Molecular neurobiology of ingestive behavior

The concepts and tools of molecular biology may be applied to almost any component of the animal involved in ingestion, but two categories of model system are particularly relevant for molecular analysis: homeostatic regulation of neuropeptide expression in the hypothalamus and neuronal plasticity underlying persistent changes in ingestive behavior. Molecular approaches to these models are reviewed, focusing on our strategy for analyzing conditioned taste aversion learning. Three questions must be answered: Where do the long-term changes occur within the distributed neural network that mediates feeding? This answer reveals the site of neuronal restructuring mediated by gene expression. When does the transition occur from short-term expression to long-term persistence of the change in behavior? This transition reveals the critical time of gene expression. What genes are expressed during the change in behavior? The expression of thousands of genes in discrete subpopulations of cells is likely to be required during critical periods of neuronal restructuring. The identification of these genes is a general challenge for molecular neurobiology. The analysis of ingestive behavior can profit from molecular tools, but ingestion also provides informative models that elucidate the principles of time- and neuron-specific gene expression mediating complex behaviors.     

Basic micro-electrophysiologic techniques used in neurobiology

Problems of application of microelectrophysiological techniques in neurobiology are addressed. Authors focused on five basic recording techniques: micro-EEG, multi unit activity, single unit activity, intracellular recording and patch clamp techniques.     

Sugars and fats: the neurobiology of preference

The appetite for specific foods and nutrients may be under neuroregulatory control. In animal studies, fat intake is increased by both opioids and galanin and reduced by enterostatin, whereas carbohydrate intake is increased by neuropeptide Y (NPY). However, what may be affected is the consumption of preferred foods rather than macronutrients. Fat and sugars are highly preferred whether consumed separately or as mixtures in foods. Studies suggest that sustained consumption of sugars and fats may have additional metabolic consequences; among these are neurochemical changes in brain sites involved in feeding and reward, some of which are also affected by drugs of abuse. Furthermore, the consumption of fats and sugars alters tissue expression of uncoupling proteins, which are also influenced by neuroregulatory peptides and may be markers of energy expenditure. These data suggest that these palatable nutrients may influence energy expenditure through changes in central neuropeptide activity. Fats and sugars could affect central reward systems, thereby increasing food intake, and might have an additional effect on energy expenditure. Such palatable substances may contribute to the observed increase in the body weight of populations from affluent societies during the past few decades.     

The neurobiology of selenium: lessons from transgenic mice

The brain represents a privileged organ with respect to selenium (Se) supply and retention. It contains high amounts of this essential trace element, which is efficiently retained even in conditions of Se deficiency. Accordingly, no severe neurological phenotype has been reported for animals exposed to Se-depleted diets. They are, however, more susceptible to neuropathological challenges. Recently, gene disruption experiments supported a pivotal role for different selenoproteins in brain function. Using these and other transgenic models, longstanding questions concerning the preferential supply of Se to the brain and the hierarchy among the different selenoproteins are readdressed. Given that genes for at least 25 selenoproteins have been identified in the human genome, and most of these are expressed in the brain, their specific roles for normal brain function and neurological diseases remain to be elucidated.     

The neurobiology of evil: psychiatric perspectives on perpetrators

Events such as the Nuremberg Trials in Germany, or the Truth and Reconciliation Commission proceedings in South Africa, raise questions about the psychology of perpetrators of crimes against humanity. While such violations occur within particular socio-political contexts, given the significant advances in clinical neuroscience in the past several decades, is it possible to outline a 'psychobiology of evil'? In this paper a preliminary approach towards this area of study is made on the basis of a review of the biological psychiatry literature. In particular, this literature is used to draw a distinction between the psychobiology of 'banal' evil and that of 'sadistic' evil. Whereas banal evil may involve a dissociation of cortico-striatal processing from limbic input (reason without passion), sadistic evil may involve a dissociation of limbic processing from frontal controls (passion without reason). A biological perspective on evil must, however, avoid several kinds of reductionism. A non-reductionistic psychobiological perspective may provide new insights into a spectrum of deviant behaviour ranging from everyday peccadilloes to pathological evil.     

Lessons in exercise neurobiology: The case of endorphins

This paper focuses on application of neuroscience techniques to exercise psychology for the purpose of obtaining better answers to questions about the effects of acute exercise on mood and other affective experiences. We do this through the lens of the popular idea that exercise can cause an endorphin-based high. Endogenous opioids and their interaction with other neurotransmitter systems are discussed, followed by a succinct historical account of the effects of acute exercise on endorphins and mood. Limitations of the approaches that have been taken are identified. A key message is that optimal progress toward truly understanding the psychological consequences of exercise will require that neuroscience techniques be combined with the strongest possible research designs.     

