- Home
- A-Z Publications
- Annual Review of Neuroscience
- Previous Issues
- Volume 21, 1998
Annual Review of Neuroscience - Volume 21, 1998
Volume 21, 1998
- Review Articles
-
-
-
GENETIC AND ENVIRONMENTAL INFLUENCES ON HUMAN BEHAVIORAL DIFFERENCES
Vol. 21 (1998), pp. 1–24More Less▪ AbstractHuman behavioral genetic research aimed at characterizing the existence and nature of genetic and environmental influences on individual differences in cognitive ability, personality and interests, and psychopathology is reviewed. Twin and adoption studies indicate that most behavioral characteristics are heritable. Nonetheless, efforts to identify the genes influencing behavior have produced a limited number of confirmed linkages or associations. Behavioral genetic research also documents the importance of environmental factors, but contrary to the expectations of many behavioral scientists, the relevant environmental factors appear to be those that are not shared by reared together relatives. The observation of genotype-environment correlational processes and the hypothesized existence of genotype-environment interaction effects serve to distinguish behavioral traits from the medical and physiological phenotypes studied by human geneticists. Behavioral genetic research supports the heritability, not the genetic determination, of behavior.
-
-
-
-
FROM BIOPHYSICS TO MODELS OF NETWORK FUNCTION
Vol. 21 (1998), pp. 25–45More Less▪ AbstractNeurons and synapses display a rich range of time-dependent processes. Which of these are critical to understanding specific integrative functions in the brain? Computational methods of various kinds are used to understand how systems of neurons interact to produce behavior. However, these models often assume that neuronal dynamics and synaptic strengths are fixed. This review presents some recent models that illustrate that short-term synaptic plasticity mechanisms such as facilitation and depression can have important implications for network function. Other features of synaptic transmission such as multi-component synaptic potentials, cotransmission, and neuromodulation with obvious potential computational implications are presented. These examples illustrate that synaptic strength and intrinsic properties in networks are continuously varying on numerous time scales as a function of the temporal patterns of activity in the network. Thus, both firing frequency of the neurons in a circuit, and the modulatory environment determine the intrinsic and synaptic properties that produce behavior.
-
-
-
LOCAL CIRCUITS IN PRIMARY VISUAL CORTEX OF THE MACAQUE MONKEY
Vol. 21 (1998), pp. 47–74More Less▪ AbstractThe basic laminar organization of excitatory local circuitry in the primary visual cortex of the macaque monkey is similar to that described previously in the cat's visual cortex (Gilbert 1983). This circuitry is described here in the context of a two-level model that distinguishes between feedforward and feedback connections. Embedded within this basic framework is a more complex organization. Within the strictly feedforward pathway, these circuits distribute unique combinations of magno-, parvo-, and koniocellular input from the lateral geniculate nucleus (LGN) to neurons in layers 2–4B. Their input is dependent on the extrastriate cortical areas they target. The local feedback connections from deep layers (5 and 6) arise from a diverse population of pyramidal neurons. Each type forms local connections with a unique relationship to more superficial layers. In the case of layer 6 neurons, these connections are closely related to layer 4 subdivisions receiving input from different functional streams.
-
-
-
RAB3 AND SYNAPTOTAGMIN: The Yin and Yang of Synaptic Membrane Fusion
Vol. 21 (1998), pp. 75–95More Less▪ AbstractSynaptic vesicle exocytosis occurs in consecutive steps: docking, which specifically attaches vesicles to the active zone; priming, which makes the vesicles competent for Ca2+-triggered release and may involve a partial fusion reaction; and the final Ca2+-regulated step that completes fusion. Recent evidence suggests that the critical regulation of the last step in the reaction is mediated by two proteins with opposite actions: synaptotagmin, a Ca2+-binding protein that is essential for Ca2+-triggered release and probably serves as the Ca2+-sensor in fusion, and rab3, which limits the number of vesicles that can be fused as a function of Ca2+ in order to allow a temporally limited, repeatable signal.
