Subjective Experiences of Space and Time: Self, Sensation, and Phenomenal Time

The investigation of subjective experiences (SEs) of space and time is at the core of consciousness research. The term ‘space’ includes the subject and objects. The SE of subject, I-ness, is defined as ‘Self’. The SEs of objects, subject’s external body, and subject’s internal states such as feelings, thoughts, and so on can be investigated using the proto-experience (PE)-SE framework. The SE of time is defined as ‘phenomenal time’ (which includes past, present and future) and the SE of space as ‘phenomenal space’. The three non-experiential materialistic models are as follows: (I) The quantum-dissipation model [25] can connect the discrete neural signals to classical electromagnetic field to ‘quantum field theory and chaos theory’ for explaining memory. (II) The soliton-catalytic model [8] hypothesizes that all living processes including micro- and macro-processes can be explained by catalysis process. (III) The ‘sensation from evolution of action’ model [13] proposes that SEs are internalized during evolution. All these models can address to some extent the function of structures, such as perception. They cannot address explanatory gap. The complementary experiential PE-SE framework [37] addresses this psycho-physical gap and elucidates the SEs of space and time

Measuring cortical connectivity in Alzheimer's disease as a brain neural network pathology: Toward clinical applications

Objectives: The objective was to review the literature on diffusion tensor imaging as well as resting-state functional magnetic resonance imaging and electroencephalography (EEG) to unveil neuroanatomical and neurophysiological substrates of Alzheimer’s disease (AD) as a brain neural network pathology affecting structural and functional cortical connectivity underlying human cognition. Methods: We reviewed papers registered in PubMed and other scientific repositories on the use of these techniques in amnesic mild cognitive impairment (MCI) and clinically mild AD dementia patients compared to cognitively intact elderly individuals (Controls). Results: Hundreds of peer-reviewed (cross-sectional and longitudinal) papers have shown in patients with MCI and mild AD compared to Controls (1) impairment of callosal (splenium), thalamic, and anterior–posterior white matter bundles; (2) reduced correlation of resting state blood oxygen level-dependent activity across several intrinsic brain circuits including default mode and attention-related networks; and (3) abnormal power and functional coupling of resting state cortical EEG rhythms. Clinical applications of these measures are still limited. Conclusions: Structural and functional (in vivo) cortical connectivity measures represent a reliable marker of cerebral reserve capacity and should be used to predict and monitor the evolution of AD and its relative impact on cognitive domains in pre-clinical, prodromal, and dementia stages of AD. (JINS, 2016, 22, 138–163

DRD4 polymorphisms modulate reward positivity and P3a in a gambling task: Exploring a genetic basis for cultural learning

Prior work shows that people respond more plastically to environmental influences, including cultural influences, if they carry the 7 or 2‐repeat (7/2R) allelic variant of the dopamine D4 receptor gene (DRD4). The 7/2R carriers are thus more likely to endorse the norms and values of their culture. So far, however, mechanisms underlying this moderation of cultural acquisition by DRD4 are unclear. To address this gap in knowledge, we tested the hypothesis that DRD4 modulates the processing of reward cues existing in the environment. About 72 young adults, preselected for their DRD4 status, performed a gambling task, while the electroencephalogram was recorded. Principal components of event‐related potentials aligned to the Reward‐Positivity (associated with bottom‐up processing of reward prediction errors) and frontal‐P3 (associated with top‐down attention) were both significantly more positive following gains than following losses. As predicted, the gain‐loss differences were significantly larger for 7/2R carriers than for noncarriers. Also, as predicted, the cultural backgrounds of the participants (East Asian vs. European American) did not moderate the effects of DRD4. Our findings suggest that the 7/2R variant of DRD4 enhances (a) the detection of reward prediction errors and (b) controlled attention that updates the context for the reward, thereby suggesting one possible mechanism underlying the DRD4 × Culture interactions.Is there a genetic basis for cultural learning? Recent work suggests carriers of 7‐ or 2‐repeat allele of the dopamine DRD4 are more likely than non‐carriers to acquire their culture’s beliefs and practices. We show carriers are more closely attuned to reward signals compared to non‐carriers. This finding offers a possible missing link in the analysis of the co‐evolutionary dynamic between genes and culture.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/162723/2/psyp13623_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/162723/1/psyp13623.pd

