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151.
Prevalence of resurgence of destructive behavior when thinning reinforcement schedules during functional communication training
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Adam M. Briggs Wayne W. Fisher Brian D. Greer Ryan T. Kimball 《Journal of applied behavior analysis》2018,51(3):620-633
Functional communication training is a well‐established treatment for socially reinforced destructive behavior that typically includes differential reinforcement of the functional communication response (FCR) in combination with extinction of destructive behavior. However, when the schedule of reinforcement for the FCR is thinned, destructive behavior may resurge (e.g., Greer, Fisher, Saini, Owen, & Jones, 2016). Currently, data are unavailable on the prevalence and characteristics of resurgence during reinforcement schedule thinning. In this study, we evaluated the prevalence of resurgence during reinforcement schedule thinning on a per‐case and per‐schedule‐step basis and also evaluated the magnitude of resurgence in relation to the functions of destructive behavior. We observed resurgence in 19 of the 25 (76%) applications of reinforcement schedule thinning. In some cases, the magnitude of resurgence exceeded the mean levels of destructive behavior observed in baseline. We discuss these results relative to prior translational and applied research on resurgence. 相似文献
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Adam M. Briggs Claudia L. Dozier Amber N. Lessor Bertilde U. Kamana Rachel L. Jess 《Journal of applied behavior analysis》2019,52(4):956-973
Previous research indicates that manipulating dimensions of reinforcement during differential reinforcement of alternative behavior (DRA) for situations in which extinction cannot be implemented is a potential approach for treating destructive behavior. Therefore, we replicated and extended previous research by determining (a) the conditions under which DRA without extinction decreased and maintained low levels of destructive behavior and (b) whether intervention effects maintained during reinforcement schedule thinning for the alternative response (i.e., compliance). Results showed that effective treatments were developed in the absence of extinction by manipulating the quality of reinforcement for compliance for 2 participants and by combining manipulations of the magnitude and quality of reinforcement for compliance for the other 2 participants. However, maintaining treatment effects during reinforcement schedule thinning required combining the magnitude and quality of reinforcement for 3 of the 4 participants. We discuss the clinical utility of this approach, review limitations of the study, and suggest directions for future research. 相似文献
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Philosophical Studies - We show that five important elements of the ‘nomological package’—laws, counterfactuals, chances, dispositions, and counterfactuals—needn’t be... 相似文献
154.
Lisa Janet Cohen Bernard Gorman Jessica Briggs Min Eun Jeon Tal Ginsburg Igor Galynker 《Suicide & life-threatening behavior》2019,49(2):413-422
In this study, we introduce the construct of the suicidal narrative, a hypothetical personal narrative linked to imminent suicide, and explore its relationship to near‐term suicidal risk and the suicide crisis syndrome (SCS). Psychiatric outpatients (N = 289) were administered the Columbia Suicide‐Severity Rating Scale (C‐SSRS), Suicide Crisis Inventory (SCI), and Suicide Narrative Inventory (SNI), a novel instrument combining the documented risk factors of Thwarted Belongingness, Perceived Burdensomeness, Humiliation, Social Defeat, Goal Disengagement, and Goal Reengagement. Dimensional measures of past month, lifetime, and past suicidal phenomena, incorporating ideation and behavior, were calculated from the C‐SSRS. Structural equation modeling was used to explore the interaction among variables. Factor analysis of the SNI yielded two orthogonal factors, termed Interpersonal and Goal Orientation. The former factor was comprised of Perceived Burdensomeness, Social Defeat, Humiliation, and Thwarted Belongingness, the latter of Goal Disengagement and Goal Reengagement. The Interpersonal factor correlated with both SCS severity and suicidal phenomena in each time frame and the Goal Orientation factor with no other variable. As hypothesized, the proposed model was significant for the past month only. Our findings support the construct of the suicidal narrative and its function as a near‐term suicidal risk factor. 相似文献
