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PubMed1981

Psychobiology of experimental hypertension: evaluation of the Dahl rat lines.

The Dahl salt-sensitive (DS) and salt-resistant (DR) rat lines were selectively bred to show opposite genetically determined blood pressure responses to excess sodium chloride ingestion. These animals have provided significant anatomical, physiological, and biochemical data concerning the pathological mechanisms of experimental hypertension. Research is also being conducted to determine the relevance of psychobiological and behavioral variables in these two lines. The rationale for the selection and maintenance of the Dahl model and the physiological, biochemical, and behavioral characteristics which distinguish DS and DR rats are presented. Although originally developed for the study of salt-induced hypertension, special attention is given to the application of this animal model in behavior genetic research, stressing its inherent advantages and limitations. The use of the Dahl model in psychobiological studies and the utility of the model for future behavioral, genetic, and psychophysiological research are also detailed.

Animals↗
PubMed2006

A hitchhiker's guide to behavioral analysis in laboratory rodents.

Genes and environment are both essential and interdependent determinants of behavioral responses. Behavioral genetics focuses on the role of genes on behavior. In this article, we aim to provide a succinct, but comprehensive, overview of the different means through which behavioral analysis may be performed in rodents. We give general recommendations for planning and performing behavioral experiments in rats and mice, followed by brief descriptions of experimental paradigms most commonly used for the analysis of reflexes, sensory function, motor function and exploratory, social, emotional and cognitive behavior. We end with a discussion of some of the shortcomings of current concepts of genetic determinism and argue that the genetic basis of behavior should be analyzed in the context of environmental factors.

Animals↗
PubMed2002

Criminality and moral dysfunctions: neurological, biochemical, and genetic dimensions.

In this article, the author attempts to demonstrate a relationship between neurobiological dysfunctions and/or genetically determined deviant behavior and personality traits as well as moral abnormalities. Data from neuroscience show that a number of neurological dysfunctions are linked to cognitive and emotional disturbances. Cognitive and emotional abnormalities, in turn, are frequently related to moral dysfunctions. Moreover, neurological disorders can produce dramatic psychological and social problems, personality changes, and behavioral problems in patients. Those mental, emotional, and psychosocial problems and related moral dysfunctions are frequently linked to violence and/or criminal behavior. Genetic research found evidence of inheritability of antisocial traits, which interfere with moral development and activities. This information has consequences for any assessment and disposition within the legal system. More research on the interrelationship between neuro(bio)logical, genetic, emotional, and mental aspects of moral dysfunctions is needed for the development of adequate treatment, prevention, and intervention programs.

Affect↗
PubMed1989

New mutants of Paramecium tetraurelia defective in a calcium control mechanism: genetic and behavioral characterizations.

The k-shy mutants of Paramecium tetraurelia are altered in several Ca2+-dependent functions which regulate ciliary motility. The isolation, genetics, and phenotypes of these mutants are described. Of six independent isolates, all contained recessive single-factor mutations and comprise two unlinked loci, ksA and ksB. All k-shy strains showed prolonged backward swimming responses to depolarizing stimuli, but gave infrequent responses to some stimuli. At least four k-shy strains displayed temperature sensitivity. Neither ksA nor ksB was allelic or linked to dancer, a mutation causing weak Ca2+ current inactivation and prolonged backward swimming. Analysis of ks+; Dn double mutants revealed synergism between the two mutations. The ksA mutant survived Ba2+ solutions longer than wild type, but was more sensitive to K+. Together with previous studies, these results are consistent with a defect in reducing intracellular Ca2+ causing both prolonged ciliary reversal and reduced Ca2+ channel activity due to more active Ca2+-dependent feedback mechanisms. The integration of the Ca2+-dependent stimulatory and inhibitory functions is therefore dependent on ks+ gene functions. The ksA mutant was rescued by microinjection of wild-type cytoplasm, suggesting a possible behavioral assay for factors related to the ksA+ gene product.

Animals↗
PubMed2004

In search of a depressed mouse: utility of models for studying depression-related behavior in genetically modified mice.

