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RATIONALE: Alcohol use disorder (AUD) is a debilitating physiological and psychiatric disorder which affects individuals globally. The current pharmacological interventions to treat AUD are limited, and hence there is an urgent need for a novel pharmacological therapy which can be effective and safe across the population. OBJECTIVE: We aimed to investigate a novel neutral cannabinoid receptor-1 (CB1R) antagonist, AM6527, in several preclinical models of ethanol consumption using male and female C57BL6/J mice. METHODS: Independent groups of male and female mice were subjected to repeated cycles of drinking in the dark (DID), or intermittent access to alcohol (IAA) procedures. Twenty minutes prior to ethanol access in each procedure, animals were treated with intraperitoneal injections of either 1, 3, and 10 mg/kg of AM6527 or its respective vehicle. Acamprosate (100, 200, 300, and 400 mg/kg) or its respective vehicle was used as a positive control. Separate groups of male mice were subjected to a chain schedule of ethanol reinforcement to gain access to ethanol wherein completion of a fixed interval (FI; 5 min) schedule (link 1: "Seeking") was reinforced with continuous access to ethanol (fixed ratio; FR1) for up to 1.8 g/kg (link 2: "consumption"). All the animals were treated with 1, 3, and 10 mg/kg of AM6527 or its respective vehicle 20 mins prior to the start of the FI chain of the procedure. Separately, AM6527 was also evaluated in male and female mice undergoing acute ethanol withdrawal following 8 weeks of intermittent or continuous access to 20% ethanol drinking. RESULTS: In both DID and IAA procedures, AM6527 reduced ethanol consumption in a dose-related manner in both male and female mice. AM6527 produced no tolerance in the DID procedure; mice treated with 3 mg/kg of AM6527 for 3 weeks continuously drank significantly smaller amounts of ethanol as compared to vehicle-treated mice over a period of three DID cycles. Moreover, in the IAA procedure, AM6527 caused an increase in water intake over the 24-h period. Acamprosate transiently reduced ethanol intake in male mice in both the DID and the IAA procedures but failed to produce any significant effect in female mice. AM6527 also produced a decrease in the FI responding ("ethanol seeking") in animals trained to self-administer ethanol. Lastly, AM6527 mitigated neurological withdrawal signs, i.e., handling induced convulsions (HIC) in mice undergoing acute ethanol withdrawal. CONCLUSIONS: Current findings support previous studies with CB1R neutral antagonist in reducing voluntary ethanol intake and seeking behavior. Based on results shown in this work, AM6527 can be developed as a first in class CB1R neutral antagonist to treat AUD in both males and females.

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BACKGROUND: Dopamine is implicated in the effort-based control of motivational processes; however, whether tonic dopamine regulates the effort-cost impact on motivation, is still debated. AIMS: The rats lacking the dopamine transporter (DAT), which have dramatically increased levels of the synaptic dopamine, were used in the present study to elucidate the role of the synaptic dopamine in motivational processes. METHODS: To study the reward-related processes, the progressive ratio 3 (PR3) operant schedule of food reinforcement (the ratio increases by 3 after each earned reinforcer) was performed in adult male rats (DAT knockouts (DAT-KO), heterozygotes (DAT-HT) and wild-types (DAT-WT)). RESULTS: During the PR3 session, the response rate of DAT-KO rats was gradually increased following the augmented required number of responses. In contrast, the local response rate of DAT-WT and DAT-HT decreased. d-Amphetamine sulfate salt (3 mg/kg, i.p.) altered the local response rate dynamics in DAT-WT, which became similar to that of DAT-KO. Interestingly, the reduction in response rate at low effort demands was associated with decreased rate of entries into the magazine tray in DAT-WT rats treated with amphetamine (3 mg/kg) but not in DAT-KO rats. CONCLUSIONS: Our results suggest that the elevated tonic synaptic dopamine can strongly affect motivation/effort-cost relation in rodents.

