One night of sleep deprivation affects reaction time, but not interference or facilitation in a Stroop task

The Stroop color-naming task is one of the most widely studied tasks involving the inhibition of a prepotent response, regarded as an executive function. Several studies have examined performance on versions of the Stroop task under conditions of acute sleep deprivation. Though these studies revealed effects on Stroop performance, the results often do not differentiate between general effects of sleep deprivation on performance and effects specifically on interference in the Stroop task. To examine the effect of prolonged wakefulness on performance on the Stroop task, we studied participants in a 40-h "constant routine" protocol during which they remained awake in constant conditions and performed a Stroop color-naming task every two hours. We found that reaction time was slowest when the color and word did not match (incongruent), fastest when the color and word did match (congruent), and intermediate when participants named the color of the non-word stimulus (neutral). Performance on all three trial types degraded significantly as a function of time awake. Extended wakefulness did not significantly change the additional time needed to respond when the color and word did not match (Stroop interference), nor did it change the amount of facilitation when color and word matched. These results indicate that one night of sleep deprivation influences performance on the Stroop task by an overall increase in response time, but does not appear to impact the underlying processes of interference or facilitation. The results suggest that the degree to which an "executive function" is affected by sleep deprivation may depend on the particular executive function studied and the degree to which it is subserved by the prefrontal cortex.     

Basolateral amygdala inactivation impairs learned (but not innate) fear response in rats

Numerous studies have suggested that the amygdala is involved in the formation of aversive memories, but the possibility that this structure is merely related to any kind of fear sensation or response could not be ruled out in previous studies. The present study investigated the effects of bilateral inactivation of the amygdaloid complex in rats tested in the plus-maze discriminative avoidance task. This task concomitantly evaluates aversive memory (by discrimination of the two enclosed arms) and innate fear (by open-arm exploration). Wistar rats (3-5 months-old) were implanted with bilateral guide cannulae into basolateral amygdala. After surgery, all subjects were given 1 week to recover before behavioral experiments. Afterwards, in experiment 1, 15 min prior to training, 0.5 μl of saline or muscimol (1 mg/ml) was infused in each side via microinjection needles. In experiment 2 the animals received injections immediately after the training session and in experiment 3 rats were injected prior to testing session (24 h after training). The main results showed that (1) pre-training muscimol prevented memory retention (evaluated by aversive arm exploration in the test session), but did not alter innate fear (evaluated by percent time in open arms); (2) post-training muscimol impaired consolidation, inducing increased percent in aversive arm exploration in the test session and (3) pre-testing muscimol did not affect retrieval (evaluated by aversive enclosed arm exploration in the test session). The results suggest that amygdala inactivation specifically modulated the learning of the aversive task, excluding a possible secondary effect of amygdala inactivation on general fear responses. Additionally, our data corroborate the hypothesis that basolateral amygdala is not the specific site of storage of aversive memories, since retention of the previously learned task was not affected by pre-testing inactivation.     

Pre-training anandamide infusion within the basolateral amygdala impairs plus-maze discriminative avoidance task in rats

Endocannabinoids (eCBs) modulate a variety of brain functions via activation of the widely expressed CB1 receptor. One site of high density of this receptor is the basolateral amygdala (BLA), a structure involved in the formation of aversive memories. The activation and blockade of CB1 receptors by systemic or hippocampal drug administrations have been shown to modify memory processing. However, little is known about the role of the BLA endocannabinoid system in aversive memories. Additionally, BLA endocannabinoid transmission seems to be related to emotional states, but the relevance of these effects to memory formation is still unknown. In this study we investigated the effects of the eCB anandamide (AEA) and the CB1 antagonist/inverse agonist AM251 infused into the BLA on the acquisition of an aversive memory task, concomitantly evaluating basal anxiety levels in rats. Male rats received pre-training micro-injection of AEA, AM251 or vehicle bilaterally into the BLA, and were studied with the plus-maze discriminative avoidance task (a paradigm that allows concomitant and independent evaluation of anxiety-like behavior and the memory of an aversive task). Our results showed that AEA into the BLA before training prevented memory retrieval 24 h later, as evaluated by exploration of the aversive arm of the maze, while AM251 into the BLA did not interfere with animals' performance. In addition, AEA had no effect on anxiety-like behavior (as evaluated by open arm exploration and risk assessment), while AM251 induced an anxiogenic effect. Our data indicate an important role of BLA CB1 receptors in aversive memory formation, and suggest that this involvement is not necessarily related to a possible modulation of anxiety states.     

Object based implicit contextual learning: a study of eye movements

Implicit contextual cueing refers to a top-down mechanism in which visual search is facilitated by learned contextual features. In the current study we aimed to investigate the mechanism underlying implicit contextual learning using object information as a contextual cue. Therefore, we measured eye movements during an object-based contextual cueing task. We demonstrated that visual search is facilitated by repeated object information and that this reduction in response times is associated with shorter fixation durations. This indicates that by memorizing associations between objects in our environment we can recognize objects faster, thereby facilitating visual search.     

Competence to be executed: An ethical analysis post Panetti

Competence to be executed evaluations in effect can prevent an execution or remove the last meaningful impediment to it. Forensic psychiatrists have primary duties to the legal system and truth and honesty, but like all other areas of medical consultation also should balance conflicting secondary traditional medical ethical duties. Participation in a legally authorized execution so violates medical roles, that it is ethically prohibited by the American Medical Association and American Psychiatric Association. This prohibition includes treatment intended to restore competence to be executed. However, despite the primary treatment intent otherwise being appropriate ethically, like relieving suffering or fostering prison safety, if competence to be executed almost predictably would be a treatment result, at least the risk of this result should be considered ethically as if it were intended. In contrast, competence to be executed assessments can be ethical. Diamond's approach of performing honest evaluations only for the defense is an ethical option for such assessments. However, it is challenging to persuade judges and juries of the objectivity of such honest legitimate assessments. Most practitioners therefore likely would consider assessing competence to be executed for either side. This ethically hazardous position necessitates sensitivity to potentially seriously conflicting duties and roles. Copyright © 2010 John Wiley & Sons, Ltd.     

