Kathryn E. Hood

A developmental-genetic analysis of aggressive behavior in mice: I. Behavioral outcomes.

In order to investigate the proposal that modifications in developmental rate may mediate differences in aggressive behavior, two series of selective breeding studies were completed. Stable lines of mice that differed in the frequency and latency of attacks were rapidly established in two series (by S1 in the first series and S3 or S4 in the second series). For evaluation of the developmental-genetic proposal, an analysis was made of the ontogeny of aggressive expression in male mice of the two series, with a detailed report provided of the S1 and S4 generations of the second breeding series. Comparisons between the results of a longitudinal design and the results of a new type of cross-sectional design (involving only siblings, or co-sibial) indicated (a) a reliable developmental course of attack expression, with a sharp rise in early maturity and a slow decline thereafter; (b) a convergence in later maturity of the behavior of lines selectively bred for high or low aggressive behavior, if the animals had been assigned to the longitudinal design; (c) a strong effect of repeated testing on attack latency and frequency, even though the dyadic tests were brief in duration and separated by long intervals. In addition, cross-generational comparisons suggested that the selective breeding differences came about primarily by changes in the behavior of the low aggressive lines, in that these animals failed to show in early maturity the sharp increases in attack occurrence that were observed in earlier generations. Certain implications of these findings for developmental and evolutionary concepts (e.g., neoteny, acceleration, heterochrony) are discussed.

Development, Microevolution, and Social Behavior

The central questions of social development--from the roots of mother-infant attachment to the plasticity of aggressive behavior--pivot on the relations between genetic and ontogenetic sources of variance. It is proposed that (a) developmental, experiential, and microevolutionary processes typically collaborate, rather than compete, in achieving social adaptation; (b) social behavior patterns are mostly closed to modification in the course of development and across generations, but avenues of vulnerability exist in ontogeny and microevolution for dynamic, rapid, and reversible changes in key features; (c) a general avenue for change is delay or acceleration in the developmental onset of one or more features of the behavior pattern, which in turn modifies the functions and properties of the adaptive configuration; and (d) the features of social behavior that are open to rapid change in ontogeny should be open as well to rapid changes in microevolution, although different underlying processes may be involved. Empirical findings from the investigation of aggressive interactions are used to illustrate this proposal on the dual genesis and coincident adaptation of social behaviors.

Handbook of developmental science, behavior, and genetics

FOREWORD. Gilbert Gottlieb and the Developmental Point of View (EvelynFox Keller, Massachusetts Institute of Technology). I. INTRODUCTION. 1. Developmental Systems, Nature-Nurture, and the Role of Genesin Behavior and Development: On the Legacy of GilbertGottlieb (Kathryn E. Hood, The Pennsylvania State University,Carolyn Tucker Halpern, University of North Carolina at ChapelHill, Gary Greenberg, Wichita State University, Richard M. Lerner,Tufts University). 2. Normally Occurring Environmental and Behavioral Influences onGene Activity: From Central Dogma to Probabilistic Epigenesis(Gilbert Gottlieb). II. THEORETICAL FOUNDATIONS FOR THE DEVELOPMENTAL STUDY OFBEHAVIOR AND GENETICS. 3. Historical and Philosophical Perspectives on BehavioralGenetics and Developmental Science (James Tabery, University ofUtah, Paul E. Griffiths, University of Sydney). 4. Development and Evolution Revisited (Mae Wan Ho, Instituteof Science in Society). 5. Probabilistic Epigenesis and Modern Behavioral and NeuralGenetics (Douglas Wahlsten, University of North Carolina atGreensboro). 6. The Roles of Environment, Experience, and Learning inBehavioral Development (George F. Michel, University of NorthCarolina at Greensboro). 7. Contemporary Ideas in Physics and Biology in Gottlieb sPsychology (Ty Partridge, Wayne State University, GaryGreenberg, Wichita State University). III. EMPIRICAL STUDIES OF BEHAVIORAL DEVELOPMENT ANDGENETICS. 8. Behavioral Development during the Mother-Young Interaction inPlacental Mammals: The Development of Behavior in the Relationshipwith the Mother (Jay S. Rosenblatt, Institute of AnimalBehavior, Rutgers). 9. Amniotic Fluid as an Extended Milieu Interieur (Scott R.Robinson, University of Iowa, Valerie Mendez-Gallardo,University of Iowa). 10. Developmental Effects of Selective Breeding for an InfantTrait (Susan A. Brunelli, Columbia University Medical Center,Betty Zimmerberg, Williams College, Myron A. Hofer, ColumbiaUniversity Medical Center). 11. Emergence and Constraint in Novel Behavioral Adaptations(Kathryn E. Hood, The Pennsylvania State University). 12. Nonhuman Primate Research Contributions to UnderstandingGenetic and Environmental Influences on Phenotypic Outcomes acrossDevelopment (Allyson Bennett and Peter J. Pierre, Wake ForestUniversity). 13. Interactive Contributions of Genes and Early Experience toBehavioural Development: Sensitive Periods and Lateralized Brainand Behaviour (Lesley J. Rogers, University of New England,Armidale). 14. Trans-Generational Epigenetic Inheritance (Lawrence V.Harper, University of California, Davis). 15. The Significance of Non-Replication of Gene-PhenotypeAssociations (Carolyn Tucker Halpern, University of NorthCarolina at Chapel Hill). 16. Canalization and Malleability Reconsidered: TheDevelopmental Basis of Phenotypic Stability and Variability(Robert Lickliter and Christopher Harshaw, Florida InternationalUniversity). IV. APPLICATIONS TO DEVELOPMENT. 17. Gene-Parenting Interplay in the Development of InfantEmotionality (Cathi B. Propper, The University of North Carolinaat Chapel Hill, Ginger A. Moore, The Pennsylvania State University,W. Roger Mills-Koonce, The University of North Carolina at ChapelHill). 18. Genetic Research in Psychiatry and Psychology: A CriticalOverview (Jay Joseph, Licensed Psychologist). 19. On the Limits of Standard Quantitative Genetic Modeling ofInter-Individual Variation: Extensions, Ergodic Conditions and aNew Genetic Factor Model of Intra-Individual Variation (Peter C.M. Molenaar, The Pennsylvania State University). 20. Songs My Mother Taught Me: Gene-Environment Interactions,Brain Development and the Auditory System: Thoughts on Non-KinRejection, Part II (Elaine L. Bearer, University of NewMexico). 21. Applications of Developmental Systems Theory to BenefitHuman Development: On the Contributions of Gilbert Gottlieb toIndividuals, Families, and Communities (Richard M. Lerner,Michelle J. Boyd, Megan K. Kiely, Christopher M. Napolitano, andKristina L. Schmid, Tufts University). Name Index. Subject Index.

