PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Genetics, Behavioral”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources

Opioid peptides as neuroregulators: potential areas for the study of genetic-behavioral mechanisms.

The opioid peptides have been related to behavior in both animal and human studies. Further investigation can be anticipated which could lead to the elucidation of genetic controls over enzymes which process these peptides and the receptors upon which the peptides act. The enzymes, both synthetic and degradative, can lead to the formation of different forms of the opiate peptides. Differential control of these enzymes or of the multiple forms of opiate receptors could lead to discrete changes in opiate status and subsequent behavioral changes. Conversely, genetically regulated behavioral modification could also lead secondarily to opiate changes.

Aminopeptidases↗

Problem behavior in early and middle childhood: an initial behavior genetic analysis.

Twin samples were used to estimate the relative importance of genetic and environmental influences on problem behavior in children, assessed by the Child Behavior Checklist (CBCL). For the younger cohort, mothers completed the CBCL/2-3, while for the older cohort the CBCL/4-18 was used. Nearly half of the older sample had also been assessed with the questionnaire for younger children at a prior date, providing tentative answers regarding continuity and change in the etiology of problem behavior. Results suggested that shared environmental influences may be more important in early childhood than in middle childhood, while the reverse holds for genetic influences.

Child↗

Circular countercurrent-distribution behavioral genetic maze.

An inexpensive, easily constructed apparatus for mass screening of taxes of small animals with a rapid and accurate assignment of individual behavior scores has been described that should be of utility in hastening a behavioral geneticist's chores and allow him to handle more populations with fewer mazes. Also, the apparatus is well suited for use within the constraints of the undergraduate laboratory.

Animals↗

Avoidance learning, behavior genetics, and aging: a critical review and comment on methodology.

Animal models of human aging problems are potentially of enormous value to gerontological research. Models of behavioral problems have not often lived up to their promise. This review examines one such model system, avoidance learning in aging rodents. This model system has become increasingly popular among behavioral gerontologists, yet it has not provided the unambiguous answers to experimental questions which investigators expected. Our effort has been to determine why the system has failed, and to provide useful suggestions for future research. At the same time we have tried to provide a comprehensive review of the relevant literature and to assess the strengths and weaknesses of studies which have been conducted in the last two decades.

Adult↗

Sensitivity, functional analysis, and behavior genetics: a response to Freeman et al.

Freeman et al. (1998) asserted that sensitivity theory is circular, unsupported by empirical evidence, and represents an "either/or" decision in regard to applied behavior analysis. We reply by showing that sensitivities are objectively measured and that our theory permits testable predictions. Further, we briefly summarize the results of recent studies that support our theory, including investigations that link sensitivities to genes and challenging behavior. Finally, we reject the idea that sensitivity theory and functional analysis represent an "either/or" viewpoint and call again for research to integrate these approaches.

Behavioral Symptoms↗

Opportunities to discover genes regulating depression and antidepressant response from rodent behavioral genetics.

Over the past several years, research has indicated that an individual's genetic makeup strongly influences not only their likelihood of developing depression, but also whether or not they will respond well to a particular antidepressant treatment. Identifying those genes regulating susceptibility to depression will increase our understanding of disease pathophysiology and direct the development of treatments that correct underlying neurobiological pathology related to stress-related psychiatric illnesses. Pharmacologically, the identification of genes regulating treatment response can lead to the design of novel pharmacological treatments and allow for more individualized, rational and successful drug treatments. Unfortunately, complex environmental and genetic mechanisms at play in depression and drug response make the discovery of susceptibility genes in humans quite difficult. Animal models may provide a more desirable system in which to discover susceptibility genes because environmental factors and tests can be regulated and more informative genetic methods can be used. Furthermore, a unique genetic opportunity exists with animal models of depression and antidepressant response because several rodent strains have been identified, or selectively bred, that display exaggerated depressive phenotypes on stress-related behavioral tests or divergent responses to antidepressant drugs. This paper reviews several of these rodent strains and illustrates the genetic strategies available to discover the long-sought susceptibility genes regulating these phenotypes.