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It has been suggested that avoiding choice represents an anxiety-avoidance strategy, which has not been investigated in the context of social media. To this end, the current study explored the relationship between social media dependency and a preference for 'forced' choice, along with its association with anxiety, intolerance of uncertainty, and experiential avoidance. The sample comprised 151 volunteer participants (18-32 years) who completed a psychometric test battery, including: the Bergen Social Media Addiction Scale; Spielberger Trait Anxiety Inventory; Intolerance of Uncertainty Scale; and Brief Experiential Avoidance Questionnaire. They also undertook a behavioural assessment based on a paradigm developed for pigeons, in which they selected either a situation with a free choice of alternatives, and one with a forced choice. Intolerance of uncertainty mediated the relationship between social media dependency and anxiety. In addition, those with lower social media dependency preferred being able to choose the contingency they worked on, while those with higher scores exhibited no such preference. This partly confirmed that social media dependency is associated with a reduced preference for freedom, but does not suggest social media dependency actively produced a preference for a lack of freedom. The speed of decision making was also faster in those with high social media dependency scores, in line with previous findings that they show higher levels of impulsive behaviours. The results suggest that anxiety and social media dependency are related, and fear of uncertainty and is linked with digital experiential avoidance.

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Progressive ratio (PR) schedules have been widely used to study motivation to work for a reinforcer. After a post-reinforcer pause, subjects engage in pressing a lever until a reinforcer is obtained. However, the discrete nature of lever presses allows alternative behaviors during inter-response time and has led to several behavioral explanations of pauses and work time. A progressive hold-down (PH) is incompatible with alternative responses and may allow a precise estimation of work time. Performance of rats trained in both PR and PH that received sucrose or intracranial self-stimulation (ICSS) as reinforcer were compared. We observed that rats mastered the PR and PH schedules. Post-reinforcer pauses (PSRP), work time and inter-reinforcer time increased as a function of the response or hold requirement. However, rats' performance suggested that the PH progression may be experienced by the rats as easier that the PR progression. Elimination of consummatory behavior with ICSS reduced post-reinforcer pause in accordance with predictions of explanatory models of fixed and variable schedules of reinforcement. In the case of PH performance, pauses showed little variation across intermediate requirements but increased rapidly on later requirements; since rats controlled their pause length and work time was close to the hold requirement, time allocation between PR and PH schedules diverged. Finally, the Mathematical Principles of Reinforcement model of Bradshaw and Killeen (Psychopharmacology 2012, 222: 549) rendered a good description of the performance in both PR and PH schedules.

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RATIONALE: Alcohol consumption is a common antecedent of aggressive behavior. The effects of alcohol on the decision to engage in aggression in preference over pro-social interaction are hypothesized to arise from augmented function within the medial prefrontal cortex (mPFC). OBJECTIVE: In a newly developed procedure, we studied social decision-making in male C57BL/6 J mice based on preferentially seeking access to either sociosexual interactions with a female partner or the opportunity to attack an intruder male. While deciding to engage in aggressive vs. sociosexual behavior, corresponding neural activation was assessed via c-Fos immunoreactivity in cortical, amygdaloid and tegmental regions of interest. A further objective was to investigate how self-administered alcohol impacted social choice. METHODS: During repeated confrontations with an intruder male in their home cage, experimental mice engaged in species-specific sequence of pursuit, threat, and attack behavior within < 2 min. Mice were then conditioned to respond at one of two separate illuminated operanda in an experimental chamber (octagon) attached to their home cage; completion of 10 responses (fixed ratio 10; FR10) was reinforced by access to either a female or a male intruder which were presented in the resident's home cage. Brains were harvested following choice between the concurrently available aggressive and sociosexual options and processed for c-Fos immunoreactivity across 10 brain regions. In two separate groups, mice were trained to rapidly self-administer ethanol prior to a social choice trial in order to examine the effects of alcohol on social choice, sociosexual, aggressive acts and postures, and concurrent c-Fos activity in the mPFC and limbic regions. RESULTS AND DISCUSSION: Eight out of 65 mice consistently chose to engage in aggressive behavior in preference to sociosexual contact with a female when each outcome was concurrently available. Self-administered alcohol (experiment 1: 1.2 ± 0.02 g/kg; experiment 2: 0, 1.0, 1.5, and 1.8 g/kg) increased responding for the aggressive option in mice that previously opted predominantly for access to sociosexual interactions with the female. When choosing the aggressive, but not the sociosexual option, the prelimbic area of the mPFC revealed increased c-Fos activity, guiding future detailed inquiry into the neural mechanisms for aggressive choice.

