Goal-directed spatial decision making video games combine spatial mapping, memory, and reward; all of which can involve hippocampal excitation through suppression of an inhibitory neurotransmitter, γ-aminobutyric acid. In this study, GABA was measured before and after 30 min of video game play within a voxel around the hippocampus. It was predicted that all participants would experience a decrease in GABA during gaming as a result of in-game rewards; and, those who were most competitive with the goal-directed spatial decision making game (...) would display lower hippocampal GABA concentrations after gaming. Those who were not competitive, because they were too skilled or not skilled enough, would demonstrate higher hippocampal GABA concentrations after gaming. While there were no significant differences in hippocampal GABA before and after gaming for gamers and non-gamers alike, there was a significant quadratic regression between performance on a spatial working memory task and post-gaming hippocampal GABA concentrations. (shrink)

CHAPTER 1 Neurotransmitter networks Elaine Perry and Allan Young i. Introduction This first chapter sets the scene for subsequent exploration of potential ...

This pioneering book explores in depth the role of neurotransmitters in conscious awareness. The central aim is to identify common neural denominators of conscious awareness, informed by the neurochemistry of natural, drug induced and pathological states of consciousness. Chemicals such as acetylcholine and dopamine, which bridge the synaptic gap between neurones, are the 'neurotransmitters in mind' that form the substance of the volume, which is essential reading for all who believe that unravelling mechanisms of consciousness must include these (...) vital systems of the brain.Up-to-date information is provided on: Psychological domains of attention, motivation, memory, sleep and dreaming that define normal states of consciousness. Effects of chemicals that alter or abolish consciousness, including hallucinogens and anaesthetics. Disorders of the brain such as dementia, schizophrenia and depression considered from the novel perspective of the way these affect consciousness, and how this might relate to disturbances in neurotransmission.(Series B). (shrink)

Many biologically active compounds including neurotransmitters, metabolic precursors, and certain drugs are accumulated intracellularly by transporters that are coupled to the transmembrane Na+ gradient. Amino acid neurotransmitter transporters play a key role in the regulation of extracellular amino acid concentrations and termination of neurotransmission in the CNSAbbreviations: CNS, central nervous system; GABA, γ‐aminobutyric acid; cDNA, complementary deoxyribonucleic acid; mRNA, messenger ribonucleic acid; NMDA, N‐methyl‐D‐aspartate; PKC, protein kinase C; PMA, phorbol 12‐myristate 13‐acetate; DAG, diacyl glycerol; R59022, DAG kinase inhibitor; AA, (...) arachidonic acid; ACHC, cis‐3‐aminocyclohexanecarboxylic acid; GAT‐A, ACHC‐sensitive GABA transporter; GAT‐B, β‐alanine‐sensitive GABA transporter; GLY‐1 and GLYT‐1, glycine transporters; PROT‐1, proline transporter; BGT‐1, betaine transporter.. Transporters for the major amino acid neurotransmitters glutamate, GABA, and glycine are found in both neurons and glial cells. Recent work has resulted in the identification of cDNAs encoding several amino acid neurotransmitter transport proteins, all of which belong to the Na+‐and Cl−‐dependent transporter gene family. The diversity of this family suggests a degree of transporter heterogeneity that is greater than that indicated by biochemical and pharmacological studies. (shrink)

Objective Manic and depressive phases of bipolar disorder (BD) show opposite psychomotor symptoms. Neuronally, these may depend on altered relationships between sensorimotor network (SMN) and subcortical structures. The study aimed to investigate the functional relationships of SMN with substantia nigra (SN) and raphe nuclei (RN) via subcortical-cortical loops, and their alteration in bipolar mania and depression, as characterized by psychomotor excitation and inhibition. -/- Method In this resting-state functional magnetic resonance imaging (fMRI) study on healthy (n = 67) and BD (...) patients (n = 100), (1) functional connectivity (FC) between thalamus and SMN was calculated and correlated with FC from SN or RN to basal ganglia (BG)/thalamus in healthy; (2) using an a-priori-driven approach, thalamus-SMN FC, SN-BG/thalamus FC, and RN-BG/thalamus FC were compared between healthy and BD, focusing on manic (n = 34) and inhibited depressed (n = 21) patients. -/- Results (1) In healthy, the thalamus-SMN FC showed a quadratic correlation with SN-BG/thalamus FC and a linear negative correlation with RN-BG/thalamus FC. Accordingly, the SN-related FC appears to enable the thalamus-SMN coupling, while the RN-related FC affects it favoring anti-correlation. (2) In BD, mania showed an increase in thalamus-SMN FC toward positive values (ie, thalamus-SMN abnormal coupling) paralleled by reduction of RN-BG/thalamus FC. By contrast, inhibited depression showed a decrease in thalamus-SMN FC toward around-zero values (ie, thalamus-SMN disconnection) paralleled by reduction of SN-BG/thalamus FC (and RN-BG/thalamus FC). The results were replicated in independent HC and BD datasets. -/- Conclusions These findings suggest an abnormal relationship of SMN with neurotransmitters-related areas via subcortical-cortical loops in mania and inhibited depression, finally resulting in psychomotor alterations. (shrink)