Animals↗

[Behavior-genetic analysis of responses in runway test as measures of emotional reactivity in rats: I.- phenotypic variations and heritability estimates based on offspring-parents regressions (author's transl)].

Individual differences of emotional reactivity were estimated from 6 kinds of responses measured in the Runway Test (modified ("Timidity Test") in 974 random-bred albino rats. 3 different estimates of heritability of these responses were calculated from the regressions of offspring on dam, sire, and midparent. The types and degree of the phenotypic variations are very different among the responses measured. Heritability estimates of 2 kinds of responses which are related to the behavior going to the remotest part of runway from starting box were relatively higher (.30-.55). Heritability estimates of starting latency, time in the starting box, and the number of sections rats traversed were medium (.20-.40). The estimates from defecation scores had lowest (.10-.30).

Animals↗

Behavior genetics of olfactory responses in Drosophila. II. An odorant-specific variant in a natural population of Drosophila melanogaster.

Homozygous second chromosome lines were extracted from a natural population of Drosophila melanogaster and tested for their olfactory responses to ethyl acetate. The chromosome lines were highly heterogeneous for this behavior, and the variability was also specific to other esters and ketones such as ethyl propionate, 2-butanone, 2-pentanone, and 3-pentanone. The responses to these odorants negatively correlated with the response to another odorant, lactic acid. A large part of this odorant-specific variation seemed to be controlled by genes located on the right arm of the second chromosome.

Animals↗

A behavioral genetic analysis of the relationship between the socialization scale and self-reported delinquency.

This investigation examined the genetic (A), and shared (C) and nonshared (E) environmental variance contributions to the relationship of self-reported delinquency (as measured by the "Delinquent Behavior Inventory" [DBI; Gibson, 1967]) to the Socialization (So) scale of the California Psychological Inventory using univariate and bivariate structural equation models. The scales were administered to 222 male (145 monozygotic; 77 dizygotic) and 159 female (107 monozygotic; 52 dizygotic) 16- to 18-year-old same-sex twin pairs. Principal components analysis with varimax rotation revealed three interpretable So factors representing family/home environment, self-concept, and behavioral control. Univariate modeling suggested sex differences in etiological influences associated with individual differences in most scales. The bivariate ACE model fit the data, suggesting that the covariance between the So scale and self-reported delinquency owes in part to shared etiological factors.

Adolescent↗

Behavior genetic analyses of drug withdrawal.

Many studies with rodent models have illustrated the role of genetic factors in determining the severity of ethanol withdrawal. In studies using inbred mouse strains and mice selectively bred for drug sensitivity, a consistent finding has been that genotypes susceptible to alcohol withdrawal are also susceptible to withdrawal from other drugs with CNS depressant effects. A new method for rough genetic mapping of genes associated with withdrawal, quantitative trait loci (QTL) gene mapping, has recently been employed in the BXD RI recombinant inbred mouse series. Several QTLs are associated with alcohol withdrawal: One such QTL on Chromosome 1 is described. An area of Chromosome 2 contains a QTL marker for a gene affecting withdrawal from acute and chronic ethanol, nitrous oxide, and high-pressure neurological syndrome Type I clonic convulsions.

Animals↗

Parent-child mutuality in early childhood: two behavioral genetic studies.

Parent-child dyadic mutuality (shared positive affect, responsiveness, and cooperation) is an important component of family socialization processes. This study sought to extend previous research on mutuality by using a quantitative genetic design to examine between- and within-family variations (e.g., sibling differences) and gene-environment processes. The first study included 125 pairs of identical and same-sex fraternal 3-year-old twins. Observations of mutuality and parents' and observers' ratings of family environment and child behavior were gathered. Greater mutuality was associated with higher socioeconomic status. Moderate sibling similarity in parent-child mutuality was accounted for by child genetic similarity, suggesting evocative gene-environment correlation and nonshared environmental processes. These findings were replicated in a 2nd study of 102 pairs of adoptive and biological siblings.

Child, Preschool↗