-
-
-
ADHESION MOLECULES AND INHERITED DISEASES OF THE HUMAN NERVOUS SYSTEM*
Vol. 21 (1998), pp. 97–125More Less▪ AbstractMutations in the human genes for the adhesion molecules Po, L1, and merosin cause severe abnormalities in nervous system development. Po and merosin are required for normal myelination in the nervous system, and L1 is essential for development of major axon pathways such as the corticospinal tract and corpus callosum. While mutations that lead to a loss of the adhesive function of these molecules produce severe phenotypes, mutations that disrupt intracellular signals or intracellular interactions are also deleterious. Geneticists have found that more than one clinical syndrome can be caused by mutations in each of these adhesion molecules, confirming that these proteins are multifunctional. This review focuses on identifying common mechanisms by which mutations in adhesion molecules alter neural development.
-
-
-
CREB AND MEMORY
Vol. 21 (1998), pp. 127–148More Less▪ AbstractThe cAMP responsive element binding protein (CREB) is a nuclear protein that modulates the transcription of genes with cAMP responsive elements in their promoters. Increases in the concentration of either calcium or cAMP can trigger the phosphorylation and activation of CREB. This transcription factor is a component of intracellular signaling events that regulate a wide range of biological functions, from spermatogenesis to circadian rhythms and memory. Here we review the key features of CREB-dependent transcription, as well as the involvement of CREB in memory formation. Evidence from Aplysia, Drosophila, mice, and rats shows that CREB-dependent transcription is required for the cellular events underlying long-term but not short-term memory. While the work in Aplysia and Drosophila only involved CREB function in very simple forms of conditioning, genetic and pharmacological studies in mice and rats demonstrate that CREB is required for a variety of complex forms of memory, including spatial and social learning, thus indicating that CREB may be a universal modulator of processes required for memory formation.
-
-
-
CORTICAL PLASTICITY: From Synapses to Maps
Vol. 21 (1998), pp. 149–186More Less▪ AbstractIt has been clear for almost two decades that cortical representations in adult animals are not fixed entities, but rather, are dynamic and are continuously modified by experience. The cortex can preferentially allocate area to represent the particular peripheral input sources that are proportionally most used. Alterations in cortical representations appear to underlie learning tasks dependent on the use of the behaviorally important peripheral inputs that they represent. The rules governing this cortical representational plasticity following manipulations of inputs, including learning, are increasingly well understood.
In parallel with developments in the field of cortical map plasticity, studies of synaptic plasticity have characterized specific elementary forms of plasticity, including associative long-term potentiation and long-term depression of excitatory postsynaptic potentials. Investigators have made many important strides toward understanding the molecular underpinnings of these fundamental plasticity processes and toward defining the learning rules that govern their induction. The fields of cortical synaptic plasticity and cortical map plasticity have been implicitly linked by the hypothesis that synaptic plasticity underlies cortical map reorganization. Recent experimental and theoretical work has provided increasingly stronger support for this hypothesis. The goal of the current paper is to review the fields of both synaptic and cortical map plasticity with an emphasis on the work that attempts to unite both fields. A second objective is to highlight the gaps in our understanding of synaptic and cellular mechanisms underlying cortical representational plasticity.
-
-
-
HUMAN AUTOIMMUNE NEUROPATHIES
Vol. 21 (1998), pp. 187–226More Less▪ AbstractPeripheral nerve diseases are among the most prevalent disorders of the nervous system. Because of the accessibility of the peripheral nervous system (PNS) to direct physiological and pathological study, neuropathies have traditionally played a unique role in developing our understanding of basic mechanism of nervous system injury and repair. At present they are providing new insight into the mechanisms of immune injury to the nervous system. A rapidly growing catalogue of PNS disorders are now suspected to be immune-mediated, and in the best understood of these disorders, the molecular and cellular targets of immune attack are known, and the pathophysiology follows directly from the specific immune injury. This review summarizes the immunologically relevant features of the PNS, then considers selected immune-mediated neuropathies, focusing on pathogenetic mechanisms. Finally, the PNS is providing a testing ground for new immunotherapies and approaches to protection and regeneration, including the use of trophic factors. The current status of treatment and implications for future approaches is reviewed.