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RATIONALE: The attraction to alcohol can be greatly increased when it is consumed in a social context. While pro-social interactions can potentiate voluntary alcohol drinking under some conditions, aversive social experience (i.e., social stress) can similarly intensify alcohol consumption. OBJECTIVE: We sought to determine how exposure to different types of chronic social stress (i.e., intermittent episodes of social defeat or continuous social stress) influences alcohol consumption and the reinforcing effects of alcohol in mice with a history of drinking. METHODS: Separate cohorts of male C57BL/6J mice were exposed to either 10 days of continuous or intermittent social defeat stress. In experiment 1, mice were assigned to 20% w/v alcohol consumption in a two-bottle choice protocol both prior to and after exposure to social defeat stress. In a second experiment, mice engaged in an operant response sequence to gain access to alcohol wherein completion of a fixed interval (FI; 5 min) schedule was reinforced with continuous access to alcohol (fixed ratio; FR1) for up to 1.8 g/kg. Alcohol-reinforced responding and subsequent alcohol consumption were assessed daily for 4 weeks prior to the 10-day social stress exposure and for 6-week post-stress. Machine learning was implemented to standardize the analysis of defeat behaviors exhibited by the intruder mouse during confrontation with an attacking resident. RESULTS: In mice with a prior history of alcohol drinking, intermittent episodes of social defeat stress produced a significant increase in 20% EtOH consumption in preference over concurrently available water. This increased intake persisted for at least 6 weeks after the final social stress experience. Intermittently stressed mice also accelerated their anticipatory responding during the fixed interval component of the operant response chain that was reinforced by alcohol. Neither unstressed controls nor mice exposed to continuous social stress exhibited significant increases in alcohol consumption and alcohol reinforcement. DISCUSSION: Episodic social defeat stress promotes the seeking and consumption of alcohol, extending earlier work to alcohol-experienced mice. We hypothesize that intermittent access to alcohol and intermittent episodes of social stress are additive and share common sensitizing neural mechanisms that engender excessive alcohol consumption.

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BACKGROUND: Individuals addicted to cocaine spend much of their time foraging for the drug. Pavlovian drug-associated conditioned stimuli exert a major influence on the initiation and maintenance of drug seeking often long into abstinence, especially when presented response-contingently, acting as conditioned reinforcers that bridge delays to drug use. The acquisition of cue-controlled cocaine seeking has been shown to depend on functional interactions between the basolateral amygdala (BLA) and the nucleus accumbens core (NAcC). However, the precise neuronal circuits underlying the acquisition of cue-controlled cocaine-seeking behavior have not been elucidated. METHODS: Here, we used a projection-specific Cre-dependent DREADD (designer receptor exclusively activated by designer drugs)-mediated causal approach to test the hypothesis that the direct projections from the BLA to the NAcC are required for the acquisition of cue-controlled cocaine-seeking behavior. RESULTS: In Sprague Dawley rats with Cre-mediated expression of the inhibitory DREADD hM4D(Gi) in the NAcC-projecting BLA neurons, treatment with clozapine N-oxide, but not vehicle, selectively prevented the impact of cocaine-associated conditioned reinforcers on cocaine seeking under a second-order schedule of reinforcement. This effect was attributable to the chemogenetic inhibition of the NAcC-projecting BLA neurons, as it was reversible, and it was absent in clozapine N-oxide-treated rats expressing an empty control virus. In contrast, chemogenetic inhibition of the anterior insula, which receives collateral projections from NAcC-projecting BLA neurons, was without effect. CONCLUSIONS: These data demonstrate that the acquisition of cue-controlled cocaine seeking that depends on the conditioned reinforcing effects of cocaine cues requires activity in the direct projections from the BLA to the NAcC.