Bits from Biology for Computational Intelligence

Computational intelligence is broadly defined as biologically-inspired computing. Usually, inspiration is drawn from neural systems. This article shows how to analyze neural systems using information theory to obtain constraints that help identify the algorithms run by such systems and the information they represent. Algorithms and representations identified information-theoretically may then guide the design of biologically inspired computing systems (BICS). The material covered includes the necessary introduction to information theory and the estimation of information theoretic quantities from neural data. We then show how to analyze the information encoded in a system about its environment, and also discuss recent methodological developments on the question of how much information each agent carries about the environment either uniquely, or redundantly or synergistically together with others. Last, we introduce the framework of local information dynamics, where information processing is decomposed into component processes of information storage, transfer, and modification -- locally in space and time. We close by discussing example applications of these measures to neural data and other complex systems

Neutral coding - A report based on an NRP work session

Neural coding by impulses and trains on single and multiple channels, and representation of information in nonimpulse carrier

Recognition memory in amnestic-mild cognitive impairment: insights from event-related potentials

Episodic memory loss is the hallmark cognitive dysfunction associated with Alzheimer’s disease (AD). Amnestic mild cognitive impairment (a-MCI) frequently represents a transitional stage between normal aging and early AD. A better understanding of the qualitative features of memory loss in a-MCI may have important implications for predicting those most likely to harbor AD-related pathology and for disease monitoring. Dual process models of memory argue that recognition memory is subserved by the dissociable processes of recollection and familiarity. Work studying recognition memory in a-MCI from this perspective has been controversial, particularly with regard to the integrity of familiarity. Event-related potentials (ERPs) offer an alternative means for assessing these functions without the associated assumptions of behavioral estimation methods. ERPs were recorded while a-MCI patients and cognitively normal (CN) age-matched adults performed a recognition memory task. When retrieval success was measured (hits versus correct rejections) in which performance was matched by group, a-MCI patients displayed similar neural correlates to that of the CN group, including modulation of the FN400 and the late positive complex (LPC) which are thought to index familiarity and recollection, respectively. Alternatively, when the integrity of these components was measured based on retrieval attempts (studied versus unstudied items), a-MCI patients displayed a reduced FN400 and LPC. Furthermore, modulation of the FN400 correlated with a behavioral estimate of familiarity and the LPC with a behavioral estimate of recollection obtained in a separate experiment in the same individuals, consistent with the proposed mappings of these indices. These results support a global decline of recognition memory in a-MCI, which suggests that the memory loss of prodromal AD may be qualitatively distinct from normal aging

The iPSC perspective on schizophrenia

Over a decade of schizophrenia research using human induced pluripotent stem cell (iPSC)-derived neural models has provided substantial data describing neurobiological characteristics of the disorder in vitro. Simultaneously, translation of the results into general mechanistic concepts underlying schizophrenia pathophysiology has been trailing behind. Given that modeling brain function using cell cultures is challenging, the gap between the in vitro models and schizophrenia as a clinical disorder has remained wide. In this review, we highlight reproducible findings and emerging trends in recent schizophrenia-related iPSC studies. We illuminate the relevance of the results in the context of human brain development, with a focus on processes coinciding with critical developmental periods for schizophrenia.Peer reviewe