Accumulation of neurotransmitters in the lumen of synaptic vesicles (SVs) relies on the activity of the vacuolar‐type H+‐ATPase. This pump drives protons into the lumen, generating a proton electrochemical gradient (ΔμH+) across the membrane. Recent work has demonstrated that the balance between the chemical (ΔpH) and electrical (ΔΨ) components of ΔμH+ is regulated differently by some distinct vesicle types. As different neurotransmitter transporters use ΔpH and ΔΨ with different relative efficiencies, regulation of this gradient balance has the potential to (...) influence neurotransmitter uptake. Nevertheless, the underlying mechanisms responsible for this regulation remain poorly understood. In this review, we provide an overview of current neurotransmitter uptake models, with a particular emphasis on the distinct roles of the electrical and chemical gradients and current hypotheses for regulatory mechanisms. -/- . (shrink)

Ductin is the highest conserved membrane protein yet found in eukaryotes. It is multifunctional, being the subunit c or proteolipid component of the vacuolar H+‐ATPase and at the same time the protein component of a form of gap junction in metazoan animals. Analysis of its structure shows it to be a tandem repeat of two 8‐kDa domains derived from the subunit c of the F0 proton pore from the F1F0 ATPase. Each domain contains two transmembrane α‐helices, which together may form (...) a four‐helix bundle. In both the V‐ATPase and gap junction channel, ductin is probably arranged as a hexamer of subunits forming a central channel of gap junction‐like proportions. The two functions appear to be seggregated by ductin having two orientations in the bilayer. Ductin is also the major component of the mediatophore, a protein complex which may aid in the release of neurotransmitters across the pre‐synaptic membrane. It is also a target for a class of poorly understood viral polypeptides. These polypeptides are small and highly hydrophobic and some have oncogenic activity. Ductin thus appears to be at the crossroads of a number of biological processes. (shrink)

The goal of this work is to compile the basic components for the construction of an electromagnetic field theory of consciousness that meets the standards of a fundamental theory. An essential cornerstone of the conceptual framework is the vacuum state of quantum electrodynamics which, contrary to the classical notion of the vacuum, can be viewed as a vibrant ocean of energy, termed zero-point field (ZPF). Being the fundamental substrate mediating the electromagnetic force, the ubiquitous ZPF constitutes the ultimate bedrock of (...) all electromagnetic phenomena. In particular, resonant interaction with the ZPF is critical for understanding rapidly forming, long-range coherent activity patterns that are characteristic of brain dynamics. Assuming that the entire phenomenal color palette is rooted in the vibrational spectrum of the ZPF and that each normal mode of the ZPF is associated with an elementary shade of consciousness, it stands to reason that conscious states are caused by the coupling of the brain to a particular set of normal modes selectively filtered from the full frequency spectrum of the ZPF. From this perspective, the brain is postulated to function as a resonant oscillator that couples to a specific range of ZPF modes, using these modes as a keyboard for the composition of an enormous variety of phenomenal states. Theoretical considerations suggest that the brain-ZPF interface is controlled by altering the concentrations of neurotransmitters, placing the detailed study of the neurotransmitter-ZPF interaction at the center of future research activities. (shrink)

