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"Brown, Richard E."
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Donald O. Hebb and the Organization of Behavior: 17 years in the writing
The Organization of Behavior
has played a significant part in the development of behavioural neuroscience for the last 70 years. This book introduced the concepts of the “Hebb synapse”, the “Hebbian cell assembly” and the “Phase sequence”. The most frequently cited of these is the Hebb synapse, but the cell assembly may be Hebb’s most important contribution. Even after 70 years, Hebb’s theory is still relevant because it is a general framework for relating behavior to synaptic organization through the development of neural networks.
The Organization of Behavior
was Hebb’s 40th publication. His first published papers in 1937 were on the innate organization of the visual system and he first used the phrase “the organization of behavior” in 1938. However, Hebb wrote a number of unpublished papers between 1932 and 1945 in which he developed the ideas published in
The Organization of Behavior
. Thus, the concept of the neural organization of behavior was central to Hebb’s thinking from the beginning of his academic career. But his thinking about the organization of behavior in 1949 was different from what it was between 1932 and 1937. This paper examines Hebb’s early ideas on the neural basis of behavior and attempts to trace the rather arduous series of steps through which he developed these ideas into the book that was published as
The Organization of Behavior
. Using the 1946 typescript and Hebb’s correspondence we can see a number of changes made in the book before it was published. Finally, a number of issues arising from the book, and the importance of the book today are discussed.
Journal Article
Hebb and Cattell: The Genesis of the Theory of Fluid and Crystallized Intelligence
Raymond B. Cattell is credited with the development of the theory of fluid and crystallized intelligence. The genesis of this theory is, however, vague. Cattell, in different papers, stated that it was developed in 1940, 1941 or 1942. Carroll (1984, Multivariate Behavioral Research, 19, 300-306) noted the similarity of Cattell's theory to \"Hebb's notion of two types of intelligence,\" which was presented at the 1941 APA meeting, but the matter has been left at that. Correspondence between Cattell, Donald Hebb and George Humphrey of Queen's University, Kingston, Ontario, however, indicates that Cattell adopted Hebb's ideas of intelligence A and B and renamed them. This paper describes Hebb's two types of intelligence, and shows how Cattell used them to develop his ideas of crystallized and fluid intelligence. Hebb and Cattell exchanged a number of letters before Cattell's paper was rewritten in such a way that everyone was satisfied. This paper examines the work of Hebb and Cattell on intelligence, their correspondence, the development of the ideas of fluid and crystallized intelligence, and why Cattell (1943, p. 179) wrote that \"Hebb has independently stated very clearly what constitutes two thirds of the present theory.\"
Journal Article
Noncanonical regulation of imprinted gene Igf2 by amyloid-beta 1–42 in Alzheimer’s disease
Reduced insulin-like growth factor 2 (IGF2) levels in Alzheimer’s disease (AD) may be the mechanism relating age-related metabolic disorders to dementia. Since
Igf2
is an imprinted gene, we examined age and sex differences in the relationship between amyloid-beta 1–42 (
Aβ
42
) accumulation and epigenetic regulation of the
Igf2/H19
gene cluster in cerebrum, liver, and plasma of young and old male and female 5xFAD mice, in frontal cortex of male and female AD and non-AD patients, and in HEK293 cell cultures. We show IGF2 levels,
Igf2
expression, histone acetylation, and
H19
ICR methylation are lower in females than males. However, elevated
Aβ
42
levels are associated with
Aβ
42
binding to
Igf2
DMR2, increased DNA and histone methylation, and a reduction in
Igf2
expression and IGF2 levels in 5xFAD mice and AD patients, independent of
H19
ICR methylation. Cell culture results confirmed the binding of
Aβ
42
to
Igf2
DMR2 increased DNA and histone methylation, and reduced
Igf2
expression. These results indicate an age- and sex-related causal relationship among
Aβ
42
levels, epigenomic state, and
Igf2
expression in AD and provide a potential mechanism for
Igf2
regulation in normal and pathological conditions, suggesting IGF2 levels may be a useful diagnostic biomarker for
Aβ
42
targeted AD therapies.
Journal Article
Why Study the History of Neuroscience?
The history of neuroscience is the memory of the discipline and this memory depends on the study of the present traces of the past; the things left behind: artifacts, equipment, written documents, data books, photographs, memoirs, etc. History, in all of its definitions, is an integral part of neuroscience and I have used examples from the literature and my personal experience to illustrate the importance of the different aspects of history in neuroscience. Each time we talk about the brain, do an experiment, or write a research article, we are involved in history. Each published experiment becomes a historical document; it relies on past research (the \"Introduction\" section), procedures developed in the past (\"Methods\" section) and as soon as new data are published, they become history and become embedded into the history of the discipline (\"Discussion\" section). In order to be transparent and able to be replicated, each experiment requires its own historical archive. Studying history means researching books, documents and objects in libraries, archives, and museums. It means looking at data books, letters and memos, talking to scientists, and reading biographies and autobiographies. History can be made relevant by integrating historical documents into classes and by using historical websites. Finally, conducting historical research can be interesting, entertaining, and can lead to travel to out-of-the-way and exotic places and meeting interesting people.