The ability to modify mice genetically has been one of the major breakthroughs in modern medical science affecting every discipline including psychiatry. It is hoped that the application of such technologies will result in the identification of novel targets for the treatment of diseases such as depression and to gain a better understanding of the molecular pathophysiological mechanisms that are regulated by current clinically effective antidepressant medications. The advent of these tools has resulted in the need to adopt, refine and develop mouse-specific models for analyses of depression-like behavior or behavioral patterns modulated by antidepressants. In this review, we will focus on the utility of current models (eg forced swim test, tail suspension test, olfactory bulbectomy, learned helplessness, chronic mild stress, drug-withdrawal-induced anhedonia) and research strategies aimed at investigating novel targets relevant to depression in the mouse. We will focus on key questions that are considered relevant for examining the utility of such models. Further, we describe other avenues of research that may give clues as to whether indeed a genetically modified animal has alterations relevant to clinical depression. We suggest that it is prudent and most appropriate to use convergent tests that draw on different antidepressant-related endophenotypes, and complimentary physiological analyses in order to provide a program of information concerning whether a given phenotype is functionally relevant to depression-related pathology.

Animals↗
PubMed2004

On the nature and nurture of antisocial behavior and violence.

This article focuses on the contribution that behavioral genetic research can make to further the understanding of how antisocial and violent behavior develops. Genetically informative study designs are particularly useful for investigating etiological heterogeneity and can refine the search for developmental pathways to persistent antisocial conduct. While the current data are not yet directly translatable for prevention programs, behavioral genetic research will have far-reaching implications for prevention and treatment. As we find genes associated with risk for antisocial behavior and develop better understanding of the mechanics of the interplay between genes and the environment, we can expect to tailor prevention and treatment to serve the specific needs of etiologically distinct subgroups of children. Furthermore, researchers involved in sharpening the knowledge base have the responsibility of trying to ensure that such findings are not misused.

Antisocial Personality Disorder↗
PubMed1991

Genetic influences in autism.

Two behavior genetic research strategies have been utilized to understand gene influences in autism. There is overwhelming evidence for gene involvement, although an exact mode of inheritance has not yet been elucidated. Family and twin studies illustrate that the clinical phenotype of autism is not sufficient to characterize the underlying genotype(s) involved. Exactly what should be included in the phenotype remains elusive. Cognitive and social deficits are indicated as milder variants of the autism phenotype, but precisely how to define these deficits requires further research. Furthermore, more complex models of inheritance (e.g., two-locus models--multifactorial and major gene) may be necessary to explain gene influences in autism. Genetic heterogeneity is indicated in autism, with an X-linked disorder, fragile X, and an autosomal dominant disorder, tuberous sclerosis, together accounting for perhaps 8% to 11% or more of cases of autism. Differences in family patterns (i.e., recurrence risks) of neuropsychiatric disorders between autism with and without mental retardation or other clinically defined groups (e.g., males and females) are suggested. Whether these differences represent genetic heterogeneity or multifactorial inheritance with varying thresholds (e.g., of severity or sex differences) cannot be distinguished on the basis of the data available to date. Autosomal recessive inheritance is suggested in a subgroup of families with autism, but the proportion of all autism that may be accounted for by autosomal recessive inheritance is unknown. Evidence exists that stoppage occurs in families with autism, however, and this can affect accurate estimates of segregation ratios when not taken into account. Future family studies need to report (1) exact ascertainment schemes and specification of probands and (2) sex and birth order of affected siblings, including sibship size, so that data may be pooled and such effects can be tested. Investigations of populations with fragile X or tuberous sclerosis as well as those with autism (without known genetic disorders) will identify the etiologic basis of these associations. Such associations may be due to linkage of genes underlying autism and those underlying the known genetic disorders (i.e., linkage disequilibrium) or shared brain pathophysiology or merely shared overt behaviors. Until such mechanisms are elucidated, we can use only empiric risk figures in genetic counseling situations of autism, assuming that no known genetic or environmental cause is identified. Pooling available data from family and twin studies, the following empiric risks are suggested for genetic counseling purposes. An average sibling risk (frequency of affected siblings among all siblings) based on pooled data is 3% (i.e., 57/1698).(ABSTRACT TRUNCATED AT 400 WORDS)

Autistic Disorder↗
PubMed2005

Behavioral versus genetic correlates of lipoproteins and adiposity in identical twins discordant for exercise.