The neurotransmitters GABA and glutamate have been suggested to play a role in Major Depressive Disorder (MDD) through an imbalance between cortical inhibition and excitation. This effect has been highlighted in higher brain areas, such as the prefrontal cortex, but has also been posited in basic sensory cortices. Based on this, magnetic resonance spectroscopy (MRS) was used to investigate potential changes to GABA+ and glutamate+glutamine (Glx) concentrations within the occipital cortex in MDD patients (n = 25) and healthy controls (...) (n = 25). No difference in occipital GABA+ or Glx concentrations, nor in the GABA+/Glx ratio, was found between groups. An analysis of an extended MDD patient and unmatched control dataset (n = 90) found no correlation between metabolite concentrations and depressive symptoms. These results were integrated with prior studies through metabolite-specific meta-analyses, revealing no difference in occipital GABA and Glx concentrations between patients and controls. An effect of publication year on GABA group differences was found, suggesting that previously reported results may have been artifacts of measurement accuracy. Taken together, our results suggest that, contrary to some prior reports, MRS measurements of occipital GABA and Glx do not differ between MDD patients and controls. (shrink)

Neurotransmitter release takes place by the exocytosis of loaded synaptic vesicles. The vesicles then fuse to the presynaptic membrane and are recycled by an endocytotic mechanism. A quantitative optical assay that detects uptake and release of a fluorescent dye during presynaptic activity was recently developed and used on the frog neauromuscular junction. I discuss a report(1) that demonstrates the effective application of this method to a Drosophila preparation. The authors use the shibire mutation and a spider venom to identify two (...) intermediates in vesicle recycling. Their report, along with other recent studies, demonstrates the power and promise of the genetic approach for the understanding of mechanisms of synapse function and development. (shrink)

GraphicalExercise, neurotransmitters, growth factors, myokines, and potential effects on the brain.As human life expectancy increases, cognitive decline and memory impairment threaten independence and quality of life. Therefore, finding prevention and treatment strategies for memory impairment is an important health concern. Moreover, a better understanding of the mechanisms involved underlying memory preservation will enable the development of appropriate pharmaceuticals drugs for those who are activity limited. Exercise training as a non-pharmacological tool, has been known to increase the mean lifespan by (...) maintaining general body health and improving the cardiovascular and nervous systems function. Among different exercise training protocols, aerobic exercise has been reported to prevent the progression of memory decline, provided adequate exertion level, duration, and frequency. Mechanisms underlying exercise training effects on memory performance have not been understood yet. Convergent evidence suggest several direct and indirect mechanisms at molecular and supramolecular levels. The supramolecular level includes improvement in blood circulation, synaptic plasticity and neurogenesis which are under controls of complex molecular signaling of neurotransmitters, neurotrophic factors, exerkines, and epigenetics factors. Among these various factors, irisin/BDNF signaling seems to be one of the important mediators of crosstalk between contracted skeletal muscles and the brain during exercise training. This review provides an affordable and effective method to improve cognitive function in old ages, particularly those who are most vulnerable to neurodegenerative disorders. (shrink)

In various documents the view emerges that contemporary biotechnosciences are currently experiencing a scientific revolution: a massive increase of pace, scale and scope. A significant part of the research endeavours involved in this scientific upheaval is devoted to understanding and, if possible, ameliorating humankind: from our genomes up to our bodies and brains. New developments in contemporary technosciences, such as synthetic biology and other genomics and “post-genomics” fields, tend to blur the distinctions between prevention, therapy and enhancement. An important dimension (...) of this development is “biomimesis”: i.e. the tendency of novel technologies and materials to mimic or plagiarize nature on a molecular and microscopic level in order to optimise prospects for the embedding of technological artefacts in natural systems such as human bodies and brains. In this paper, these developments are read and assessed from a psychoanalytical perspective. Three key concepts from psychoanalysis are used to come to terms with what is happening in research laboratories today. After assessing the general profile of the current revolution in this manner, I will focus on a particular case study, a line of research that may serve as exemplification of the vicissitudes of contemporary technosciences, namely viral biomaterials. Viral life forms can be genetically modified (their genomes can be rewritten) in such a manner that they may be inserted in human bodies in order to produce substances at specific sites such as hormones (testosterone), neurotransmitters (dopamine), enzymes (insulin) or bone and muscle tissue. Notably, certain target groups such as top athletes, soldiers or patients suffering from degenerative diseases may become the pioneers serving as research subjects for novel applications. The same technologies can be used for various purposes ranging from therapy up to prevention and enhancement. (shrink)