Journal Article
Genetically modified mice for research on human diseases: A triumph for Biotechnology or a work in progress?
Genetically modified mice are engineered as models for human diseases. These mouse models include inbred strains, mutants, gene knockouts, gene knockins, and ‘humanized’ mice. Each mouse model is engineered to mimic a specific disease based on a theory of the genetic basis of that disease. For example, to test the amyloid theory of Alzheimer’s disease, mice with amyloid precursor protein genes are engineered, and to test the tau theory, mice with tau genes are engineered. This paper discusses the importance of mouse models in basic research, drug discovery, and translational research, and examines the question of how to define the “best” mouse model of a disease. The critiques of animal models and the caveats in translating the results from animal models to the treatment of human disease are discussed. Since many diseases are heritable, multigenic, age-related and experience-dependent, resulting from multiple gene-gene and gene-environment interactions, it will be essential to develop mouse models that reflect these genetic, epigenetic and environmental factors from a developmental perspective. Such models would provide further insight into disease emergence, progression and the ability to model two-hit and multi-hit theories of disease. The summary examines the biotechnology for creating genetically modified mice which reflect these factors and how they might be used to discover new treatments for complex human diseases such as cancers, neurodevelopmental and neurodegenerative diseases.
Journal Article
What are We Measuring When We Test Strain Differences in Anxiety in Mice?
We examined measures of locomotor and anxiety-like behavior in male and female mice of 15 inbred strains on the elevated-plus maze, light/dark transition box and open field. Strain differences were found on all measures of locomotor activity and anxiety. Strain means for measures of locomotor activity on the three apparatus were significantly correlated, but strain means for commonly used measures of anxiety were not correlated. Principal component analysis revealed a common locomotor activity factor, which accounted for 28.6 % of the variance, but no common anxiety factor. Species-typical behaviors (defecations, stretch-attend postures, grooming) accounted for smaller proportions (<11 %) of the variance. These results plus comparisons with previously published data suggest that the elevated-plus maze, light/dark box and open field measure different facets of anxiety, and that the reliability of genetic differences on anxiety is highly dependent on apparatus, procedural variables and laboratory factors. Locomotor activity, however, is a stable trait that differs across strains and is reliably measured in different apparatus and laboratories. We conclude that anxiety traits of inbred mouse strains are best reflected by species-typical behaviors in each apparatus. These results suggest that new ways of measuring trait anxiety are required in order to determine the neural and genetic correlates of anxiety-like behaviour in mice.
Journal Article
Sex Differences in Healthspan Predict Lifespan in the 3xTg-AD Mouse Model of Alzheimer’s Disease
Mouse models of Alzheimer's disease (AD) exhibit marked differences in life expectancy depending on their genotype and sex. The assessment of frailty could provide a measure of healthspan to facilitate comparisons between different AD models. We used a validated mouse frailty index (FI) assessment tool to explore genotype and sex differences in lifespan and healthspan of 3xTg-AD mice and their B6129F2 wild-type (WT) controls. This tool is based on an approach commonly used in people and quantifies frailty by counting the accumulation of age-related health deficits. The number of deficits in an individual divided by the total number measured yields an FI score theoretically between 0 and 1, with higher scores denoting more frailty. Male 3xTg-AD mice aged 300-600 days had higher FI scores (Mean FI = 0.21 ± 0.03) than either male WT (Mean FI = 0.15 ± 0.01) or female 3xTg-AD mice (Mean FI = 0.10 ± 0.01), and the elevated frailty scores were accompanied by parallel increases in mortality. Frailty increased exponentially with age, and higher rates of deficit accumulation elevated mortality risk in all groups of mice. When mice were stratified by FI score, frailty predicted mortality, at least in females. Therefore, the mouse clinical FI provides a valuable tool for evaluating healthspan in mouse models of AD with different lifespans.
Journal Article
The Hebb Synapse Before Hebb: Theories of Synaptic Function in Learning and Memory Before Hebb (1949), With a Discussion of the Long-Lost Synaptic Theory of William McDougall
Since the work of Semon was rediscovered by Schacter in 1978, there has been a renewed interest is searching for the “engram” as the locus of memory in the brain and Hebb’s cell assembly has been equated with Semon’s engram. There have been many theories of memory involving some concept of synaptic change, culminating in the “Hebb Synapse” theory in 1949. However, Hebb said that the idea that any two cells or systems of cells that are repeatedly active at the same time will tend to become “associated,” was not his idea, but an old one. In this manuscript we give an overview of some of the theories of the neural basis of learning and memory before Hebb and describe the synaptic theory of William McDougall, which appears to have been an idea ahead of its time; so far ahead of its time that it was completely ignored by his contemporaries. We conclude by examining some critiques of McDougall’s theory of inhibition and with a short discussion on the fate of neuroscientists whose ideas were neglected when first presented but were accepted as important many decades later.
Journal Article