and function, and aberrant dendritic morphology characterizes neuropsychiatric disorders. Here, we identify the adhesion-GPCR BAI1 as an important regulator of dendritic arborization. BAI1 loss from mouse or rat hippocampal neurons causes dendritic hypertrophy, whereas BAI1 overexpression precipitates dendrite retraction. These defects specifically manifest as dendrites transition from growth to stability. BAI1-mediated growth arrest is independent of its Rac1-dependent synaptogenic function. Instead, BAI1 couples to the small GTPase RhoA, driving late RhoA activation in dendrites coincident with growth arrest. BAI1 loss lowers RhoA activation and uncouples it from dendrite dynamics, causing overgrowth. None of BAI1’s known downstream effectors mediates BAI1-dependent growth arrest. Rather, BAI1 associates with the Rho-GTPase regulatory protein Bcr late in development and stimulates its cryptic RhoA-GEF activity, which functions together with its Rac1-GAP activity to terminate arborization. Our results reveal a late-acting signaling pathway mediating a key transition in dendrite development.