Research in the neurosciences continues to provide evidence that sleep plays a role in the processes of learning and memory. There is less of a consensus, however, regarding the precise stages of memory development during which sleep is considered a requirement, simply favorable, or not important. This article begins with an overview of recent studies regarding sleep and learning, predominantly in the procedural memory domain, and is measured against our current understanding of the mechanisms that govern memory formation. Based on (...) these considerations, I offer a new neurocognitive framework of procedural learning, consisting first of acquisition, followed by two specific stages of consolidation, one involving a process of stabilization, the other involving enhancement, whereby delayed learning occurs. Psychophysiological evidence indicates that initial acquisition does not rely fundamentally on sleep. This also appears to be true for the stabilization phase of consolidation, with durable representations, resistant to interference, clearly developing in a successful manner during time awake (or just time, per se). In contrast, the consolidation stage, resulting in additional/enhanced learning in the absence of further rehearsal, does appear to rely on the process of sleep, with evidence for specific sleep-stage dependencies across the procedural domain. Evaluations at a molecular, cellular, and systems level currently offer several sleep specific candidates that could play a role in sleep-dependent learning. These include the upregulation of select plasticity-associated genes, increased protein synthesis, changes in neurotransmitter concentration, and specific electrical events in neuronal networks that modulate synaptic potentiation. Key Words: consolidation; enhancement; learning; memory; plasticity; sleep; stabilization. (shrink)

There is converging evidence that high doses of hallucinogenic drugs can produce significant alterations of self-experience, described as the dissolution of the sense of self and the loss of boundaries between self and world. This article discusses the relevance of this phenomenon, known as “drug-induced ego dissolution (DIED)”, for cognitive neuroscience, psychology and philosophy of mind. Data from self-report questionnaires suggest that three neuropharmacological classes of drugs can induce ego dissolution: classical psychedelics, dissociative anesthetics and agonists of the kappa opioid (...) receptor (KOR). While these substances act on different neurotransmitter receptors, they all produce strong subjective effects that can be compared to the symptoms of acute psychosis, including ego dissolution. It has been suggested that neuroimaging of DIED can indirectly shed light on the neural correlates of the self. While this line of inquiry is promising, its results must be interpreted with caution. First, neural correlates of ego dissolution might reveal the necessary neurophysiological conditions for the maintenance of the sense of self, but it is more doubtful that this method can reveal its minimally sufficient conditions. Second, it is necessary to define the relevant notion of self at play in the phenomenon of DIED. This article suggests that DIED consists in the disruption of subpersonal processes underlying the “minimal” or “embodied” self, i.e., the basic experience of being a self rooted in multimodal integration of self-related stimuli. This hypothesis is consistent with Bayesian models of phenomenal selfhood, according to which the subjective structure of conscious experience ultimately results from the optimization of predictions in perception and action. Finally, it is argued that DIED is also of particular interest for philosophy of mind. On the one hand, it challenges theories according to which consciousness always involves self-awareness. On the other hand, it suggests that ordinary conscious experience might involve a minimal kind of self-awareness rooted in multisensory processing, which is what appears to fade away during DIED. (shrink)

Like the cracking of the genetic code and the creation of the atomic bomb, the discovery of how the brain's neurons work is one of the fundamental scientific developments of the twentieth century. The discovery of neurotransmitters revolutionized the way we think about the brain and what it means to be human yet few people know how they were discovered, the scientists involved, or the fierce controversy about whether they even existed. The War of the Soups and the Sparks (...) tells the saga of the dispute between the pharmacologists, who had uncovered the first evidence that nerves communicate by releasing chemicals, and the neurophysiologists, experts on the nervous system, who dismissed the evidence and remained committed to electrical explanations. The protagonists of this story are Otto Loewi and Henry Dale, who received Nobel Prizes for their work, and Walter Cannon, who would have shared the prize with them if he had not been persuaded to adopt a controversial theory (how that happened is an important part of this history). Valenstein sets his story of scientific discovery against the backdrop of two world wars and examines the fascinating lives of several scientists whose work was affected by the social and political events of their time. He recounts such stories as Loewi's arrest by Nazi storm troopers and Dale's efforts at helping key scientists escape Germany. The War of the Soups and the Sparks reveals how science and scientists work. Valenstein describes the observations and experiments that led to the discovery of neurotransmitters and sheds light on what determines whether a novel concept will gain acceptance among the scientific community. His work also explains the immense importance of Loewi, Dale, and Cannon's achievements in our understanding of the human brain and the way mental illnesses are conceptualized and treated. (shrink)