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Lag reinforcement schedules have been shown in previous research to be an effective intervention for teaching verbal and nonverbal response variability to individuals with developmental disabilities. In more recent research, variability itself has been considered a reinforceable behavior in its own right (Susa & Schlinger, The Analysis of Verbal Behavior, 18, 125-130, 2012). Lag x schedules of reinforcement can be used to teach variability by using contingencies that require responses to differ from previous responses. The present study extended Susa and Schlinger's, The Analysis of Verbal Behavior, 18, 125-130, (2012) research by using 3 social questions instead of 1 in a random rotation and included probes to test for generality. A changing-criterion design was used to evaluate the results with one 11-year-old female participant diagnosed with autism. During baseline, the participant provided little variability, with rote responses. During the Lag 1 and Lag 2 phases, appropriate variable verbal responding increased with the use of echoic prompts, visual aids, and an error correction procedure. Further, the results also showed that the participant learned to vary her responses by demonstrating the ability to emit 11 novel prompted responses and 13 spontaneous responses. In addition, the participant was able to retain the skills learned in a maintenance probe conducted 4 weeks postintervention.

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A challenge for developing effective treatments for substance use disorders (SUDs) is understanding how environmental variables alter the efficacy of therapeutics. Environmental enrichment (EC) enhances brain development and protects against behaviors associated with drug abuse vulnerability when compared to rats reared in isolation (IC) or standard conditions (SC). EC rearing enhances the expression and function of metabotropic glutamate receptor2/3 (mGlurR2/3) and activating mGluR2/3 reduces psychostimulant self-administration (SA). However, the ability for mGluR2/3 activation to suppress amphetamine (AMP) SA in differentially reared rats is not determined. Therefore, we tested the hypothesis EC reduces AMP (SA) by augmenting mGluR2/3 function. At postnatal day 21, male Sprague-Dawley rats were assigned to EC, IC, or SC environments for 30 days. Then, they acquired AMP SA and were moved to a progressive ratio (PR) schedule of reinforcement. EC, IC, and SC rats were pretreated with LY379268 (vehicle, 0.3 and 1 mg/kg), a selective mGluR2/3 agonist, before PR behavioral sessions. Linear mixed effects analysis determined EC rats had reduced motivation for AMP SA when compared to IC or SC rats and that LY379268 dose-dependently suppressed AMP SA, but there was no evidence of an interaction. Cumming/Gardner-Altman estimation plots illustrate that the 0.3 mg/kg dose suppressed infusions in EC rats while the 1 mg/kg dose suppressed infusions in SC rats. LY379268 was incapable of suppressing the motivation for AMP SA in IC rats. Controlling for baseline differences in differentially reared rats remains a challenge. Normalizing to a baseline introduced error which is illustrated in the precision of the estimated effect size differences. The data indicate that environmental enrichment enhances the ability of a selective mGluR2/3 agonist to suppress AMP SA and indicates the functional status of the mGluR2/3 is formed during development. Therefore, environmental history must be considered when evaluating pharmacological therapeutics particularly those aimed at the mGluR2/3.

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The prevalence of autism continues to rise, yet the ability to receive treatment or caregiver training through traditional in-person methods continues to be a precluding factor for many families. Studies have shown that parent training provides benefits to caregivers and children through increased success of interventions, implementation, and generalization of skills. This study evaluated the effect of using technology for remote caregiver training of a token economy for use during routine non-preferred activities. A multiple-baseline design was implemented across two participants, through three phases. Additional surveys and interviews were conducted to evaluate social validity. Results revealed that caregivers acquired necessary skills to implement the fixed interval schedule of reinforcement with token system and participants reported experiencing greater positive interactions with the children. Limitations of this study included no data were collected on the children's behavior, nor were they trained on token economy use. Extraneous variables may have affected the results, such as unplanned household events. Results suggest that remote caregiver training can increase desirable interactions between caregiver and child, improve socially significant behaviors, and extend resources not typically available to all families.