BACKGROUND: Lipoprotein and weight differences between vigorously active and sedentary monozygotic (MZ) twins were used to (1) estimate the effects of training while controlling for genotype and (2) estimate genetic concordance (ie, similarity) in the presence of divergent lifestyles. METHODS AND RESULTS: Thirty-five pairs of MZ twins (25 male, 10 female) were recruited nationally who were discordant for vigorous exercise (running distances differed by > or =40 km in male and > or =32 km in female twins). The active twins ran an average (mean+/-SD) of 63.0+/-20.4 km/wk, whereas the mostly sedentary twins averaged 7.0+/-13.5 km/wk. The active twins had significantly lower body mass index (difference+/-SE, -2.12+/-0.57 kg/m2, P=0.0007) and significantly higher HDL cholesterol (0.14+/-0.04 mmol/L, P=0.004), HDL2 (2.71+/-1.04 U, P=0.01), and apolipoprotein (apo) A-I (0.10+/-0.03 g/L, P=0.004). Despite the difference in lifestyle, when adjusted for sex, the correlations between the discordant MZ twin pairs were significant (P<0.01) for HDL cholesterol (r=0.69), apoA-I (r=0.58), and HDL2 (r=0.67). There was no significant MZ twin correlation for body mass index (r=0.17). None of the active twins having an overweight twin were themselves overweight. CONCLUSIONS: Behavior (vigorous exercise) may reduce genetic influences on body mass index. In contrast, genetics (or shared environment) substantially influences HDL cholesterol and HDL subclasses, even in the presence of extreme behavioral differences. There may be greater individual control over moderate degrees of obesity, whereas low HDL cholesterol may be largely predetermined and less effectively treated by vigorous exercise.

Adiposity↗
PubMed2004

Cell behaviors and genetic lineages of the mesencephalon and rhombomere 1.

Brain structures derived from the mesencephalon (mes) and rhombomere 1 (r1) modulate distinct motor and sensory modalities. The precise origin and cellular behaviors underpinning the cytoarchitectural organization of the mes and r1, however, are unknown. Using a novel inducible genetic fate mapping approach in mouse, we determined the fate and lineage relationships of mes/r1 cells with fine temporal and spatial resolution. We demonstrate that the mes and r1 are neuromeres that along with the isthmic organizer are partitioned along the anterior-posterior axis by lineage restriction boundaries established sequentially between E8.5 and E9.5. Furthermore, a small group of cells originating from the most posterior mes exhibit anterior intracompartmental expansion and contribute throughout the inferior colliculus. Finally, we also uncovered transient and differential genetic lineages of ventral midbrain dopaminergic and ventral hindbrain serotonergic neuronal precursors with respect to Wnt1 and Gli1 expression.

Animals↗
PubMed1999

Genetic and behavioral risk factors for self-reported joint pain among a population-based sample of Swedish twins.

Self-reported joint pain, a typical manifestation of osteoarthritis, was examined using 335 twin pairs from the Swedish Adoption/Twin Study of Aging to estimate relative genetic and environmental influences on self-reported joint pain and to examine the relationships between joint pain, health behavior, and psychological variables. Findings suggest that family resemblance for self-reported joint pain represents similar environments more than genetic similarity. Data from the early 1970s, including exercise, physical activity at work, obesity, and neuroticism, were used to predict joint pain in 1993. For men, moderate amounts of exercise decreased the likelihood of joint pain, but strenuous amounts of physical activity in the workplace had the opposite effect. For women, exercise and physical activity were not significant predictors, but past obesity and higher levels of neuroticism increased the likelihood of reporting joint pain in 1993.

Aged↗
PubMed2005

Remote control of behavior through genetically targeted photostimulation of neurons.

