Interference with reelin signaling in the lateral entorhinal cortex impairs spatial memory

Entorhinal neurons receive extensive intracortical projections, and form the primary input to the hippocampus via the perforant pathway. The glutamatergic cells of origin for the perforant pathway are distinguished by their expression of reelin, a glycoprotein involved in learning and synaptic plasticity. The functional significance of reelin signaling within the entorhinal cortex, however, remains unexplored. To determine whether interrupting entorhinal reelin signaling might have consequences for learning and memory, we administered recombinant receptor-associated protein (RAP) into the lateral entorhinal cortex (LEC) of young Long-Evans rats. RAP prevents reelin from binding to its receptors, and we verified the knockdown of reelin signaling by quantifying the phosphorylation state of reelin’s intracellular signaling target, disabled-1 (DAB1). Effective knockdown of reelin signaling was associated with impaired performance in the hippocampus-dependent version of the water maze. Moreover, inhibition of reelin signaling induced a localized loss of synaptic marker expression in the LEC. These observations support a role for entorhinal reelin signaling in spatial learning, and suggest that an intact reelin signaling pathway is essential for synaptic integrity in the adult entorhinal cortex.     

Bidirectional metabolic regulation of neurocognitive function

The efficiency of somatic energy metabolism is correlated with cognitive change over the lifespan. This relationship is bidirectional, with improved overall fitness associated with enhanced synaptic function and neuroprotection, and synaptic endangerment occurring in the context of impaired energy metabolism. In this review, we discuss recent advancements in the fields of exercise, dietary energy intake and diabetes, as they relate to neuronal function in the hippocampus. Because hippocampal neurons have energy requirements that are relatively higher than those of other brain regions, they are uniquely poised to benefit from exercise, and to be harmed by diabetes. We view exercise and dietary energy restriction as being associated with enhanced hippocampal plasticity at one end of a continuum, with obesity and diabetes accompanied by cognitive impairment at the other end of the continuum. Understanding the mechanisms for this continuum may yield novel therapeutic targets for the prevention and treatment of cognitive decline following aging, disease, or injury.     

Do common systems control eye movements and motion extrapolation?

People are able to judge the current position of occluded moving objects. This operation is known as motion extrapolation. It has previously been suggested that motion extrapolation is independent of the oculomotor system. Here we revisited this question by measuring eye position while participants completed two types of motion extrapolation task. In one task, a moving visual target travelled rightwards, disappeared, then reappeared further along its trajectory. Participants discriminated correct reappearance times from incorrect (too early or too late) with a two-alternative forced-choice button press. In the second task, the target travelled rightwards behind a visible, rectangular occluder, and participants pressed a button at the time when they judged it should reappear. In both tasks, performance was significantly different under fixation as compared to free eye movement conditions. When eye movements were permitted, eye movements during occlusion were related to participants' judgements. Finally, even when participants were required to fixate, small changes in eye position around fixation (<2°) were influenced by occluded target motion. These results all indicate that overlapping systems control eye movements and judgements on motion extrapolation tasks. This has implications for understanding the mechanism underlying motion extrapolation.     

On the theoretical error bound for estimating psychometric functions

The theoretical limits to the amount of error, or the Cramer-Rao bounds, were derived for estimating psychometric functions. These theoretical error bounds were compared with the variability of psychometric functions estimated from human as well as computer-simulated observers. For the simulated observers, due to the limited efficiency of the sampling strategies, including the placement of the signals and the distribution of the trials, the variances of the estimated parameters are seven times the theoretical bound for threshold and 22 times that for slope. For the human observers, the variance is 18 times the theoretical bounds for threshold and 80 times that for slope. Therefore, a major portion of the variances (60% for threshold and 73% for slope) for the human observers is associated with factors other than sampling strategies. Further improvement of the accuracy for estimating psychometric functions will depend on not only optimizing the sampling strategy, but also better understanding the various sources of error related to the behavior of human observers.     

Unimpaired trace classical eyeblink conditioning in Purkinje cell degeneration (pcd) mutant mice

Young adult Purkinje cell degeneration (pcd) mutant mice, with complete loss of cerebellar cortical Purkinje cells, are impaired in delay eyeblink classical conditioning. In the delay paradigm, the conditioned stimulus (CS) overlaps and coterminates with the unconditioned stimulus (US), and the cerebellar cortex supports normal acquisition. The ability of pcd mutant mice to acquire trace eyeblink conditioning in which the CS and US do not overlap has not been explored. Recent evidence suggests that cerebellar cortex may not be necessary for trace eyeblink classical conditioning. Using a 500 ms trace paradigm for which forebrain structures are essential in mice, we assessed the performance of homozygous male pcd mutant mice and their littermates in acquisition and extinction. In contrast to results with delay conditioning, acquisition of trace conditioning was unimpaired in pcd mutant mice. Extinction to the CS alone did not differ between pcd and littermate control mice, and timing of the conditioned response was not altered by the absence of Purkinje cells during acquisition or extinction. The ability of pcd mutant mice to acquire and extinguish trace eyeblink conditioning at levels comparable to controls suggests that the cerebellar cortex is not a critical component of the neural circuitry underlying trace conditioning. Results indicate that the essential neural circuitry for trace eyeblink conditioning involves connectivity that bypasses cerebellar cortex.     