-
-
-
SENSE AND THE SINGLE NEURON: Probing the Physiology of Perception
Vol. 21 (1998), pp. 227–277More Less▪ AbstractThe newly defined field of cognitive neuroscience attempts to draw together the study of all brain mechanisms that underlie our mental life. Historically, the major sensory pathways have provided the most trustworthy insights into how the brain supports cognitive functions such as perception, attention, and short-term memory. The links between neural activity and perception, in particular, have been studied revealingly in recent decades. Here we review the striking progress in this area, giving particular emphasis to the kinds of neural events that underlie the perceptual judgments of conscious observers.
-
-
-
SIGNAL TRANSDUCTION IN THE CAENORHABDITIS ELEGANS NERVOUS SYSTEM
Vol. 21 (1998), pp. 279–308More Less▪ AbstractCaenorhabditis elegans interacts with its environment by sensing chemicals, touch, and temperature; genetic analysis of each of these responses has led to the identification of candidate signaling molecules within sensory neurons. A molecular model for touch sensation has emerged from studies of the mechanosensory response; the receptors and signal transduction mechanisms in olfactory neurons are being elucidated; and an unusual neuroendocrine role for a TGF-β-related peptide in chemosensory neurons has been discovered. Presynaptic and postsynaptic components of neuronal synapses have been identified in behavioral and pharmacological mutant screens. Mutations have been found in multiple classes of nicotinic acetylcholine receptor genes, excitatory and inhibitory glutamate receptor genes, and candidate gap junction genes, allowing their function to be studied in vivo. Different G-protein signaling pathways have characteristic effects on behavior, neuronal degeneration, and embryonic development.
-
-
-
THE EPHRINS AND EPH RECEPTORS IN NEURAL DEVELOPMENT
Vol. 21 (1998), pp. 309–345More Less▪ AbstractThe Eph receptors are the largest known family of receptor tyrosine kinases. Initially all of them were identified as orphan receptors without known ligands, and their specific functions were not well understood. During the past few years, a corresponding family of ligands has been identified, called the ephrins, and specific functions have now been identified in neural development. The ephrins and Eph receptors are implicated as positional labels that may guide the development of neural topographic maps. They have also been implicated in pathway selection by axons, the guidance of cell migration, and the establishment of regional pattern in the nervous system. The ligands are anchored to cell surfaces, and most of the functions so far identified can be interpreted as precise guidance of cell or axon movement. This large family of ligands and receptors may make a major contribution to the accurate spatial patterning of connections and cell position in the nervous system.
-
-
-
ZINC AND BRAIN INJURY
Dennis W. Choi, and Jae Y. KohVol. 21 (1998), pp. 347–375More Less▪ AbstractZinc is an essential catalytic or structural element of many proteins, and a signaling messenger that is released by neural activity at many central excitatory synapses. Growing evidence suggests that zinc may also be a key mediator and modulator of the neuronal death associated with transient global ischemia and sustained seizures, as well as perhaps other neurological disease states. Manipulations aimed at reducing extracellular zinc accumulation, or cellular vulnerability to toxic zinc exposure, may provide a novel therapeutic approach toward ameliorating pathological neuronal death in these settings.
-
-
-
INDUCIBLE GENE EXPRESSION IN THE NERVOUS SYSTEM OF TRANSGENIC MICE
Vol. 21 (1998), pp. 377–405More Less▪ AbstractGene function during mammalian development is often studied by making irreversible changes to the genome. This approach has a major drawback in that the function of the gene in question must be deduced from the phenotype of animals that have been deficient for the product of the disrupted gene throughout ontogeny. Compensation for the loss of the gene product could yield an apparently unaltered phenotype. Alternatively, the changes in the regulation of other genes could yield a misleading phenotype. If the genetic manipulation results in embryonic or neonatal lethality, gene function at later stages of development cannot be analyzed. It would thus be highly advantageous if the expression of a particular gene could be restricted both temporally and spatially through the use of an inducible genetic system. This paper describes the various inducible genetic expression systems developed for use in mammalian cells, with particular emphasis on their application in the nervous system of transgenic mice.
