The Popular Policeman and Other Cases

In this compelling title, two distinguished scholars share their experiences as expert witnesses in cases ranging from eyewitness testimony, person identification and recovered memories, to false confessions, collaborative storytelling and causal attribution, in the context of various interrogation techniques and their ability to deliver reliable results. Each chapter describes in lucid, entertaining prose a representative case in the context of scholarly literature to date, showing how psychological expertise has been (and can be) used in a legal setting. The cases include petty and serious crime, from illegal gambling, infringed trademarks and risqué courtship behaviour, to honour killing and death on the climbing wall. The authors' findings and recommendations apply to legal systems worldwide. There is no other English-language textbook covering a similarly wide range of offences, and this volume will fill a gap in the existing literature and demonstrate how psychological expertise can be used in a much larger area than is often realised.Psychologisch onderzoek is voor de rechter niet altijd gemakkelijk toe te passen binnen de context van een strafrechtelijk of civiel geding. Inzichten in de werking van het geheugen, het gedrag, logisch denkvermogen en het nemen van beslissingen kunnen uitkomst bieden als er sprake is van valse voorwendselen, fraude, diefstal of zelfs moord, maar vaak is daar wel de toelichting van een deskundige voor nodig. Op onderhoudende en toegankelijke wijze beschrijven rechtspsychologen Willem Albert Wagenaar en Hans Crombag tot in detail vijftien representatieve zaken uit de Nederlandse rechtspraak, hun rol daarin als deskundige, en hoe het afliep. Naast de betrouwbaarheid van ooggetuigenverklaringen en bekentenissen is er aandacht voor de psychologische aspecten van minder gangbare onderwerpen zoals illegaal gokken, verwarrende consumentenvoorlichting en seksuele intimidatie. The Popular Policeman and Other Cases vult een belangrijke lacune in de bestaande literatuur over de psychologie in de rechtszaal. Niet eerder werd er buiten de Verenigde Staten in één boek zo uitgebreid en gedetailleerd aandacht besteed aan zoveel uiteenlopende zaken. Het boek is in eerste instantie geschreven voor het hoger onderwijs, maar ook buiten de collegezaal zal dit boek op de nodige belangstelling kunnen rekenen

Addiction is a brain disease, and it doesn’t matter: prior choice in drug use blocks leniency in criminal punishment

Our aim was to explore how (neuro)scientific understanding of addiction as a brain-disease impacts criminal sentencing decisions in courts in England and Wales, where legal rules concerning intoxication, prior-fault and mental disease conflict, and sentencing guidelines lack clarity. We hypothesized that despite significant neuropsychiatric overlap of addiction and other brain-disorders, variables in relation to etiology would moderate magistrates’ sentencing decisions in cases involving addicted offenders. Using a questionnaire-based, quantitative design, and combining frequentist and Bayesian analysis approaches, we probed court magistrates’ sentencing decisions, and underlying rationale, for defendants presenting with brain damage resulting from a (fictional) disease, addiction to heroin, or more complex, mixed etiologies. When identical neuropsychiatric profiles resulted from disease, but not heroin addiction, prison sentences were significantly reduced. Study 1 (N=109) found the pivotal factor preventing addiction from mitigating sentences was perceived choice in its acquisition; removing choice from addiction increased the odds of sentence reduction (~20- fold) and attaching choice to disease aggravated or reversed earlier leniency. Study 2 (N=276) replicated these results and found that when heroin use led to disease or vice versa, magistrates found middle ground. These differences were independent of the age of first drug use. Finally, evidence of addiction was more likely to evoke punishment considerations by magistrates, rather than rehabilitation. Consistent with legal rules relating to intoxication but running counter to norms around mental-illness and choice, our results demonstrate the need for greater clarity in sentencing guidance on addiction specifically, and mental disorders more generally

Debating intoxication: response to commentaries

The lack of scientific or clinical clarity faced by courts dealing with cases involving intoxicated criminal defendants is unavoidable, but introducing further legal ambiguity to meet policy goals introduces ever greater risk of problematic (including unjust) legal outcomes