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Procedural modifications can modulate drug effects in delay discounting, such as signaling the delay to reinforcement and altering the order in which delays are presented. Although the schedule of reinforcement can alter the rate at which animals discount a reinforcer, research has not determined if animals trained on different schedules of reinforcement are differentially affected by pharmacological manipulations. Similarly, research has not determined if using different delays to reinforcement can modulate drug effects in delay discounting. Male Sprague Dawley rats (n = 36) were split into four groups and were trained in a delay-discounting procedure. The schedule of reinforcement (fixed ratio [FR] 1 vs. FR 10) and delays to reinforcement (0, 5, 10, 20, and 50 s vs. 0, 10, 30, 60, 100 s) were manipulated for each group. Following behavioral training, rats were treated with d-amphetamine (0, 0.25, 0.5, and 1.0 mg/kg) and MK-801 (0, 0.03, and 0.06 mg/kg). Results showed that amphetamine decreased impulsive choice when a FR 1 schedule was used, but only when the short delay sequence was used. Conversely, amphetamine decreased impulsive choice when a FR 10 schedule was used, but only when rats were trained on the long delay sequence. MK-801 decreased impulsive choice in rats trained on a FR 1 schedule, regardless of delay sequence, but did not alter choice in rats trained on a FR 10 schedule. These results show that schedule of reinforcement and delay length can modulate drug effects in delay discounting.

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A common assumption in the study of fixed-interval (FI) timing is that FI performance is largely stable within sessions, once it is stable between sessions. Within-session changes in FI performance were examined in published data (Daniels and Sanabria, 2017), wherein some rats were trained on a FI 30-s schedule of food reinforcement (FI30) and others on a FI 90-s schedule (FI90). Following stability, FI90 rats were pre-fed for five sessions. Response rates declined as a function of trial, due more to latency lengthening than to run-rate reduction. Latencies were best described by a dynamic gamma-exponential mixture distribution, in which latency lengthening was driven by the growth of the criterion pulse count for a response and not by a reduction in the speed of an endogenous clock. The speed of the clock was selectively sensitive to the length of the FI; the prevalence and length of exponentially-distributed latencies were selectively sensitive to pre-feeding. These findings reveal (a) that parameters governing FI latencies are selectively sensitive to a range of manipulations, (b) a potential degradation of the criterion pulse count between consecutive sessions, and (c) a subsequent recovery of the criterion pulse count within sessions.

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Sodium cyanide (NaCN) is a commonly and widely used industrial and laboratory chemical reagent that is highly toxic. Its availability and rapid harmful/lethal effects combine to make cyanide a potential foodborne/waterborne intentional-poisoning hazard. Thus, laboratory studies are needed to understand the dose-dependent progression of toxicity/lethality following ingestion of cyanide-poisoned foods/liquids. We developed an oral-dosing method in which a standard pipette was used to dispense a sodium cyanide solution into the cheek, and the rat then swallowed the solution. Following poisoning (4-128 mg/kg), overt toxic signs were recorded and survival was evaluated periodically up to 30 hours thereafter. Toxic signs for NaCN doses higher than 16 mg/kg progressed quickly from head burial and mastication, to lethargy, convulsions, gasping/respiratory distress, and death. In a follow-on study, trained operant-behavioral performance was assessed immediately following cyanide exposure (4-64 mg/kg) continuously for 5 h and again the following day. Onset of behavioral intoxication (i.e., behavioral suppression) occurred more rapidly and lasted longer as the NaCN dose increased. This oral-consumption method with concomitant operantbehavioral assessment allowed for accurate dosing and quantification of intoxication onset, severity, and recovery, and will also be valuable in characterizing similar outcomes following varying medical countermeasure drugs and doses.

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The present study examined how systemic low doses of nicotine affect the microstructure of reinforced food-seeking behavior in rats. Rats were first given an acute saline or nicotine treatment (0.1-0.6mg/kg, with an inter-injection interval of at least 48h), and then a chronic saline or nicotine treatment (0.3mg/kg/day for 10 consecutive days). Immediately after each injection, rats were required to press a lever five times to obtain food that was available at unpredictable times (on average every 80s) with constant probability. Acute nicotine dose-dependently suppressed behavior prior to the delivery of the first reinforcer, but enhanced food-reinforced behavior afterwards. These effects were primarily observed in the time it took rats to initiate food-seeking behavior. Enhancing effects were also observed in the microstructure of food-seeking behavior, with lower nicotine doses (0.1-0.3mg/kg) increasing the rate at which response bouts were initiated, and higher doses (0.3-0.6mg/kg) increasing within-bout response rates. A pre-feeding control suggests that changes in appetite alone cannot explain these effects. Over the course of chronic nicotine exposure, tolerance developed to the suppressive, but not to the enhancing effects of nicotine on food-seeking behavior. These results suggest that (a) lower doses of nicotine enhance the reward value of food and/or food-associated stimuli, (b) higher doses of nicotine enhance motoric activity, and (c) ostensive sensitization effects of nicotine on behavior partially reflect a tolerance to its transient suppressive motoric effects.

