Alcoholic neurobiology: Changes in dependence and recovery

This article presents the proceedings of a symposium held at the meeting of the International Society for Biomedical Research on Alcoholism (ISBRA) in Mannheim, Germany, in October, 2004. Chronic alcoholism follows a fluctuating course, which provides a naturalistic experiment in vulnerability, resilience, and recovery of human neural systems in response to presence, absence, and history of the neurotoxic effects of alcoholism. Alcohol dependence is a progressive chronic disease that is associated with changes in neuroanatomy, neurophysiology, neural gene expression, psychology, and behavior. Specifically, alcohol dependence is characterized by a neuropsychological profile of mild to moderate impairment in executive functions, visuospatial abilities, and postural stability, together with relative sparing of declarative memory, language skills, and primary motor and perceptual abilities. Recovery from alcoholism is associated with a partial reversal of CNS deficits that occur in alcoholism. The reversal of deficits during recovery from alcoholism indicates that brain structure is capable of repair and restructuring in response to insult in adulthood. Indirect support of this repair model derives from studies of selective neuropsychological processes, structural and functional neuroimaging studies, and preclinical studies on degeneration and regeneration during the development of alcohol dependence and recovery from dependence. Genetics and brain regional specificity contribute to unique changes in neuropsychology and neuroanatomy in alcoholism and recovery. This symposium includes state-of-the-art presentations on changes that occur during active alcoholism as well as those that may occur during recovery-abstinence from alcohol dependence. Included are human neuroimaging and neuropsychological assessments, changes in human brain gene expression, allelic combinations of genes associated with alcohol dependence and preclinical studies investigating mechanisms of alcohol induced neurotoxicity, and neuroprogenetor cell expansion during recovery from alcohol dependence.

Evolutionary neurobiology and art

In his important book on evolutionary theory, Darwin's Dangerous Idea, Daniel Dennett warns that Darwin's idea seeps through every area of human discourse like a "universal acid" (Dennett, 1995). Art and the aesthetic response cannot escape its influence. So my approach in this chapter is essentially naturalistic. Friedrich Nietzsche writes of observing the human comedy from afar, "like a cold angel...without anger, but without warmth" (Nietzsche, 1872, p. 164). Whether Nietzsche, of all people, could have done this is a matter of debate. But we know what he means. It describes a stance outside the human world as if looking down on human folly from Mount Olympus. From this stance, humans, their art and neurology are all part of the natural world, all part of the evolutionary process, the struggle for existence. The anthropologist David Dutton, in his contribution to the Routledge Companion to Aesthetics, says that all humans have an aesthetic sense (Dutton, 2001). It is a human universal. Biologists argue that such universals have an evolutionary basis. Furthermore, many have argued that not only humans but also animals, at least the higher mammals and birds, have an appreciation of the beautiful and the ugly (Eibl-Eibesfeldt, 1988).11Charles Darwin indeed writes "Birds appear to be the most aesthetic of all animals, excepting, of course, man, and they have nearly the same sense of the beautiful that we have" (1871, The Descent of Man and Selection in Relation to Sex, London: John Murray, vol.2, xiii, 39). This again suggests that aesthetics has an evolutionary origin. In parenthesis here, I should perhaps say that I am well aware of the criticism leveled at evolutionary psychology. I am well aware that it has been attacked as just so many "just-so" stories. This is neither the time nor the place to mount a defense but simply just to say that I believe that a defense is eminently feasible. © 2006 Elsevier Inc. All rights reserved.