Prior fault and contrived criminal defences: coming to the law with clean hands

The concept of ‘prior fault’ presents a number of significant challenges for the criminal law. The focus of criminal law (offences and defences) is necessarily event specific; we target and assess liability in relation to a snap-shot moment in time or a short series of acts, not as a judgement of prior or more general culpability or character. Therefore, prior fault should be largely an irrelevance at the liability stage. However, remaining faithful to this narrow focus in all circumstances would lead to considerable unfairness, creating an opportunity for defendants to manipulate legal rules to their own advantage. Some of the clearest examples of this arise in so-called contrived defence cases. Let’s take the example of self-defence, a general and complete defence where the defendant’s (D’s) use of force against the victim (V) is both necessary and reasonably proportionate. The standard operation of this defence is largely uncontroversial; people should be empowered to defend themselves from unlawful attack. However, what if D manufactures the circumstances of that ‘attack’ in order to use the law of self-defence to ‘justify’ her pre-planned use of force against V. For example, D wants to kill V. D hands V a knife and then goads V continuously until V (as anticipated) lashes out at D. D shoots and kills V in self-defence. In order to understand and analyse examples such as the one above, we must distinguish two points in time within each potential criminal event. First, and standardly, we must look at the time where the potential criminal offence is committed (T2), asking whether the elements of the potential offence are completed, and if so, whether the elements of a potential defence can be found. In our example above, it is likely that the offence of murder was committed by D, but D would also be able to raise self-defence because of the attack from V. Secondly, we must look at D’s conduct prior to the potential crime (T1), to ask if D has done anything to undermine her future use of a defence at T2. In our example, this could be D’s prior fault in planning, and in manipulating V, in order to create the circumstances of her own defence. It is at this second stage, looking back to T1, that legal rules relating to prior fault must be identified and applied. Issues of prior fault are (potentially) relevant across every criminal defence, and this has given rise to a variety of legal rules designed to prevent the application of contrived defences. However, the legal rules relating to prior fault are often unclear and inconsistent between different defences. Basic questions about what D must have done at T1, what she must have intended, and how this can impact liability at T2, all require investigation. In this article, we provide such an investigation. In Part 1 we explore the application of legal rules relating to prior fault within the current law, exposing areas of inconsistency and incoherence. Part 2 discusses the academic response to this inconsistency, including different models of prior fault that have been recommended in an effort to bring coherence to this area of law. Finally, in Part 3, building upon the academic analysis, we set out our own model of legal rules relating to prior fault; a model that we believe can (and should) be applied across all criminal defences. It is contended that the issue of prior fault can be addressed consistently, and that such rules should form part of any codification project

A selective role for neuronal activity regulated pentraxin in the processing of sensory-specific incentive value

Neuronal activity regulated pentraxin (Narp) is a secreted neuronal product which clusters AMPA receptors and regulates excitatory synaptogenesis. Although Narp is selectively enriched in brain, its role in behavior is not known. As Narp is expressed prominently in limbic regions, we examined whether Narp deletion affects performance on tasks used to assess motivational consequences of food-rewarded learning. Narp knock-out (KO) mice were unimpaired in learning simple pavlovian discriminations, instrumental lever pressing, and in acquisition of at least two aspects of pavlovian incentive learning, conditioned reinforcement and pavlovian-instrumental transfer. In contrast, Narp deletion resulted in a substantial deficit in the ability to use specific outcome expectancies to modulate instrumental performance in a devaluation task. In this task, mice were trained to respond on two levers for two different rewards. After training, mice were prefed with one of the two rewards, devaluing it. Responding on both levers was then assessed in extinction. Whereas control mice showed a significant preference in responding on the lever associated with the nondevalued reward, Narp KO mice responded equally on both levers, failing to suppress responding on the lever associated with the devalued reward. Both groups consumed more of the nondevalued reward in a subsequent choice test, indicating Narp KO mice could distinguish between the rewards themselves. These data suggest Narp has a selective role in processing sensory-specific information necessary for appropriate devaluation performance, but not in general motivational effects of reward-predictive cues on performance

Regional differences in striatal neuronal ensemble excitability following cocaine and extinction memory retrieval in Fos-GFP mice

Learned associations between drugs of abuse and the drug administration environment play an important role in addiction. In rodents, exposure to a drug-associated environment elicits conditioned psychomotor activation, which may be weakened following extinction learning. While widespread drug-induced changes in neuronal excitability have been observed, little is known about specific changes within neuronal ensembles activated during the recall of drugenvironment associations. Using a cocaine conditioned locomotion procedure, the present study assessed the excitability of neuronal ensembles in the nucleus accumbens core and shell (NAccore and NAcshell), and dorsal striatum (DS) following cocaine conditioning and extinction in Fos-GFP mice that express green fluorescent protein (GFP) in activated neurons (GFP+). During conditioning, mice received repeated cocaine injections (20 mg/kg) paired with a locomotor activity chamber (Paired) or home cage (Unpaired). 7-13 days later both groups were re-exposed to the activity chamber under drug-free conditions, and Paired, but not Unpaired, mice exhibited conditioned locomotion. In a separate group of mice, conditioned locomotion was extinguished by repeatedly exposing mice to the activity chamber under drugfree conditions. Following the expression and extinction of conditioned locomotion, GFP+ neurons in the NAccore (but not NAcshell and DS) displayed greater firing capacity compared to surrounding GFP– neurons. This difference in excitability was due to a generalized decrease in GFP– excitability following conditioned locomotion, and a selective increase in GFP+ excitability following its extinction. These results suggest a role for both widespread and ensemble-specific changes in neuronal excitability following recall of drug-environment associations

Incentive learning underlying cocaine relapse requires mGluR5 receptors located on dopamine D1 receptor-expressing neurons