This article considers the roles played by brain images (e.g., from PET scans) in mass media as experienced by people suffering from mental illness, and as used by scientists and activist groups in demonstrating a biological basis for mental illness. Examining the rhetorical presentation of images in magazines and books, the article describes the persuasive power that brain images have in altering the understanding people have of their own body—their objective self. Analyzing first-person accounts of encounters with brain images, it (...) argues that people come to understand themselves as having neurotransmitter imbalances that are the cause of their illnesses via received facts and images of the brain, but that this understanding is incomplete and in tension with the sense that they are their brain. The article concludes by querying the emergence of a pharmaceutical self, in which one experiences one's brain as if on drugs, as a new form of objective self-fashioning. (shrink)

_Spiritual practices have been proposed to have many beneficial effects as far as mental health is concerned. The exact neural basis of these effects is slowly coming to light and different imaging techniques have elucidated the neural basis of meditative practices. The evidence though preliminary and based on studies replete with methodological constraints, points toward the involvement of the prefrontal and parietal cortices. The available data on meditation focus on activated frontal attentional network. Neuroimaging studies have shown that meditation results (...) in an activation of the prefrontal cortex, activation of the thalamus and the inhibitory thalamic reticular nucleus and a resultant functional deafferentation of the parietal lobe. The neurochemical change as a result of meditative practices involves all the major neurotransmitter systems. The neurotransmitter changes contribute to the amelioration of anxiety and depressive symptomatology and in part explain the psychotogenic property of meditation. This overview highlights the involvement of multiple neural structures, the neurophysiological and neurochemical alterations observed in meditative practices._. (shrink)

Moral enhancement is a topic that has sparked much current interest in the world of bioethics. The possibility of making people ‘better,’ not just in the conventional enhancement sense of improving health and other desirable qualities and capacities, but by making them somehow more moral, more decent, altogether better people, has attracted attention from both advocates 1 2 and sceptics 3 alike. The concept of moral enhancement, however, is fraught with difficult questions, theoretical and practical. What does it actually mean (...) to be ‘more moral’? How would moral enhancement be defined and would it necessarily, as some have claimed, make the world a better or safer place? How would or could such enhancement be achieved safely and without undue constraint on personal liberty and autonomy? On this subject, a recent paper by Crockett et al 4 investigating the effects of the neurotransmitter serotonin on moral decision-making provides an intriguing scientific basis for examining what might or might not constitute moral enhancement. The study involved treatment with citalopram, a drug that increases the action of serotonin in the brain, and subsequent analysis of participants' decision-making behaviour in two different situations involving moral dilemmas: the well-known ‘Trolley Problem’ 5 and the ‘Ultimatum Game’. 6 The researchers found that citalopram promoted what they call ‘prosocial behaviour’, increasing the participants' aversion to causing direct harm to others: in the first scenario, they were less likely to select the option that required killing one in order to save five, and in the second, less likely to reject unfair offers at the expense of others. The Crockett study is fascinating both for its insight into human behaviour and because it appears to demonstrate that, at least on some accounts of moral behaviour, serotonin may in fact be a …. (shrink)

Aversive experiences have been thought to provoke or exacerbate clinical depression. The present review provides a brief survey of the stress-depression literature and suggests that the effects of stressful experiences on affective state may be related to depletion of several neurotransmitters, including norepinephrine, dopamine, and serotonin. A major element in determining the neurochemical changes is the organism's ability to cope with the aversive stimuli through behavioral means. Aversive experiences give rise to behavioral attempts to cope with the stressor, coupled (...) with increased utilization and synthesis of brain amines to contend with environmental demands. When behavioral coping is possible, neurochemical systems are not overly taxed, and behavioral pathology will not ensue. However, when there can be no behavioral control over the stressful stimuli, or when the aversive experience is perceived as uncontrollable, increased emphasis is placed on coping through endogenous neurochemical mechanisms. Amine utilization increases appreciably and may exceed synthesis, resulting in a net reduction of amine stores, which in turn promotes or exacerbates affective disorder. The processes governing the depletions may be subject to sensitization or conditioning, such that exposure to traumatic experiences may have long-term repercussions when the organism subsequently encounters related stressful stimuli. With continued uncontrollable stimulation, adaptation occurs in the form of increased activity of synthetic enzymes, and levels of amines approach basal values. It is suggested that either the initial amine depletion provoked by aversive experiences or a dysfunction of the adaptive processes, resulting in persistent amine depletion, contributes to behavioral depression. Aside from the contribution of behavioral coping, several organismic, experiential, and environmental variables will influence the effects of aversive experiences on neurochemical activity, and may thus influence vulnerability to depression. (shrink)