Dopamine, empathy and the neurobiology of leadership

Objectives: Organisational Psychologists have long sought after methods by which to train individuals to become more effective leaders. Indeed considerable sums of money are spent on the design of such training programs. Yet it is not clear whether or not leadership skills can be taught or whether they are innate. Social leadership is a varied construct consisting of many diverse aspects, yet the ability to empathise with subordinates is a core skill that underpins effective transformational leadership. This type of leadership consists of four characteristics which are labelled ‘idealized influence’, ‘inspirational motivation’, ‘intellectual stimulation’ and ‘individualized consideration’. This is distinct from the transactional style of leadership, which is based on offering contingent rewards for completion of specific tasks. By identifying a specific gene that mediates distinct leadership traits, more effective training regimes can be designed. Design: There are two likely candidate genes that may mediate empathic leadership. The first is catechol-O-methyltransferase (COMT) which is involved with dopamine synthesis, and the second is the serotonin transporter promoter gene (5-HTTLPR). Both these genes mostly appear in the general population in their heterozygotic form. Thus by comparing phenotypes in leadership traits a measure of base line differences can be examined. Methods: 115 volunteers completed the Multifactor Leadership questionnaire (MLQ), which is a standard 12-item leadership psychometric scale and also underwent buccal swab for subsequent genotyping. Results: Of the 115 subjects 37 were heterozygotic for the COMT gene and 47 heterozygotic for 5-HTTLPR. Of the 12 MLQ subscales, the scores for two of the subscales only differed between the two participant groups. Individuals who were heterozygotic for the COMT gene scored higher on the ‘Inspirational motivation’ t(84)=1.99, p=0.05 and ‘Intellectual stimulation’ t(82)=1.94, p=0.05 scales compared to the carriers for the heterozygotic 5HTPP gene. Conclusions: Given that the behaviours described by these two MLQ subscales require leaders to empathise with subordinates, the current results suggest that dopamine may play a role in this important social task. The fact that both heterozygotic carriers for COMT and 5HTPP were compared allows a comparison to be made between the genotypes most prevalent in the general population.

Elements of molecular neurobiology:instruction manual to 2r.e

Extensively updated, revised and illustrated this unique introductory text presents a molecular account of the structure, function and development of the brain and nervous systems. This book describes the latest research in neurobiology made possible by modern molecular biology techniques. The author synthesizes this new knowledge and demonstrates how an understanding at the molecular level can contribute towards a theory of the brain in health and disease.

Origins of molecular neurobiology:The role of the physicists

The revolution in the foundations of physics at the beginning of the twentieth century suggested to several of its most prominent workers that biology was ripe for something similar. In consequence, a number of physicists moved into biology. They were highly influential in initiating a molecular biology in the 1950s. Two decades later it seemed to several of these migrants, and those they had influenced, that the major problems in molecular biology had been solved, and that it was time to move on to what seemed to them the final problem: the nervous system, consciousness, and the age-old mind-body problem. This paper reviews this "double migration" and shows how the hopes of the first generation of physicist-biologists were both realized and dashed. No new physical principles were discovered at work in the foundations of biology or neuroscience. On the other hand, the mind-set of those trained in physics proved immensely valuable in analyzing fundamental issues in both biology and neuroscience. It has been argued that the outcome of the molecular biology of the 1950s was a change in the concept of the gene from that of "a mysterious entity into that of a real molecular object" (Watson, 1965, p.6); the gates and channels which play such crucial roles in the functioning of nervous systems have been transformed in a similar way. Studies on highly simplified systems have also opened the prospect of finding the neural correlatives of numerous behaviors and neuropathologies. This increasing understanding at the molecular level is invaluable not only in devising rational therapies but also, by defining the material substrate of consciousness, in bringing the mind-body problem into sharper focus. Copyright © Taylor & Francis Inc.

Elements of molecular neurobiology

This edition of the popular text incorporates recent advances in neurobiology enabled by modern molecular biology techniques. Understanding how the brain works from a molecular level allows research to better understand behaviours, cognition, and neuropathologies. Since the appearance six years ago of the second edition, much more has been learned about the molecular biology of development and its relations with early evolution. This "evodevo" (as it has come to be known) framework also has a great deal of bearing on our understanding of neuropathologies as dysfunction of early onset genes can cause neurodegeneration in later life. Advances in our understanding of the genomes and proteomes of a number of organisms also greatly influence our understanding of neurobiology. This book will be of particular interest to biomedical undergraduates undertaking a neuroscience unit, neuroscience postgraduates, physiologists, pharmacologists. It is also a useful basic reference for university libraries.

Elements of molecular neurobiology

Extensively updated, revised and illustrated this unique introductory text presents a molecular account of the structure, function and development of the brain and nervous systems. This book describes the latest research in neurobiology made possible by modern molecular biology techniques. The author synthesizes this new knowledge and demonstrates how an understanding at the molecular level can contribute towards a theory of the brain in health and disease.

Elements of molecular neurobiology

The 1980s have seen spectacular advances in our understanding of the molecular bases of neurobiology. Biological membranes, channel proteins, cytoskeletal elements, and neuroactive peptides have all been illuminated by the molecular approach. The operation of synapses can be seen to be far more subtle and complex than has previously been imagined, and the development of the brain and physical basis of memory have both been illuminated by this new understanding. In addition, some of the ways in which the brain may go wrong can be traced to malfunction at the molecular level. This study attemps a synthesis of this new knowledge, to provide an indication of how an understanding at the molecular level can help towards a theory of the brain in health and disease. The text will be of benefit to undergraduate students of biochemistry, medical science, pharmacy, pharmacology and general biology.