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Tetramethylenedisulfotetramine (tetramine, or TETS) is a highly toxic rodenticide that has been responsible for over 14,000 accidental and intentional poisonings worldwide. Although the vast majority of TETS poisonings involved tainted food or drink, the laboratory in vivo studies of TETS intoxication used intraperitoneal injection or gavage for TETS exposure. Seeking to develop and characterize a more realistic model of TETS intoxication in the present study, rats were trained to rapidly and voluntarily consume a poisoned food morsel. Initially, the overt toxic effects of TETS consumption across a large range of doses were characterized, then a focused range of doses was selected for more intensive behavioral evaluation (in operant test chambers providing a variable-interval schedule of food reinforcement). The onset of intoxication following voluntary oral consumption of TETS was rapid, and clear dose-dependent response-rate suppression was observed across multiple performance measures within the operant-chamber environment. At most doses, recovery of operant performance did not occur within 30h. Food consumption and body weight changes were also dose dependent and corroborated the behavioral measures of intoxication. This voluntary oral-poisoning method with concomitant operant-behavioral assessment shows promise for future studies of TETS (and other toxic chemicals of interest) and may be extremely valuable in characterizing treatment outcomes.

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BACKGROUND: Walking is a widely accepted and frequently targeted health promotion approach to increase physical activity (PA). Interventions to increase PA have produced only small improvements. Stronger and more potent behavioral intervention components are needed to increase time spent in PA, improve cardiometabolic risk markers, and optimize health. OBJECTIVE: Our aim is to present the rationale and methods from the WalkIT Trial, a 4-month factorial randomized controlled trial (RCT) in inactive, overweight/obese adults. The main purpose of the study was to evaluate whether intensive adaptive components result in greater improvements to adults' PA compared to the static intervention components. METHODS: Participants enrolled in a 2x2 factorial RCT and were assigned to one of four semi-automated, text message-based walking interventions. Experimental components included adaptive versus static steps/day goals, and immediate versus delayed reinforcement. Principles of percentile shaping and behavioral economics were used to operationalize experimental components. A Fitbit Zip measured the main outcome: participants' daily physical activity (steps and cadence) over the 4-month duration of the study. Secondary outcomes included self-reported PA, psychosocial outcomes, aerobic fitness, and cardiorespiratory risk factors assessed pre/post in a laboratory setting. Participants were recruited through email listservs and websites affiliated with the university campus, community businesses and local government, social groups, and social media advertising. RESULTS: This study has completed data collection as of December 2014, but data cleaning and preliminary analyses are still in progress. We expect to complete analysis of the main outcomes in late 2015 to early 2016. CONCLUSIONS: The Walking Interventions through Texting (WalkIT) Trial will further the understanding of theory-based intervention components to increase the PA of men and women who are healthy, insufficiently active and are overweight or obese. WalkIT is one of the first studies focusing on the individual components of combined goal setting and reward structures in a factorial design to increase walking. The trial is expected to produce results useful to future research interventions and perhaps industry initiatives, primarily focused on mHealth, goal setting, and those looking to promote behavior change through performance-based incentives. TRIAL REGISTRATION: ClinicalTrials.gov NCT02053259; https://clinicaltrials.gov/ct2/show/NCT02053259 (Archived by WebCite at http://www.webcitation.org/6b65xLvmg).