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Rachel Briggs Adrienne Epps Naomi Brookes Robyn Tate Suncica Lah 《Journal of Neuropsychology》2023,17(1):193-209
The Westmead Post-Traumatic Amnesia Scale (WPTAS) is routinely used for the assessment of post-traumatic amnesia (PTA) in children who sustained traumatic brain injury (TBI). Yet, the WPTAS' predictive validity for functional outcomes is largely unknown. We aimed to determine whether PTA duration measured by the WPTAS (i) differentially predicts functional outcomes and (ii) contributes to predictions of outcomes beyond the Glasgow Coma Scale (GCS) in children who sustained TBI. Participants were children and adolescents with moderate-to-severe TBI (n = 55) aged 8–15 years. PTA duration was assessed with the WPTAS. Outcomes at the first outpatient follow-up were scored on the Kings Outcome Scale for Childhood Head Injury (KOSCHI) and the TBI Outcome Domain Scale-Extended (ODS-E). Longer PTA and lower GCS were both significantly correlated with worse (i) global outcomes: presence of disability on the KOSCHI and lower score on the ODS-E and (ii) select specific outcomes on the ODS-E: mobility, mood and cognition. PTA duration predicted cognitive outcome on the ODS-E independently, beyond GCS. Together, PTA duration and GCS, predicted the global KOSCHI outcome, as well as the ODS-E mobility and mood outcomes. Neither GCS nor PTA duration correlated with the ODS-E communication, impulsivity/disinhibition, headache, fatigue, sensory impairments or somatic complaints outcomes. PTA duration measured by the WPTAS is a significant unique predictor of functional cognitive outcomes in children who sustained moderate-to-severe TBI, and in combination with the GCS, a significant predictor of global, and several specific functional outcomes. 相似文献
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Sherri B. Briggs Reilly Hannapel Janavi Ramesh Marise B. Parent 《Learning & memory (Cold Spring Harbor, N.Y.)》2021,28(6):187
Research into the neural mechanisms that underlie higher-order cognitive control of eating behavior suggests that ventral hippocampal (vHC) neurons, which are critical for emotional memory, also inhibit energy intake. We showed previously that optogenetically inhibiting vHC glutamatergic neurons during the early postprandial period, when the memory of the meal would be undergoing consolidation, caused rats to eat their next meal sooner and to eat more during that next meal when the neurons were no longer inhibited. The present research determined whether manipulations known to interfere with synaptic plasticity and memory when given pretraining would increase energy intake when given prior to ingestion. Specifically, we tested the effects of blocking vHC glutamatergic N-methyl-D-aspartate receptors (NMDARs) and activity-regulated cytoskeleton-associated protein (Arc) on sucrose ingestion. The results showed that male rats consumed a larger sucrose meal on days when they were given vHC infusions of the NMDAR antagonist APV or Arc antisense oligodeoxynucleotides than on days when they were given control infusions. The rats did not accommodate for that increase by delaying the onset of their next sucrose meal (i.e., decreased satiety ratio) or by eating less during the next meal. These data suggest that vHC NMDARs and Arc limit meal size and inhibit meal initiation.Research into the higher-order cognitive controls of eating behavior has demonstrated that hippocampal neurons, which are critical for learning and memory, also regulate energy intake (Benoit et al. 2010; Parent 2016; Kanoski and Grill 2017). The hippocampus is functionally divided along its longitudinal axis into dorsal (posterior in primates) and ventral (anterior in primates) poles (Moser and Moser 1998; Fanselow and Dong 2010; Strange et al. 2014). Generally, dorsal hippocampal (dHC) neurons are necessary for episodic and spatial memory, whereas ventral hippocampal (vHC) neurons are essential for affective and motivational processes and emotional memory (Fanselow and Dong 2010; Strange et al. 2014). dHC and vHC have different anatomical connections, cellular and circuit properties and patterns of gene expression that likely contribute to the different functions that they serve (Moser and Moser 1998; Thompson et al. 2008; Dong et al. 2009; Barkus et al. 2010; Fanselow and Dong 2010; Bienkowski et al. 2018).vHC neurons, in particular, are poised to integrate energy-related signals with mnemonic processes because they contain receptors