Optically gated ion channels were expressed in circumscribed groups of neurons in the Drosophila CNS so that broad illumination of flies evoked action potentials only in genetically designated target cells. Flies harboring the "phototriggers" in different sets of neurons responded to laser light with behaviors specific to the sites of phototrigger expression. Photostimulation of neurons in the giant fiber system elicited the characteristic escape behaviors of jumping, wing beating, and flight; photostimulation of dopaminergic neurons caused changes in locomotor activity and locomotor patterns. These responses reflected the direct optical activation of central neuronal targets rather than confounding visual input, as they persisted unabated in carriers of a mutation that eliminates phototransduction. Encodable phototriggers provide noninvasive control interfaces for studying the connectivity and dynamics of neural circuits, for assigning behavioral content to neurons and their activity patterns, and, potentially, for restoring information corrupted by injury or disease.

Action Potentials↗
PubMed2004

[Identification of the memory component that decays with age in Drosophila].

No one can escape from memory decay with advancing age. Understanding molecular mechanisms underlying age-related memory impairment (AMI) is important not only from the scientific viewpoint but also for elucidating novel targets that may eventually lead to developing therapeutics for combating memory loss. AMI had been generally considered to be an overall or nonspecific decay of memory processes that results from dysfunction of neural networks. However, behavioral genetic tests of this hypothesis have not been carried out. Using Drosophila, we have demonstrated the first extensive behavioral-genetic characterization of AMI. We discovered that AMI results from the specific decay of only one memory component, amnesiac-dependent middle-term memory, and not other components. In support of this finding, we show that memory in aged flies is identical to that of amnesiac mutants, and while other memory mutants show a further decrease in memory upon aging, amnesiac flies do not. These results provide the first identification of a specific gene pathway underlying AMI.

Aging↗
PubMed2006

Geographic variation of genetic and behavioral traits in northern and southern tüngara frogs.

We use a combination of microsatellite marker analysis and mate-choice behavior experiments to assess patterns of reproductive isolation of the túngara frog Physalaemus pustulosus along a 550-km transect of 25 populations in Costa Rica and Panama. Earlier studies using allozymes and mitochondrial DNA defined two genetic groups of túngara frogs, one ranging from Mexico to northern Costa Rica (northern group), the second ranging from Panama to northern South America (southern group). Our more fine-scale survey also shows that the northern and southern túngara frogs are genetically different and geographically separated by a gap in the distribution in central Pacific Costa Rica. Genetic differences among populations are highly correlated with geographic distances. Temporal call parameters differed among populations as well as between genetic groups. Differences in calls were explained better by geographic distance than by genetic distance. Phonotaxis experiments showed that females preferred calls of males from their own populations over calls of males from other populations in about two-thirds to three-fourths of the contrasts tested. In mating experiments, females and males from the same group and females from the north with males from the south produced nests and tadpoles. In contrast, females from the south did not produce nests or tadpoles with males from the north. Thus, northern and southern túngara frogs have diverged both genetically and bioacoustically. There is evidence for some prezygotic isolation due to differences in mate recognition and fertilization success, but such isolation is hardly complete. Our results support the general observation that significant differences in sexual signals are often not correlated with strong genetic differentiation.

Animals↗
PubMed1995

Using high-efficiency mouse germline mutagenesis to investigate complex biological phenomena: genetic diseases, behavior, and development.

A valuable approach to investigating a biological process is to study the effect of mutations in the involved genes. By studying a diverse set of such mutations, one can gain important insights into the roles that the given gene product plays in the biological process. Although this approach has long been recognized, the scarcity of mammalian mutations has largely limited such investigations to simple organisms. It has recently been shown that highly efficient mutagenesis of the mouse germline with a random point mutagen can produce mutations that are valuable in several important ways. First, it can produce numerous different types of mutations. Second, it can be used to mutate genes that have yet to be cloned or characterized. Genes that have been marked by mutation can ultimately yield molecular access after mapping to high resolution and cloning from map position. Such new investigative capabilities will ultimately allow one to gain intimate knowledge of the molecular basis of complex biological processes like behavior and development. Third, mutations can be induced that yield animal models of human heritable diseases. Such disease models allow for intensive research into the etiology of the given disease and also permit the facile evaluation of new therapeutic regimens.

Animals↗