Preparing to move and deciding not to move

A commentary is given on Trevena and Miller (2010). The comparability of their experimental task and of the potential they recorded with those used and recorded by Libet, Gleason, Wright, and Pearl (1983a) is questioned. An interpretation is given for the similarity of event-related potentials recorded when subjects decided to move and when they decided not to move.     

Death Anxiety and Symbolic Immortality in Relatives at Risk for Familial Amyloid Polyneuropathy Type I (FAP I,ATTR V30M)

This study is an investigation of the impact of familial amyloid polyneuropathy type I (FAP I, ATTR V30M) on death anxiety and symbolic immortality. Templer and Drolet’s scales were administered to 524 individuals: (1) 84 relatives at risk, (2) 92 relatives not at risk for FAP I; and (3) a control group (n = 348) with no known hereditary disease in their families. At-risk relatives had, on average, a higher score for death anxiety and a lower score for symbolic immortality, than either those not-at-risk or controls. There were no significant differences in scores on either measure for those not-at-risk versus controls. Being at risk increases death anxiety and threatens the sense of symbolic immortality and psychosocial wellbeing. This may be true for other serious hereditary disorders as well. Genetic counsellors should become familiar with these concepts, feel comfortable initiating discussions about death with their patients, and be able to identify and reinforce their patients’ and family members’ sense of symbolic immortality.     

Factor structure and behavioural correlates of the Psychopathy Checklist-Revised [PCL-R] in a Brazilian prisoner sample

The present study examines the reliability, factor structure, and criterion-related validity of Hare (2003) Revised Psychopathy Checklist [PCL-R] in a Latin American forensic context. Brazilian male inmates (124) were administered the PCL-R, along with relevant subscales of an inventory of normal personality [Personality Factorial Inventory], an intelligence scale [Standard Progressive Matrices], and a semi-structured interview based in DSM IV. Criminal offence records were obtained from prison files. Several theoretical factorial structures for the PCL-R were tested and compared. A bifactor model with three factors, one general factor reflecting the overlap across all items, and two independent subfactors reflecting the unique covariation among particular groups of items, shows the better fit. Overall scores on the PCL-R correlated with the number of criminal offenses committed by participants. No significant correlations were found between PCL-R scores and personality or intelligence measures. It was concluded that the PCL-R is a reliable and valid instrument for the assessment of psychopathy in the Brazilian male forensic population.     

Autophosphorylation of alphaCaMKII is differentially involved in new learning and unlearning mechanisms of memory extinction

Accumulating evidence indicates the key role of alpha-calcium/calmodulin-dependent protein kinase II (alphaCaMKII) in synaptic plasticity and learning, but it remains unclear how this kinase participates in the processing of memory extinction. Here, we investigated the mechanism by which alphaCaMKII may mediate extinction by using heterozygous knock-in mice with a targeted T286A mutation that prevents the autophosphorylation of this kinase (alphaCaMKII(T286A+/-)). Remarkably, partial reduction of alphaCaMKII function due to the T286A(+/-) mutation prevented the development of extinction without interfering with initial hippocampus-dependent memory formation as assessed by contextual fear conditioning and the Morris water maze. It is hypothesized that the mechanism of extinction may differ depending on the interval at which extinction training is started, being more akin to "new learning" at longer intervals and "unlearning" or "erasure" at shorter intervals. Consistent with this hypothesis, we found that extinction conducted 24 h, but not 15 min, after contextual fear training showed spontaneous recovery (reappearance of extinguished freezing responses) 21 d following the extinction, representing behavioral evidence for new learning and unlearning mechanisms underlying extinction 24 h and 15 min post-training, respectively. Importantly, the alphaCaMKII(T286A+/-) mutation blocked new learning of contextual fear memory extinction, whereas it did not interfere with unlearning processes. Our results demonstrate a genetic dissociation of new learning and unlearning mechanisms of extinction, and suggest that alphaCaMKII is responsible for extinguishing memories specifically through new learning mechanisms.     

Systemic administration of a nitric oxide synthase inhibitor impairs fear sensitization in the plus-maze

The aim of the present study was to evaluate the occurrence of fear sensitization in rats previously treated with an inhibitor of the NO syntheses and submitted to Trial1/Trial2 plus-maze (PM) procedure. Male Wistar rats received a systemic treatment with N(omega)-nitro-L-Arginine-methyl ester (L-NAME; 5, 10 or 50 mg kg(-1)) and were submitted to PM Trial1. In the following day the animals were re-exposed to the PM with no drug administration (Trial2). Some standards spatial-temporal measures, such as the percentage of entries (% Open arm entries) and time spent (% Open arm time) in the open arms and risk assessment frequency were recorded and used to estimate the animal level of fear sensitization in PM Trial2. The results showed that animals receiving L-NAME (50 mg kg(-1)) displayed increased % Open arm entries and % Open arm time in Trial2 in relation to the group receiving 0.9% saline, which is compatible with impaired fear/anxiety acquisition during Trial1/Trial2 PM procedure. In addition, rats treated with L-NAME (50 mg kg(-1)) exhibited low level of risk assessment in Trial2 in relation to the group treated with 0.9% saline, which indicates low level of fear/anxiety during PM re-exposure. The number of entries into the enclosed arms was not changed by any L-NAME treatment, which suggests no bias of the drug treatments on animal locomotor activity. The data suggest that NO synthesis may mediate the fear sensitization process in the PM.