-
-
-
GENE DISCOVERY IN DROSOPHILA: New Insights for Learning and Memory
Josh Dubnau, and Tim TullyVol. 21 (1998), pp. 407–444More Less▪ AbstractGenetic approaches have been used to investigate increasingly complex biological systems. Here we review the current state of genetic analysis of learning and memory in the fruitfly, Drosophila melanogaster. Emerging findings support two main themes. First, discovery and manipulation of genes involved with behavioral plasticity in genetically accessible systems such as D. melanogaster enables dissection of the biochemical, cellular, anatomical, and behavioral pathways of learning and memory. Second, because core cellular mechanisms of simple forms of learning are evolutionarily conserved, biological pathways discovered in invertebrates are likely to be conserved in vertebrate systems as well.
-
-
-
REGIONALIZATION OF THE PROSENCEPHALIC NEURAL PLATE
Vol. 21 (1998), pp. 445–477More Less▪ AbstractRecent embryological studies are beginning to establish that the underlying organization of the forebrain may be reduced to relatively simple elements that are common to all vertebrates. We begin this chapter by reviewing studies that describe the similarities in prospective fate and molecular organization of the developing neural plate in fish, frogs, chickens, and mice. The chapter next addresses mechanisms that regulate regional specification in the anterior central nervous system. There is now evidence that the axial mesendoderm anterior to the notochord (the prechordal plate) has a central role in induction of the floor and basal plate primordia (hypothalamus) of the forebrain. Patterning of the anterolateral neural plate (telencephalon) may be regulated by FGF8 produced in the anterior neural ridge. Thus, the synthesis of information from fate mapping and experimental embryological and genetic studies is illuminating the mechanisms that generate the different components of the forebrain.
-
-
-
MUTANT GENES IN FAMILIAL ALZHEIMER'S DISEASE AND TRANSGENIC MODELS
Vol. 21 (1998), pp. 479–505More Less▪ AbstractThe most common cause of dementia occurring in mid- to late-life is Alzheimer's disease (AD). Some cases of AD, particularly those of early onset, are familial and inherited as autosomal dominant disorders linked to the presence of mutant genes that encode the amyloid precursor protein (APP) or the presenilins (PS1 or PS2). These mutant gene products cause dysfunction/death of vulnerable populations of nerve cells important in memory, higher cognitive processes, and behavior. AD affects 7–10% of individuals >65 years of age and perhaps 40% of individuals >80 years of age. For the late-onset cases, the principal risk factors are age and apolipoprotein (apoE) allele type, with apoE4 allele being a susceptibility factor. In this review, we briefly discuss the clinical syndrome of AD and the neurobiology/neuropathology of the disease and then focus attention on mutant genes linked to autosomal dominant familial AD (FAD), the biology of the proteins encoded by these genes, and the recent exciting progress in investigations of genetically engineered animal models that express these mutant genes and develop some features of AD.
-
Previous Volumes
-
Volume 46 (2023)
-
Volume 45 (2022)
-
Volume 44 (2021)
-
Volume 43 (2020)
-
Volume 42 (2019)
-
Volume 41 (2018)
-
Volume 40 (2017)
-
Volume 39 (2016)
-
Volume 38 (2015)
-
Volume 37 (2014)
-
Volume 36 (2013)
-
Volume 35 (2012)
-
Volume 34 (2011)
-
Volume 33 (2010)
-
Volume 32 (2009)
-
Volume 31 (2008)
-
Volume 30 (2007)
-
Volume 29 (2006)
-
Volume 28 (2005)
-
Volume 27 (2004)
-
Volume 26 (2003)
-
Volume 25 (2002)
-
Volume 24 (2001)
-
Volume 23 (2000)
-
Volume 22 (1999)
-
Volume 21 (1998)
-
Volume 20 (1997)
-
Volume 19 (1996)
-
Volume 18 (1995)
-
Volume 17 (1994)
-
Volume 16 (1993)
-
Volume 15 (1992)
-
Volume 14 (1991)
-
Volume 13 (1990)
-
Volume 12 (1989)
-
Volume 11 (1988)
-
Volume 10 (1987)
-
Volume 9 (1986)
-
Volume 8 (1985)
-
Volume 7 (1984)
-
Volume 6 (1983)
-
Volume 5 (1982)
-
Volume 4 (1981)
-
Volume 3 (1980)
-
Volume 2 (1979)
-
Volume 1 (1978)
-
Volume 0 (1932)