Neurobiology and clinical implications of lucid dreaming

Several lines of evidence converge to the idea that rapid eye movement sleep (REMS) is a good model to foster our understanding of psychosis. Both REMS and psychosis course with internally generated perceptions and lack of rational judgment, which is attributed to a hyperlimbic activity along with hypofrontality. Interestingly, some individuals can become aware of dreaming during REMS, a particular experience known as lucid dreaming (LD), whose neurobiological basis is still controversial. Since the frontal lobe plays a role in self-consciousness, working memory and attention, here we hypothesize that LD is associated with increased frontal activity during REMS. A possible way to test this hypothesis is to check whether transcranial magnetic or electric stimulation of the frontal region during REMS triggers LD. We further suggest that psychosis and LD are opposite phenomena: LD as a physiological awakening while dreaming due to frontal activity, and psychosis as a pathological intrusion of dream features during wake state due to hypofrontality. We further suggest that LD research may have three main clinical implications. First, LD could be important to the study of consciousness, including its pathologies and other altered states. Second, LD could be used as a therapy for recurrent nightmares, a common symptom of depression and post-traumatic stress disorder. Finally, LD may allow for motor imagery during dreaming with possible improvement of physical rehabilitation. In all, we believe that LD research may clarify multiple aspects of brain functioning in its physiological, altered and pathological states.

The Role of Cannabinoids in the Neurobiology of Sensory Gating: A firing rate model study

Gating of sensory (e.g. auditory) information has been demonstrated as a reduction in the auditory-evoked potential responses recorded in the brain of both normal animals and human subjects. Auditory gating is perturbed in schizophrenic patients and pharmacologically by drugs such as amphetamine, phencyclidine or ketamine, which precipitate schizophrenic-like symptoms in normal subjects. The neurobiological basis underlying this sensory gating can be investigated using local field potential recordings from single electrodes. In this paper we use such technology to investigate the role of cannabinoids in sensory gating. Cannabinoids represent a fundamentally new class of retrograde messengers which are released postsynaptically and bind to presynaptic receptors. In this way they allow fine-tuning of neuronal response, and in particular can lead to so-called depolarization-induced suppression of inhibition (DSI). Our experimental results show that application of the exogenous cannabinoid WIN55, 212-2 can abolish sensory gating as measured by the amplitude of local field responses in rat hippocampal region CA3. Importantly we develop a simple firing rate population model of CA3 and show that gating is heavily dependent upon the presence of a slow inhibitory (GABAB) pathway. Moreover, a simple phenomenological model of cannabinoid dynamics underlying DSI is shown to abolish gating in a manner consistent with our experimental findings.

Neurobiology and clinical implications of lucid dreaming

Several lines of evidence converge to the idea that rapid eye movement sleep (REMS) is a good model to foster our understanding of psychosis. Both REMS and psychosis course with internally generated perceptions and lack of rational judgment, which is attributed to a hyperlimbic activity along with hypofrontality. Interestingly, some individuals can become aware of dreaming during REMS, a particular experience known as lucid dreaming (LD), whose neurobiological basis is still controversial. Since the frontal lobe plays a role in self-consciousness, working memory and attention, here we hypothesize that LD is associated with increased frontal activity during REMS. A possible way to test this hypothesis is to check whether transcranial magnetic or electric stimulation of the frontal region during REMS triggers LD. We further suggest that psychosis and LD are opposite phenomena: LD as a physiological awakening while dreaming due to frontal activity, and psychosis as a pathological intrusion of dream features during wake state due to hypofrontality. We further suggest that LD research may have three main clinical implications. First, LD could be important to the study of consciousness, including its pathologies and other altered states. Second, LD could be used as a therapy for recurrent nightmares, a common symptom of depression and post-traumatic stress disorder. Finally, LD may allow for motor imagery during dreaming with possible improvement of physical rehabilitation. In all, we believe that LD research may clarify multiple aspects of brain functioning in its physiological, altered and pathological states.

The organisation of action in complex neurobiological systems

This chapter elucidates key ideas behind neurocomputational and ecological dynamics and perspectives of understanding the organisation of action in complex neurobiological systems. The need to study the close link between neurobiological systems and their environments (particularly their sensory and movement subsystems and the surrounding energy sources) is advocated. It is proposed how degeneracy in complex neurobiological systems provides the basis for functional variability in organisation of action. In such systems processes of cognition and action facilitate the specific interactions of each performer with particular task and environmental constraints.