The repeated use of psychostimulants in humans has been associated with progressive enhancement of anxiety, panic attacks, and eventually paranoid psychosis. The appearance of such behaviors has been termed behavioral sensitization, which forms part of the basic pathological mechanisms involved in drug addiction. Psychostimulants act via a circuit involving the ventral tegmental area (VTA), prefrontal cortex (PFC), and nucleus accumbens. The PFC sends glutamatergic projections that activate dopaminergic neurons in the VTA. These projections provide an extremely important excitatory drive necessary for the development of sensitization. The effects of cocaine administration on the response of dopaminergic VTA cells to activation of the PFC have not been reported. Here the effects of acute cocaine administration on VTA cell response to PFC stimulation are examined. Statistical analysis of the changes in spontaneous activity and evoked response revealed a significant decrease in spontaneous activity at 1.0 mg/kg i.v. after cocaine treatment compared to baseline levels. The net effect was an increase in signal‐to‐noise ratio. Treatment with MK‐801 at a dose of 2 mg/kg showed that the excitatory response was, at least partially, NMDA‐mediated. Prazosin pretreatment (0.5 mg/kg i.p.) did not prevent a significant decrease in spontaneous activity brought about by cocaine (15 mg/kg, i.p.). Nonetheless, prazosin alone induced a significant decrease in the response to PFC stimulation when compared to baseline. In addition, iontophoretic application of norepinephrine (NE) onto VTA cells revealed that NE potentiated (19.2%), enhanced (26.9%), or suppressed (46.2%) the glutamate‐evoked response in VTA cells. The results suggest that a possible role of cocaine in the process of sensitization might be to amplify the PFC‐induced excitation at the VTA. Since the iontophoretic release of NE in almost half of the sampled cells produced similar effects to those of cocaine it may suggest a possible NE‐mediated mechanism for cocaine actions.

Although functional analysis (FA) methodology has been used to identify treatments for elopement, the results of some of these analyses have been confounded by the retrieval of participants. Recently, researchers have used latency-based FAs, which eliminate the retrieval component during a session, to assess elopement. In the current study, we replicated previous research using latency-based FAs to assess elopement exhibited by three children with autism. In addition, we evaluated function-based treatments for each participant. The treatments effectively decreased elopement for all participants, partially validating the latency-based FAs. K E Y W O R D Selopement, functional analysis, latency-based measure | INTRODUCTIONElopement is defined as leaving a designated area without caregiver permission (Lehardy et al., 2013). Research suggests that approximately 25%-50% of children diagnosed with autism spectrum disorder (ASD) elope. In community contexts, elopement poses a risk of bodily harm (e.g., when eloping into traffic or to a body of water) and individuals who elope are often required to remain in restricted environments to reduce their risk of injury (Anderson et al., 2012). This risk also places a significant burden on the caregiver. Due to the potentially lifethreatening nature of elopement, the development of accurate and efficient assessment and treatment methods is needed.Functional analysis (FA) has been used to address elopement (Boyle & Adamson, 2017); however, the results of many of these analyses have been difficult to interpret. Elopement often produces sudden reactions from caregivers to intervene. The response required from caregivers to maintain safety may inadvertently strengthen

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