Chronic cigarette smoking: implications for neurocognition and brain neurobiology

Compared to the substantial volume of research on the general health consequences associated with chronic smoking, little research has been specifically devoted to the investigation of its effects on human neurobiology and neurocognition. This review summarizes the peer-reviewed literature on the neurocognitive and neurobiological implications of chronic cigarette smoking in cohorts that were not seeking treatment for substance use or psychiatric disorders. Studies that specifically assessed the neurocognitive or neurobiological (with emphasis on computed tomography and magnetic resonance-based neuroimaging studies) consequences of chronic smoking are highlighted. Chronic cigarette smoking appears to be associated with deficiencies in executive functions, cognitive flexibility, general intellectual abilities, learning and/or memory processing speed, and working memory. Chronic smoking is related to global brain atrophy and to structural and biochemical abnormalities in anterior frontal regions, subcortical nuclei and commissural white matter. Chronic smoking may also be associated with an increased risk for various forms of neurodegenerative diseases. The existing literature is limited by inconsistent accounting for potentially confounding biomedical and psychiatric conditions, focus on cross-sectional studies with middle aged and older adults and the absence of studies concurrently assessing neurocognitive, neurobiological and genetic factors in the same cohort. Consequently, the mechanisms promoting the neurocognitive and neurobiological abnormalities reported in chronic smokers are unclear. Longitudinal studies are needed to determine if the smoking-related neurobiological and neurocognitive abnormalities increase over time and/or show recovery with sustained smoking cessation.     

The neurobiology of reward and cognitive control systems and their role in incentivizing health behavior

ObjectiveThis article reviews the neurobiology of cognitive control and reward processes and addresses their role in the treatment of addiction. We propose that the neurobiological mechanisms involved in treatment may differ from those involved in the etiology of addiction and consequently are worthy of increased investigation.MethodWe review the literature on reward and control processes and evidence of differences in these systems in drug addicted individuals. We also review the relatively small literature on neurobiological predictors of abstinence.ResultsWe conclude that prefrontal control systems may be central to a successful recovery from addiction. The frontal lobes have been shown to regulate striatal reward-related processes, to be among the regions that predict treatment outcome, and to show elevated functioning in those who have succeeded in maintaining abstinence.ConclusionThe evidence of the involvement of the frontal lobes in recovery is consistent with the hypothesis that recovery is a distinct process that is more than the undoing of those processes involved in becoming addicted and a return to the pre-addiction state of the individual. The extent to which these frontal systems are engaged by treatment interventions may contribute to their efficacy.     

Further developments in the neurobiology of food and addiction: update on the state of the science

Over the past three decades, obesity has become a major public health crisis in the United States. The prevalence of obesity in the United States and in other parts of the world has led to a new word, "globesity," being used to describe the problem. As a result of this increased emphasis on understanding the causes and consequences of obesity, novel theories have stimulated new research aimed to prevent, intervene in and ameliorate the effects and decrease the incidence and medical consequences of globesity. One theory that has gained popularity in recent years, is based on the idea that an excessive intake of highly palatable foods shares similarities with the effects on brain and behavior that are seen with some drugs of abuse. Although this theory is not new, empirically-based translational research has only recently provided strong support for this hypothesis. In the present article, we review the present state of the science in this area and describe some newer clinical and preclinical works that shed light on innovative and interesting overlaps between excessivly palatable food intake and drug use.     

Functional magnetic resonance imaging in studies of the neurobiology of suicidal behavior in adolescents with alcohol use disorders

Functional MRI of the brain is a technique that localizes regions of activity in the brain following task activation. It is useful to neuroscientists interested in interrogating the localization of certain brain functions. Alcohol misuse is a complex, multidimensional disorder involving problematic ethanol ingestion and reflected in behavior. Genetic factors play an important role in the etiopathogenesis of alcohol abuse in adolescents. Alcohol use disorders tend to run in families with 40-60% of the variance of risk explained by genetic influences. Numerous well-designed twin, adoption, and family studies have demonstrated that genetic factors are important in determining vulnerability to alcohol use disorders. There is a tendency for people who misuse alcohol to marry individuals who also abuse alcohol (assortative mating). Thus, many adolescent alcohol misusers are from families with a high proportion of alcohol abuse or dependence. It has been shown that alcohol abusing adolescents have a number of cognitive deficits. Neuropsychological studies of adolescents with alcohol use disorders have reported decrements in language skills, problem solving, verbal and non-verbal retention, working memory, and visuospatial performance. Some cognitive deficits may be present before an adolescent starts drinking and contribute to the development of alcohol use disorders. Data suggest that neuropsychological dysfunction may play a role in determining risk for suicidal acts. Therefore, studies of cognitive impairments and the neural substrate of these impairments in alcohol abusing adolescents may help develop methods of identifying teenagers who are at increased risk for suicide and contribute to our knowledge of the neurobiology of suicidal behavior and may lead to the development of new treatment methods.