Increased GABAA-dependent chloride uptake in mice selectively bred for low aggressive behavior

Selective breeding for aggressive behavior alters GABA-dependent chloride uptake and behavioral response to benzodiazepine treatment. Pharmacological and biochemical studies examined subjects from three lines of adult male ICR mice selectively bred for either high levels or low levels of aggressive behavior, as well as unselected controls. Selective breeding produced two lines of behaviorally distinct males. During 5-min dyadic confrontations with an outbred stimulus animal, untreated low-aggressive mice spent more time in walking, rearing, and social interaction than untreated high-aggressive mice. The three lines also showed different responsiveness to the aggression increasing and decreasing effects as well as the sedative effects of benzodiazepine treatment. High doses of chlordiazepoxide (17, 30 mg/kg) reduced motor behaviors (walk, rear and groom) in the low-aggressive line without altering these behaviors in the high aggressive line. In the high-aggressive line, the same doses of chlordiazepoxide (17, 30 mg/kg) produced a behavioral shift; aggressive behaviors were reduced while social behaviors increased to levels similar to the untreated low-aggressive line. In contrast, only the unselected line pursued and threatened more after a low dose of chlordiazepoxide (3 mg/kg). The three lines also showed alterations at the GABAA-benzodiazepine receptor complex. Specific uptake of [3H]Ro-15-1788 was increased in cerebral cortex, hypothalamus and hippocampus in the low-aggressive line, and was reduced in these areas in high-aggressive line when compared with unselected controls. Similarly, GABA-dependent chloride uptake in cortical synaptoneurosomes was augmented in low-aggressive mice and decreased in high-aggressive mice when compared to unselected controls. These data suggest a direct relationship between GABAA-benzodiazepine receptor function and the predisposition to initiate aggressive behavior.

Developmental effects of early immune stress on aggressive, socially reactive, and inhibited behaviors

The origins of individual differences in social development are examined in relation to early stress (immune challenge) and social milieu (maternal behavior) in a genetic-developmental analysis using an animal model. Neonatal male mice (5 or 6 days of age) from two lines of mice selectively bred for high versus low levels of inter-male aggressive behavior received a standard immune challenge (i.p. injections of 0.05 mg/kg endotoxin or saline). Animals were reared by their line-specific biological dam or by a foster dam from a line bred without selection. Adult levels of social behaviors were assessed in a dyadic test (age 45-50 days). Mice from the high-aggressive line show more developmental sensitivity to immune challenge than mice from the low-aggressive line, and line differences persist regardless of the early maternal environment. As adults, endotoxin-treated mice from the high-aggressive line have lower levels of aggressive behavior, longer latency to attack, and higher rates of socially reactive and inhibited behaviors compared to saline controls. Developmental effects of endotoxin in the low-aggressive line are minimal: endotoxin increases socially reactive behaviors, compared to saline controls, but only for mice reared by their biological dams. Rearing by foster dams increases social exploration in the low-aggressive line. The findings raise novel questions regarding the openness of behavioral systems to effects of nonobvious but omnipresent features of the environment, such as antigenic load, how these effects are integrated to affect social development and psychopathology, and the nature of intrinsic factors that contribute to individual differences in sensitivity to early stressors.

