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This chapter examines the neuromolecular and plastic brain. Ideas about plasticity and the openness of brains to environment influences, from initial evidence about nerve development, through the recognition that synaptic plasticity was the very basis of learning and memory, to evidence about the influence of environment on gene expression and the persistence throughout life of the capacity to make new neurons—all this made the neuromolecular brain seem exquisitely open to its milieu, with changes at the molecular level occurring throughout the course of a human life and thus shaping the growth, organization, and regeneration of neurons and neuronal circuits at time scales from the millisecond to the decade. This was an opportunity to explore the myriad ways in which the milieu got “under the skin,” implying an openness of these molecular processes of the brain to biography, sociality, and culture, and hence perhaps even to history and politics.

Meso-diencephalic dopaminergic (mdDA) neurons play a key role in several human brain functions and are thus also involved in the pathophysiology of severe neurological and psychiatric disorders. The prospect of regenerative therapies for some of these disorders has fueled the interest of developmental neurobiologists in deciphering the molecular cues and processes controlling the generation of the mdDA neurons in the vertebrate brain. Rodents, in particular the mouse, have served as the classical model organism due to their phylogenetic relationship to humans, their relatively well-characterized mdDA system on both the anatomical and physiological levels, and the propensity of the mouse to undergo genetic manipulation. This chapter focuses on in vivo data obtained from the analyses of mutant mice, as several reports have indicated that cell culture-based in vitro data do not always recapitulate the in vivo situation.

A wide variety of well-studied phenomena associated with mindreading are surveyed to probe the consistency of what is known about them with our version of simulation theory. These phenomena include key ontogenetic stages such as gaze following, early intention tracking, and role play, as well as the psychopathology of autism. A link between mirror-neuron dysfunction and autism provides suggestive support for the simulation approach. Our distinction between low-level and high-level simulation fits comfortably with dual-process theories in cognitive science that draw a fundamental distinction between automatic and controlled processes. A tentative conjecture is offered about the evolution of simulation and mindreading, at least for more primitive kinds of simulation.

Following their birth in the prenatal period, dopamine neurons of the mesencephalon undergo a complex series of cellular events in response to external cues, which ultimately result in the establishment of their phenotype. This chapter focuses on a single important event in the postnatal development of mesencephalic dopamine neurons: the determination of their final adult number. The postnatal development of mesencephalic dopamine neurons follows the fundamental principles of classic neurotrophic theory. There is an apoptotic naturally occurring cell death (NCD) event that is maximal in both rodents and primates during the period of maximal development of target contact. As proposed by classic theory, this NCD event is regulated by target contact and retrograde neurotrophic support. In addition, there is evidence that it may also be regulated by afferent anterograde influences and autocrine control.

This chapter details early studies on the neuron doctrine. The neuron doctrine arose as an organizing principle for the nervous system in the late 19th century. The advances in the 1950s provided the first adequate tests of its validity, bringing about a revolution in the functional concept of the neuron. Much of this revolution concerns the functional significance of the short processes, the dendrites, at the next higher level of organization of the neuron above the synapse.

This chapter summarizes the wealth of structural, histological, and physiological information available for hippocampal neurons. Most of the data on this topic come from studies of the rat hippocampal formation. The chapter begins with the CA1 pyramidal neuron since it is the most studied class of neuron in the brain and probably better understood from both structural and functional points of view than any other type of neuron in the hippocampus. It then compares the function of the other pyramidal neurons in the hippocampus: those in CA3 and the subiculum. It covers two nonpyramidal excitatory neurons in the hippocampus: granule cells of the dentate gyrus and mossy cells of the hilus. It also describes the properties of a variety of neurons in other regions comprising the hippocampal formation: the entorhinal cortex, presubiculum, and parasubiculum. Finally, the many types of interneurons found in the hippocampus are considered.

The interaction of two populations of integrate-and-fire-or-burst neurons representing thalamocortical cells from the dorsal lateral geniculate nucleus (dLGN) and thalamic reticular cells from the perigeniculate nucleus (PGN) is studied using a population density approach. A two-dimensional probability density function that evolves according to a time-dependent advection-reaction equation gives the distribution of cells in each population over the membrane potential and de-inactivation level of a low-threshold calcium current. In the absence of retinal drive, the population density network model exhibits rhythmic bursting. In the presence of constant retinal input, the aroused LGN/PGN population density model displays a wide range of responses depending on cellular parameters and network connectivity.