Understanding the psychobiological basis of relapse remains a challenge in developing therapies for drug addiction. Relapse in cocaine addiction often occurs following exposure to environmental stimuli previously associated with drug taking. The metabotropic glutamate receptor, mGluR5, is potentially important in this respect; it plays a central role in several forms of striatal synaptic plasticity proposed to underpin associative learning and memory processes that enable drug-paired stimuli to acquire incentive motivational properties and trigger relapse. Using cell type-specific RNA interference, we have generated a novel mouse line with a selective knock-down of mGluR5 in dopamine D1 receptor-expressing neurons. Although mutant mice self-administer cocaine, we show that reinstatement of cocaine-seeking induced by a cocaine-paired stimulus is impaired. By examining different aspects of associative learning in the mutant mice, we identify deficits in specific incentive learning processes that enable a reward-paired stimulus to directly reinforce behavior and to become attractive, thus eliciting approach toward it. Our findings show that glutamate signaling through mGluR5 located on dopamine D1 receptor-expressing neurons is necessary for incentive learning processes that contribute to cue-induced reinstatement of cocaine-seeking and which may underpin relapse in drug addiction

Extinction of cue-evoked food seeking recruits a GABAergic interneuron ensemble in the dorsal medial prefrontal cortex of mice

Animals must quickly adapt food-seeking strategies to locate nutrient sources in dynamically changing environments. Learned associations between food and environmental cues that predict its availability promote food-seeking behaviors. However, when such cues cease to predict food availability, animals undergo 'extinction' learning, resulting in the inhibition of food-seeking responses. Repeatedly activated sets of neurons, or 'neuronal ensembles', in the dorsal medial prefrontal cortex (dmPFC) are recruited following appetitive conditioning and undergo physiological adaptations thought to encode cue-reward associations. However, little is known about how the recruitment and intrinsic excitability of such dmPFC ensembles are modulated by extinction learning. Here, we used in vivo 2-Photon imaging in male Fos-GFP mice that express green fluorescent protein (GFP) in recently behaviorally-activated neurons to determine the recruitment of activated pyramidal and GABAergic interneuron mPFC ensembles during extinction. During extinction, we revealed a persistent activation of a subset of interneurons which emerged from a wider population of interneurons activated during the initial extinction session. This activation pattern was not observed in pyramidal cells, and extinction learning did not modulate the excitability properties of activated neurons. Moreover, extinction learning reduced the likelihood of reactivation of pyramidal cells activated during the initial extinction session. Our findings illuminate novel neuronal activation patterns in the dmPFC underlying extinction of food-seeking, and in particular, highlight an important role for interneuron ensembles in this inhibitory form of learning

An open-source pipeline for analysing changes in microglial morphology

Changes in microglial morphology are powerful indicators of the inflammatory state of the brain. Here, we provide an open-source microglia morphology analysis pipeline that first cleans and registers images of microglia, before extracting 62 parameters describing microglial morphology. It then compares control and 'inflammation' training data and uses dimensionality reduction to generate a single metric of morphological change (an 'inflammation index'). This index can then be calculated for test data to assess inflammation, as we demonstrate by investigating the effect of short-term high-fat diet consumption in heterozygous Cx3CR1-GFP mice, finding no significant effects of diet. Our pipeline represents the first open-source microglia morphology pipeline combining semi-automated image processing and dimensionality reduction. It uses free software (ImageJ and R) and can be applied to a wide variety of experimental paradigms. We anticipate it will enable others to more easily take advantage of the powerful insights microglial morphology analysis provides

Changes in appetitive associative strength modulates nucleus accumbens, but not orbitofrontal cortex neuronal ensemble excitability

Cues that predict the availability of food rewards influence motivational states and elicit food-seeking behaviors. If a cue no longer predicts food availability, animals may adapt accordingly by inhibiting food seeking responses. Sparsely activated sets of neurons, coined neuronal ensembles, have been shown to encode the strength of reward-cue associations. While alterations in intrinsic excitability have been shown to underlie many learning and memory processes, little is known about these properties specifically on cue-activated neuronal ensembles. We examined the activation patterns of cue-activated orbitofrontal cortex (OFC) and nucleus accumbens (NAc) shell ensembles using wild-type and Fos-GFP mice following appetitive conditioning with sucrose and extinction learning. We also investigated the neuronal excitability of recently activated, GFP+ neurons in these brain areas using whole-cell electrophysiology in brain slices. Exposure to a sucrose cue elicited activation of neurons in both the NAc shell and OFC. In the NAc shell, but not the OFC, these activated GFP+ neurons were more excitable than surrounding GFP– neurons. Following extinction, the number of neurons activated in both areas was reduced and activated ensembles in neither area exhibited altered excitability. These data suggest that learning-induced alterations in the intrinsic excitability of neuronal ensembles is regulated dynamically across different brain areas. Furthermore, we show that changes in associative strength modulate the excitability profile of activated ensembles in the NAc shell