Plasticity in development: Concepts and issues for intervention☆

Abstract Because of its pertinence both to key theoretical issues and to applied concerns, plasticity is a central concept within developmental psychology. Our concept of plasticity derives from a comparative developmental, probabilistic epigenetic perspective: Plasticity is the relative flexibility, or capacity to modify behavior to fit contextual demands, shown by a species (or individual) at its most advanced level of development. We argue that processes of development should be conceived of as plastic, and that they should be studied in relation to constancies and constraints on change. Finally, we indicate that, for intervenors, plasticity represents a double-edged sword: Processes available to be changed for the better may be also changed for tho worse. As such, we discuss several developmental and contextual issues that must be confronted by intervenors if a persons potential plasticity across life is to be actualized in the service of enhancing or optimizing the life course.

Effects of peripheral immune activation on social behavior and adrenocortical activity in aggressive mice: Genotype‐environment interactions

To explore genetic-developmental differences in the biobehavioral effects of induced illness, males from two lines of mice selectively bred for high or low levels of aggressive behavior were injected with endotoxin (Escherichia coli, LPS: 0.25 mg/kg, 1.25 mg/kg, or 2.5 mg, i.p.) or saline. Body temperature, weight, and locomotor activity were monitored immediately before and 8 and 24 hr after injection. Twenty-four hours after injection, social behaviors were assessed in a 10-min dyadic test, and hypothalamus, spleen, and serum were collected. In both lines, endotoxin treatment increased behavioral immobility (freezing) and decreased social exploration. Other effects showed line differences : Males from the high-aggressive line had a lower threshold to endotoxin-induced effects on body temperature, weight loss, spleen weight, and corticosterone. Social reactivity (startle response to mild social investigation) increased in the high-aggressive line and decreased in the low-aggressive line after treatment. In the high-aggressive line only, endotoxin decreased attack frequency and increased latency to attack. The interactions between selected line (genotype) and endotoxin treatment (environment) demonstrate that genetic-developmental differences in social and aggressive behavior may indicate the extent to which immune stimuli (e.g., bacteria, viruses, cytokines) function as biobehavioral stressors.

Genetic–environment analysis of sensitivity and acute tolerance to ethanol in mice

The purpose of this study was to characterize initial sensitivity (IS), acute functional tolerance (AFT), and rate of tolerance development to ethanol in lines of mice selected for aggression mice as well as to investigate the impact of isolate housing on these phenotypes. The results showed that for IS, there were no differences among treatment groups. For acute tolerance and rate of tolerance development, a Line x Sex x Housing interaction was present, with the response to housing being more pronounced in the low aggressive line than the high aggressive line, and the females being more affected than the males. Correlational analysis showed low to moderate associations between rate of tolerance development and IS, as well as between rate of tolerance and AFT. Housing condition significantly influenced female expression of ethanol phenotypes as compared to males. The line of the subject also influenced the magnitude of expression of these phenotypes. These findings suggest that environmental and genetic influences interact to influence acute tolerance and rate of tolerance development.

Times of Life and Timing in Developmental Psychology

For the many aspects of psychological time, there are many approaches to understanding, including cultural theories, psychological studies, philosophical analyses and mathematical models. A useful approach is to assume that there are many kinds of psychological time in coexistence, and to distinguish their different cultural and meaning-based contexts, as do Yamada and Kato (2006). From a different perspective, Rudolph (2006) presents rigorous mathematical models of psychological time, in the hope that psychologists will apply them as ways to gain insights into experience and change. This discussion enjoins some qualities of time, attention and ambivalence (Rudolph’s themes) to properties of dialectical structures (Hood, 1995), with fluctuation as a source of individuality within the spiraling cycles of reversible time proposed by Yamada and Kato. Fluctuations at a border, especially a fractal border, may show the way in which a present experience contains traces of the past and constructions of the future. Applications of mathematical models in cultural contexts serve here to more fully elaborate the qualities of psychological time, rather than to reduce them as statistical products. This approach suggests a reconsideration of the distinctive roles of different kinds of time in the study of life cycles.