Mental-state attribution drives rapid, reflexive gaze following

When presented with a face stimulus whose gaze is diverted, observers’ attention shifts to locations fixated by the face. Such “gaze following” has been characterized by some previous studies as a consequence of sophisticated theory of mind processes, but by others (particularly those employing the “gaze-cuing” paradigm) as an involuntary response that is triggered directly and reflexively by the physical features of a face. To address this apparent contradiction, we modified the gaze-cuing paradigm using a deception procedure to convince observers that prerecorded videos of an experimenter making head turns and wearing mirrored goggles were a “live” video link to an adjacent room. In two experiments, reflexive gaze following was found when observers believed that the model was wearing transparent goggles and could see, but it was significantly reduced when they believed that the experimenter wore opaque goggles and could not see. These results indicate that the attribution of the mental state “seeing” to a face plays a role in controlling even reflexive gaze following.     

Religiosity and Spirituality: A Psychometric Evaluation of the Santa Clara Strength of Religious Faith Questionnaire

The Santa Clara Strength of Religious Faith Questionnaire (SCSORF) was administered to 124 undergraduate college students attending a private Catholic university and the result was compared to measures of spirituality, religious behavior, religious coping, and affect. The present study found that the SCSORF was strongly related to spirituality, in particular, seeking support from one's spirituality. However, the SCSORF was not correlated with an openness to new spiritual experiences. The SCSORF was also related to religious behavior and religious coping. The SCSORF was not related to affect, indicating that scores on the SCSORF were not affect-dependent. Results from this study provide additional evidence that the SCSORF is a reliable and valid measure of religious faith.     

Increased brain serotonin turnover in panic disorder patients in the absence of a panic attack: reduction by a selective serotonin reuptake inhibitor

Since the brain neurotransmitter changes characterising panic disorder remain uncertain, we quantified brain noradrenaline and serotonin turnover in patients with panic disorder, in the absence of a panic attack. Thirty-four untreated patients with panic disorder and 24 matched healthy volunteers were studied. A novel method utilising internal jugular venous sampling, with thermodilution measurement of jugular blood flow, was used to directly quantify brain monoamine turnover, by measuring the overflow of noradrenaline and serotonin metabolites from the brain. Radiographic depiction of brain venous sinuses allowed differential venous sampling from cortical and subcortical regions. The relation of brain serotonin turnover to serotonin transporter genotype and panic disorder severity were evaluated, and the influence of an SSRI drug, citalopram, on serotonin turnover investigated. Brain noradrenaline turnover in panic disorder patients was similar to that in healthy subjects. In contrast, brain serotonin turnover, estimated from jugular venous overflow of the metabolite, 5-hydroxyindole acetic acid, was increased approximately 4-fold in subcortical brain regions and in the cerebral cortex (P < 0.01). Serotonin turnover was highest in patients with the most severe disease, was unrelated to serotonin transporter genotype, and was reduced by citalopram (P < 0.01). Normal brain noradrenaline turnover in panic disorder patients argues against primary importance of the locus coeruleus in this condition. The marked increase in serotonin turnover, in the absence of a panic attack, possibly represents an important underlying neurotransmitter substrate for the disorder, although this point remains uncertain. Support for this interpretation comes from the direct relationship which existed between serotonin turnover and illness severity, and the finding that SSRI administration reduced serotonin turnover. Serotonin transporter genotyping suggested that increased whole brain serotonin turnover most likely derived not from impaired serotonin reuptake, but from increased firing in serotonergic midbrain raphe neurons projecting to both subcortical brain regions and the cerebral cortex.     

The Adult Attachment Interview and self-reports of attachment style: an empirical rapprochement

Although 10 studies have been published on the empirical overlap of the Adult Attachment Interview (AAI) and measures of self-reported attachment style, results in this literature have been inconsistently interpreted in narrative reviews. This report was designed as a rapprochement of the AAI and attachment style literatures and includes 3 studies. Study 1 (combined N = 961) is a meta-analytic review showing that by J. Cohen's (1992) criteria (mean r = .09), the association between AAI security and attachment style dimensions is trivial to small. Study 2 (N = 160) confirms meta-analytic results with state-of-the-art assessments of attachment security and also examines attachment dimensions in relation to the Big 5 personality traits. Finally, Study 3 is an investigation of 50 engaged couples that shows that developmental and social psychological measures of attachment security predict somewhat distinct--though theoretically anticipated--aspects of functioning in adult relationships.