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Studies indicate that when abstinence is initiated, escalating reinforcement schedules maintain continuous abstinence longer than fixed reinforcement schedules. However, these studies were conducted for shorter durations than most clinical trials and also resulted in larger reinforcer value for escalating participants during the 1st week of the experiment. We tested whether escalating reinforcement schedules maintained abstinence longer than fixed reinforcement schedules in a 12-week clinical trial. Smokers (146) were randomized to an escalating reinforcement schedule, a fixed reinforcement schedule, or a control condition. Escalating reinforcement participants received $5.00 for their first breath carbon monoxide (CO) sample <3 ppm, with a $0.50 increase for each consecutive sample. Fixed reinforcement participants received $19.75 for each breath CO sample <3 ppm. Control participants received payments only for delivering a breath CO sample. Similar proportions of escalating and fixed reinforcement participants met the breath CO criterion at least once. Escalating reinforcement participants maintained criterion breath CO levels longer than fixed reinforcement and control participants. Similar to previous short-term studies, escalating reinforcement schedules maintained longer durations of abstinence than fixed reinforcement schedules during a clinical trial.

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Mild traumatic brain injury (mTBI) and post-traumatic stress disorder (PTSD) are pressing medical issues for the Warfighter. Symptoms of mTBI can overlap with those of PTSD, suggesting the possibility of a causal or mediating role of mTBI in PTSD. To address whether mTBI can exacerbate the neurobiological processes associated with traumatic stress, we evaluated the impact of mTBI from a blast overpressure (BOP) on the expression of a conditioned fear. In the rat, conditioned fear models are used to evaluate the emotional conditioning processes that are known to become dysfunctional in PTSD. Rats were first trained on a variable interval (VI), food maintained, operant conditioning task that established a general measure of performance. Inescapable electric shock (IES) was paired with an audio-visual conditioned stimulus (CS) and followed 1day later by three daily exposures to BOP (75kPa). Subsequently, the CS alone was presented once every 7days for 2months, beginning 4days following the last BOP. The CS was presented during the VI sessions allowing a concurrent measure of performance. Treatment groups (n=10, each group) received IES+BOP, IES+sham-BOP, sham-IES+BOP or sham-IES+sham-BOP. As expected, pairing the CS with IES produced a robust conditioned fear that was quantified by a suppression of responding on the VI. BOP significantly decreased the expression of the conditioned fear. No systematic short- or long-term performance deficits were observed on the VI from BOP. These results show that mTBI from BOP can affect the expression of a conditioned fear and suggests that BOP caused a decrease in inhibitory behavioral control. Continued presentation of the CS produced progressively less response suppression in both fear conditioned treatments, consistent with extinction of the conditioned fear. Taken together, these results show that mTBI from BOP can affect the expression of a conditioned fear but not necessarily in a manner that increases the conditioned fear or extends the extinction process.

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We evaluated functional communication training (FCT) combined with a chained schedule of reinforcement procedure for the treatment of challenging behavior exhibited by two individuals diagnosed with Asperger syndrome and autism. Following functional analyses that suggested that challenging behavior served multiple functions for both participants, we implemented FCT in which mands for a discriminative stimulus (S(D); wristband) were reinforced with access to the S(D) and all three functional reinforcers. Next, we modified the procedure by incorporating delays to increase ease of implementation and promote toleration of delays to reinforcement. Last, we made additional modifications to the procedure by incorporating a chained schedule of reinforcement such that (a) mands for the wristband were reinforced with access to the wristband and (b) specific mands for respective functional reinforcers were reinforced in the presence of the wristband. The results showed that the procedure successfully treated challenging behavior with multiple functions. Future directions in the evaluation and development of treatments that simultaneously address multiple functions are discussed.

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Research has shown that reinforcing novel behaviors can increase the number of different ways that an individual behaves (Goetz & Baer, 1973; Pryor, Haag, & O'Reilly, 1969). However, it was not until more recently that researchers began to consider variability to be a reinforceable operant in and of itself (Neuringer, 2002). More specifically, Neuringer suggested that variability can be taught using a Lag x schedule of reinforcement, in which x refers to the number of previous responses from which the current response must differ in order for reinforcement to occur (Page & Neuringer, 1985). The purpose of the present study was to extend one of the first studies of a Lag x schedule on verbal responses with human subjects (Lee, McComas, & Jawor, 2002), by increasing the lag criteria while attempting to address some of methodological limitations of the study. The participant was a 7-year-old male with autism. A changing criterion design was used and results showed that 3 novel responses were acquired and varied according to the lag schedule of reinforcement.