This article examines the neurobiological basis of the healing power attributed to shamanic practices in the Andes and Brazil in light of the pharmacology of neurotransmitters and the new technological explorations of brain functioning. The psychotropic plants used in shamanic psychiatric cures interfere selectively with the intrinsic neuromediators of the brain. Mainly they may alter: (1) the neuroendocrine functioning through the adrenergic system by controlling stressful conditions, (2) the dopaminergic system in incentive learning and emotions incorporation, (3) the serotoninergic (...) system in modulating behaviors, and mood, and (4) basic functions implied in anxiety or depression. PET scans and functional magnetic resonance imaging studies of hypnotic trance and altered states of consciousness may provide a useful model for the neurophysiological phenomena of shamanic drum-and-dance trance. The reorganization of cortical areas and the direct interconnections between the prefrontal cortex and the dopaminergic reward centers in the limbic system are of particular significance for human social judgment and symbolic processing. Those centers—including the hypothalamus and the amygdala (associated with psychosomatic equilibrium, memory, and emotion) are enhanced. This arousal may be amplified in order to induce a cathartic crisis—the shamanic trance. It is suggested that through this holistic approach the shaman empirically interferes in neurobiological dysfunctions. (shrink)

Glutamate is the major excitatory neurotransmitter in the mammalian brain, with receptors on every neuron in the central nervous system; it has major roles in fast synaptic transmission and in the establishment of certain forms of memory. More than 20 years ago Olney and his colleagues(1) described the [Excitotoxic Hypothesis] which postulates that, in addition to its normal function in the healthy brain, glutamate can kill neurons by prolonged, receptorsmediated depolarization resulting in irreversible disturbances in ion homeostasis. Therefore, glutamate is (...) a two‐edged sword; in certain undefined, adverse conditions it undergoes a transition from neurotransmitter to neurotoxin. Its toxicity has been implicated in the death of neurons in ischemia, epilepsy, and the neurodegenerative disorders such as Alzheimer's, Huntington's, and Parkinson's diseases(2–5). Recent advances in the molecular cloning of the genes for the glutamate family of receptors has revealed a plethora of receptor subtypes and an unexpected level of complexity in the mechanisms of receptor expression and function. (shrink)

In his "Let the drugs lead the way! On the unfolding of a research program in psychiatry," Shai Mulinari nicely lays out the evolution of theories of depression since the late 1950s; that is, understanding depression as ultimately a brain disorder centering on the functioning of monoamine neurotransmitters. Moreover, the emergence of various psychotropic drug treatments have provided researchers with a "pharmacological bridge" to gain a more precise understanding of depression by observing the effects of these drugs on patients' (...) monoamines and mood. This evolution, Mulinari argues, fits Imre Lakatos's concept of a research program. Mulinari's narrative is clear, compelling, and informative and it generates some... (shrink)

Twenty five years ago, Sir John Carew Eccles together with Friedrich Beck proposed a quantum mechanical model of neurotransmitter release at synapses in the human cerebral cortex. The model endorsed causal influence of human consciousness upon the functioning of synapses in the brain through quantum tunneling of unidentified quasiparticles that trigger the exocytosis of synaptic vesicles, thereby initiating the transmission of information from the presynaptic towards the postsynaptic neuron. Here, we provide a molecular upgrade of the Beck and Eccles model (...) by identifying the quantum quasiparticles as Davydov solitons that twist the protein α-helices and trigger exocytosis of synaptic vesicles through helical zipping of the SNARE protein complex. We also calculate the observable probabilities for exocytosis based on the mass of this quasiparticle, along with the characteristics of the potential energy barrier through which tunneling is necessary. We further review the current experimental evidence in support of this novel bio-molecular model as presented. (shrink)