for numerous food-related signals (Kanoski and Grill 2017) and project to several brain regions critical for food intake (Namura et al. 1994; Cenquizca and Swanson 2006; Radley and Sawchenko 2011; Hsu et al. 2015b). vHC lesions increase food consumption and body mass (Davidson et al. 2009, 2012, 2013), and activation of vHC receptors for gut hormones affects food intake and food-related memory (Kanoski et al. 2011, 2013; Hsu et al. 2015a, 2017, 2018). Additionally, vHC glutamatergic projections to the bed nucleus of the stria terminalis, lateral septum, and prefrontal cortex inhibit energy intake (Sweeney and Yang 2015; Hsu et al. 2017).It is possible that vHC neurons contribute to the representation of the memory of a meal and inhibit subsequent intake. In support, we have shown that vHC neurons inhibit energy intake during the postprandial period. Specifically, optogenetic inhibition of vHC principle glutamatergic neurons given after the end of a sucrose or chow meal, timed to occur when the memory of the meal would be undergoing consolidation, accelerates the onset of the next meal and increases the amount eaten during the next meal when the neurons are no longer inhibited (Hannapel et al. 2019). Inactivation of these neurons given after a saccharin meal also hastens the initiation of the next saccharin meal and increases the size of that next meal, suggesting that vHC inhibition does not increase intake by disrupting the processing of interoceptive visceral signals (Hannapel et al. 2019).If vHC neurons inhibit intake through a process that involves memory, then well-defined molecular events necessary for vHC synaptic plasticity should play a role in controlling meal timing and meal size because synaptic plasticity at hippocampal excitatory synapses is a critical mechanism underlying memory formation (Bailey et al. 2015; Bartsch and Wulff 2015). Activation of glutamatergic N-methyl-D-aspartate receptors (NMDARs) is required for most forms of hippocampal synaptic plasticity (Malenka and Nicoll 1993; Volianskis et al. 2015). NMDAR-dependent increases in intracellular calcium activate proteins and stimulate mRNA synthesis and protein translation that collectively act to increase glutamate AMPA receptor function in the postsynaptic cell, thereby increasing glutamate signaling and synaptic strength (Shanley et al. 2001; Bevilaqua et al. 2005; Herring and Nicoll 2016). Synaptic plasticity in vHC is NMDAR-dependent and vHC NMDARs are often necessary for vHC-dependent memory (Zhang et al. 2001; Xu et al. 2005; Kent et al. 2007; Czerniawski et al. 2012; Portero-Tresserra et al. 2014; Zhu et al. 2014; Clark et al. 2015; Maggio et al. 2015). Of note, feeding-related hormones such as insulin and leptin enhance NMDAR functionality in hippocampal cultured neurons and slices (Liu et al. 1995; Shanley et al. 2001).Hippocampal synaptic plasticity is also dependent on the activation of the immediate early gene (IEG) activity-regulated cytoskeleton-associated protein (Arc). Arc is considered a master regulator of synaptic plasticity (Bramham et al. 2010; Korb and Finkbeiner 2011; Shepherd and Bear 2011). It is downstream from many molecular signaling pathways and is necessary for virtually every type of synaptic plasticity (Bramham et al. 2008; Korb and Finkbeiner 2011; Shepherd and Bear 2011). Learning experiences produce small but significant increases in Arc that are typically maximal within 15 min of the experience, and unlike other IEGs, Arc expression reflects synaptic plasticity rather than neuronal activity (Fletcher et al. 2006; Guzowski et al. 2006; Carpenter-Hyland et al. 2010). vHC Arc is necessary for memory consolidation because disrupting vHC Arc expression with Arc antisense (anti-Arc) oligodeoxynucleotides (ODN) disrupts vHC-dependent memory (Czerniawski et al. 2011, 2012; Chia and Otto 2013). We have shown that sucrose consumption increases vHC Arc expression during the early postprandial period (Hannapel et al. 2017), suggesting that ingestion activates molecular processes required for synaptic plasticity in vHC.Although it is well established that vHC neurons influence energy regulation, it is unknown whether vHC neurons regulate energy intake through a process that requires NMDARs and Arc. In the present experiments, we tested the prediction that disrupting vHC NMDAR activation and Arc expression would increase meal size and decrease the interval between meals. Specifically, NMDAR antagonists or anti-Arc ODNs were infused into the vHC and subsequent intake of sucrose was assessed. 相似文献