The etiology of ADHD

Attention Deficit/Hyperactivity Disorder (“ADHD”) is a complex multi-factorial disorder that was first described in the late 1800s as a defect in moral control. By the early 1900s, ADHD shifted away from being a behavioral-based to a neurobiological-based disorder. During this period, individuals with ADHD were classified as having minimal brain damage. Early studies focused on the clinical presentation of ADHD. As advances in neuroimaging and molecular marker techniques started to develop, researchers were able to focus more on the neurobiological aspects of ADHD. This shift was instrumental to both the diagnosis and treatment of ADHD. This paper surveys the existing literature on ADHD in an attempt to elucidate its etiology. While several areas of research seem promising, so far, no single major contributor to ADHD has been identified. This paper first looks at the history behind ADHD. The historical background was instrumental in directing the course of ADHD research. Next, the Diagnostic and Statistical Manual of Mental Disorders (“DSM”) is examined with a focus on the changes made to DSM-IV and reflected in DSM-V. While DSM is a valuable diagnostic tool, its purpose in elucidating the etiology behind ADHD is questionable. Despite that, discussion of the DSM is necessary as it is impossible to study a disorder without delineating the normal from the abnormal. What follows this discussion is a brief overview of comorbidities that are often associated, and possibly share, a common etiology with ADHD. The paper then examines the theories promulgated by researchers as to the neurobiological basis of ADHD. This examination is followed by a discussion of recent findings into the pathology behind ADHD, which mainly centers around differences in brain structure and connectivity. Further analysis of these studies reveals that sex plays an instrumental role in the type of brain abnormalities found in ADHD children. In addition, delays in brain development are analyzed, and age is discussed as a factor in the presentation of ADHD. This paper goes on to examine genetics as a contributor to the etiology of ADHD. This examination proves fruitful as several genes of interest seem to indicate a hereditary component of ADHD. Finally, treatment options such as psychosocial therapy and medications that help ADHD patients maintain a quality of life, are discussed. By studying the mechanism of action underlying these medications, additional clues as to the etiology of ADHD may be discovered. There is still a long way to go before a complete picture of ADHD emerges. Already, studies are showing that race and environmental factors play a role in how ADHD presents. These two areas have rarely been studied and doing so will only serve to enhance the current understanding of ADHD. Despite an incomplete picture, the scientific community has come a long way from the 1800s where ADHD was thought to result from a defect in moral control. With early diagnosis and proper treatment, the ADHD individuals of today can live a life as close to that of their neurotypical peers as possible

The influence of acute aerobic exercise on excitability and rapid plasticity in the primary motor cortex

The aim of this thesis was to explore the influence of a single session of aerobic exercise on excitability changes and markers of short-term plasticity in the human primary motor cortex (M1). To that end, this thesis consists of 4 studies. In the first experiment, we explored whether acute exercise alone could modulate resting excitability in M1. We demonstrated that 20 minutes of moderate-intensity stationary biking could suppress intracortical inhibition and enhance intracortical facilitation in a non-exercised upper limb muscle for up to 30 minutes following exercise completion. Since decreases in inhibition are a necessary precursor to neuroplastic changes, we then investigated whether exercise could enhance the induction of rapid plasticity. We used paired-associative stimulation (PAS), a technique that reliably induces long-term potentiation (LTP)-like plasticity in M1 and found that a preceding bout of exercise enhanced the effectiveness of the intervention. Next, we examined whether these cortical changes were consistent across the entire cortical representation of the target muscle and if they were related to any measurable changes in motor performance. We paired exercise with a bimanual motor training task and observed that while performance was not enhanced compared to training alone, exercise facilitated training-related cortical excitability increases throughout the representation of the trained muscle. Finally, we demonstrated that exercise has opposite effects on the induction of long-term depression (LTD), suggesting that exercise is biased towards increasing excitability, and that this influence is evident even when exercise is performed following, rather than prior to, plasticity induction. This thesis demonstrates that aerobic exercise may optimize the conditions for experience-dependent plasticity to occur and provides a rationale for the use of exercise as an adjunct to interventions that aim to induce LTP in human motor cortex