A comparative method of studying the biological bases of personality compares human trait dimensions with likely animal models in terms of genetic determination and common biological correlates. The approach is applied to the trait of sensation seeking, which is defined on the human level by a questionnaire, reports of experience, and observations of behavior, and on the animal level by general activity, behavior in novel situations, and certain types of naturalistic behavior in animal colonies. Moderately high genetic determination has been (...) found for human sensation seeking, and marked strain differences in rodents have been found in open-field behavior that may be related to basic differences in brain neurochemistry. Agonistic and sociable behaviors in both animals and humans and the trait measure of sensation seeking in humans have been related to certain common biological correlates such as gonadal hormones, monoamine oxidase (MAO), and augmenting of the cortical evoked potential.The monoamine systems in the rodent brain are involved in general activity, exploratory behavior, emotionality, socialization, dominance, sexual and consummately behaviors, and intracranial self-stimulation. Preliminary studies have related norepinephrine and enzymes involved in its production and degradation to human sensation seeking. A model is suggested that relates mood, behavioral activity, sociability, and clinical states to activity of the central catecholamine neurotransmitters and to neuroregulators and other transmitters that act in opposite ways on behavior or stabilize activity in the arousal systems. Stimulation and behavioral activity act on the catecholamine systems in a brain–behavior feedback loop. At optimal levels of catecholamine systems activity (CSA) mood is positive and activity and sociability are adaptive. At very low or very high levels of CSA mood is dysphoric, activity is restricted or stereotyped, and the organism is unsocial or aggressively antisocial. Novelty, in the absence of threat, may be rewarding through activation of noradrenergic neurons. (shrink)

Language has been argued to arise, both ontogenetically and phylogenetically, from specific patterns of brain wiring. We argue that it can further be shown that core features of language processing emerge from particular phasal and cross-frequency coupling properties of neural oscillations; what has been referred to as the language ‘oscillome’. It is expected that basic aspects of the language oscillome result from genetic guidance, what we will here call the language ‘oscillogenome’, for which we will put forward a list of (...) candidate genes. We have considered genes for altered brain rhythmicity in conditions involving language deficits: autism spectrum disorders, schizophrenia, specific language impairment and dyslexia. These selected genes map on to aspects of brain function, particularly on to neurotransmitter function. We stress that caution should be adopted in the construction of any oscillogenome, given the range of potential roles particular localized frequency bands have in cognition. Our aim is to propose a set of genome-to-language linking hypotheses that, given testing, would grant explanatory power to brain rhythms with respect to language processing and evolution. (shrink)

The electric activities of cortical pyramidal neurons are supported by structurally stable, morphologically complex axo-dendritic trees. Anatomical differences between axons and dendrites in regard to their length or caliber reflect the underlying functional specializations, for input or output of neural information, respectively. For a proper assessment of the computational capacity of pyramidal neurons, we have analyzed an extensive dataset of three-dimensional digital reconstructions from the NeuroMorphoOrg database, and quantified basic dendritic or axonal morphometric measures in different regions and layers of (...) the mouse, rat or human cerebral cortex. Physical estimates of the total number and type of ions involved in neuronal electric spiking based on the obtained morphometric data, combined with energetics of neurotransmitter release and signaling fueled by glucose consumed by the active brain, support highly efficient cerebral computation performed at the thermodynamically allowed Landauer limit for implementation of irreversible logical operations. Individual proton tunneling events in voltage-sensing S4 protein alpha-helices of Na+, K+ or Ca2+ ion channels are ideally suited to serve as single Landauer elementary logical operations that are then amplified by selective ionic currents traversing the open channel pores. This miniaturization of computational gating allows the execution of over 1.2 zetta logical operations per second in the human cerebral cortex without combusting the brain by the released heat. (shrink)

Almost all computational models of the mind and brain ignore details about neurotransmitters, hormones, and other molecules. The neglect of neurochemistry in cognitive science would be appropriate if the computational properties of brains relevant to explaining mental functioning were in fact electrical rather than chemical. But there is considerable evidence that chemical complexity really does matter to brain computation, including the role of proteins in intracellular computation, the operations of synapses and neurotransmitters, and the effects of neuromodulators such (...) as hormones. Neurochemical computation has implications for understanding emotions, cognition, and artificial intelligence. (shrink)