This chapter examines how space is represented in the primate hippocampus, how this is related to the memory and spatial functions performed by the hippocampus, and how the hippocampus performs these functions. It is shown that in the primate hippocampal spatial-view cells could be involved in arbitrary associations with the objects and rewards which are presented at particular viewed locations. A new investigation of object-place recall memory is described, which shows some of the representations that become active within the hippocampus when places are recalled from objects.

This chapter reviews over thirty years of findings from behavioral neurophysiological recordings in the monkey hippocampus. It shows that consistent with the memory space hypothesis, hippocampal neurons provide a rich array of responses that signal all aspects of the ongoing memory trial. It also discuss more recent studies showing strong associative learning signals as well as long-term memory signals in the monkey hippocampus that provide further insight into the plastic and mnemonic properties of hippocampal neurons.

Along with place cells, the hippocampal theta rhythm is one of the most predominant and well-studied physiological patterns in the hippocampal literature. This chapter outlines the major behavioral correlates of theta rhythm, particularly pertaining to learning and memory, and then discusses the relationship between theta rhythm and the activity of individual neurons (including place cells) in hippocampus. Computational models that have been used to link learning and memory functions to theta rhythm and theta-related hippocampal unit firing are reviewed to generate hypotheses for future experimental studies.

This chapter reviews current knowledge about aged neural ensembles in the hippocampus and how alterations in the dynamics of these circuits are linked to memory decline. Topics discussed include fundamental properties of place cells in young and old rats, advanced age and the dynamic properties of hippocampal place cells, and memory decline. It is shown that old rats have notable differences in the dynamic properties of CA1 place fields, and several of these differences correspond with observed age-associated behavioral deficits. Aged rats fail to show experience-dependent place field expansion plasticity to the same extent as young rats. Between episodes of experience in a single environment, aged rats are also impaired at maintaining stable spatial representations in the CA1 subregion of the hippocampus. This observation is consistent with the finding that old rats exhibit impaired performance on tasks requiring the solution of an allocentric spatial reference frame.

This chapter reviews attempts to determine how activity of neurons in the place system — place cells and the more recently discovered head direction and entorhinal grid cells — relates to what the animal “knows”, as manifest by how it behaves. Beginning with O'Keefe and Nadel's cognitive map hypothesis, the chapter explores the extent to which behavioral experiments have supported this idea, before turning to the question of how, if at all, these neurons contribute to episodic memory. It argues that while data suggesting a role for place cells in encoding transient events are scarce, data suggesting that cells may encode the spatial-contextual scaffolding for the attachment of episodic memory are plentiful and plausible.

This chapter examines the hypothesis that attention aids memory formation by providing neuromodulatory input that turns transient, homosynaptic plasticity to long-lasting heterosynaptic plasticity. It addresses the following questions. Are the firing patterns of hippocampal neurons learned? Do they require plasticity like that seen in reduced hippocampal preparations? Are the firing properties of hippocampal neurons attentionally modulated? Evidence suggests that place fields require experience to be constructed, and that plasticity is involved in this process, thus, the first two questions can be answered positively even though the mechanistic details remain elusive. However, the role of attention in the firing patterns of hippocampal neurons, remains more problematic. This is not surprising because this part deals with cognitive rather than cellular mechanisms, and the mechanistic understanding of cognitive neuroscience is still in its infancy relative to that of cellular neuroscience.

Drugs and foods can affect your brain and therefore your behavior. It is becoming increasingly difficult to define what is a drug (i.e., something that your brain wants or needs in order to function optimally) and what is a food (i.e., something that your body wants or needs in order to function optimally). The contents of your diet will only act upon your brain if in some way they chemically resemble an actual neurotransmitter within the brain, or if they are able to interact with an essential biochemical processes in your brain that influences the production, release, or inactivation of a neurotransmitter. Drugs and the contents of our diet often interact with these processes and alter how you think and feel. For example, the constant consumption of caffeine, nicotine, sugar, or heroin can produce changes within your brain that lead to craving with their absence from the diet. As far as your brain is concerned, everything you consume is a drug.

This chapter argues that spontaneously occurring brain rhythms during slow wave sleep (SWS) produce plastic changes in thalamic and neocortical neurons. It discusses the role played by augmenting responses elicited by stimuli at 10 Hz, which are the experimental model of sleep spindles, in producing plastic changes in neuronal properties through the rhythmic repetition of spike-bursts and spike-trains fired by thalamic and cortical neurons.