The intelligence of heritability.

Abstract: The influences of heredity and environment on behaviour are sometimes quantified as a heritability ratio, which assigns a percentage of variation in test scores to variation in the genotypes of individuals. There are compelling reasons, both biological and statistical, to doubt the validity of the common practice of partitioning variance in this manner. This paper outlines the conceptual foundations and explains the weaknesses of heritability analysis, reviews evidence of heredity-environment interaction during development, and argues for an alternative research strategy to detect and understand the functions of specific genes relevant for individual differences in behaviour. Article: The importance of heredity for human intelligence and other mental attributes is a perennial topic of debate in psychology with a history extending to Rousseau and earlier. Since 1970 these questions have been addressed by a specialization in psychology calling itself behaviour genetics and having its own professional society and journal. The dominant school of thought in this subdiscipline asserts that almost every human characteristic is determined by both the genetic inheritance and the life experience of the individual, and it seeks to estimate the relative strengths of these two factors. The index commonly used to summarize the results for a specific behaviour is the heritability coefficient, which is the most salient feature of the academic discipline of behaviour genetics. Studies of twins and adopted children have claimed substantial heritability of everything from time spent watching television to religious conservatism and what brand of beer you prefer (Plomin ct al., 1990; Heritability in the broad sense (h B 2 ) is said to estimate the proportion of variance in a measure of behaviour or other phenotype (V Y ) in a breeding population that is attributable to genetic variation (h B 2 = V G / V Y ). The estimation of this parameter involves a model based on the inheritance of genes via the principles of Mendel, which are well established, plus assumptions about how genetic effects are related to environment and behaviour, which are still contentious. Genetic Facts Before presenting the main argument, a few genetic facts should be considered. A gene is a segment of a DNA molecule occurring at a specific locus or place along the DNA, and it codes for the structure of a polypeptide molecule that may function as a protein, enzyme or hormone. A person's genotype is the pair of genes he or she has at the locus, one coming from each parent. There are perhaps 50,000 (possibly as many as 100,000) different genes in the 23 human chromosomes, each coding for a specific polypeptid

Retarded Formation of the Hippocampal Commissure in Embryos From Mouse Strains Lacking a Corpus Callosum

formation of the hippocampal commissure in embryos from mouse strains lacking a corpus callosum. Hippocampus, 1997, 7, 2- A precise description of the timing and route traveled by axons traversing the telencephalic midline through the ventral hippocampal commissure (HC) is essential for understanding the role it plays in the formation of the corpus callosum (CC). A normal baseline of HC development was described in B6D2F 2 hybrid mice and then compared with two inbred strains of mice displaying callosal agenesis, BALB/cWah1 (50% CC defect) and 129/J (70% CC defect), their F 2 hybrid (C129F 2 -33% CC defect), and a recombinant inbred strain (RI-1-100% CC defect) derived from pairs of C129F 2 mice. Embryos weighing from 0.25 gto0.70 g(E14.5-E17) were collected and fixed by perfusion. Axon tracts were labeled using crystals of the lipophilic dyes DiI and DiA inserted into the hippocampal fimbria and cerebral cortex. HC axons in B6D2F 2 mice first cross the midline at about 0.350 g body weight (E14.8) by traveling over the dorsal septum and along the pia membrane lining the longitudinal fissure. Earlier crossing was prevented by the presence of a deep cleft formed by the longitudinal fissure extending down into the septal region. Subsequent axons fasciculated along existing axons, gradually building the dorsoventral height of the HC to about 200 μm by 0.600 g. The earliest callosal axons from frontal cortex crossed the midline at 0.620 g and were clearly seen fasciculating along and between existing hippocampal axons at the dorsal surface of the HC as they crossed. In the acallosal strains, HC formation was delayed by the continued presence of the cleft deep in the septal region. This delay in time of crossing was correlated with later CC defect expression. Initial HC crossing occurred at about 0.470 g (E1 6.25) in BALB mice and about 0.520 g (E1 6.5) in 129 mice. In the RI-1 embryos, first HC crossing was estimated at about 0.750 g (E1 7.5), although several older embryos showed no crossing. These results show the importance of the HC for successful CC formation and suggest that absent CC arises as a consequence of a developmental defect which affects the formation of the hippocampal commissure prior to arrival of CC axons at midplane

Precision Stereotaxic Procedure for the Mouse (Mus musculus): Method and Instrumentation

Abstract: A precision stereotaxic procedure for mouse brain research is described accompanied by a new design in mouse stereotaxic head holder and a new device used to guarantee accurate alignment of the skull in the stereotaxic device. This method and instrumentation when applied in forthcoming research will contribute to the development of investigations of structure/function relationships in mouse brain. Keywords: Stereotaxic, Brain Surgery, Mouse Article: Experimentation on the brain of the laboratory mouse poses serious problems of accuracy simply because the mouse brain, although very complex in organization, is quite small, rarely exceeding a volume of 0.5 cc. A number of researchers have found the mouse to be a useful animal for stereotaxic surgery, but careful studies have encountered problems of accuracy (e.g., [1]). Slotnick A recent study in our laboratory has identified several sources of error in stereotaxic surgery with mice This new method has been employed successfully in a study of strain-specific stereotaxic coordinates The head holder (se

Digit ratio (2D:4D) and behavioral differences between inbred mouse strains

Abstract: Digit ratio (2D:4D) is a trait, which is sexually differentiated in a variety of species. In humans, males typically have shorter second digits (2Ds) (index fingers) compared to fourth digits (4Ds) (ring fingers) whereas females' fingers are more equal in length. Smaller, more masculine, digit ratios are thought to be associated with higher prenatal testosterone levels, greater sensitivity to prenatal androgens or both. Men with more masculine digit ratios have shown increased ability, achievement and speed in sports and tend to report that they are more physically aggressive. Previous research has shown the same sexually differentiated pattern in the hind paws of laboratory mice as in human hands, males have lower 2D:4D than females. We measured hind paw digit ratio in mice of eight inbred strains. These measurements were made while blind to strain, sex and whether the paw was from the left or right side. We found large differences in digit ratio between the strains and suggest that inbred mice are a promising system for investigating the correlation between digit ratio and behavioral traits

Coming to terms with heritability

The complex mechanisms of heredity are little appreciated by non-specialists, in some measure, because of misunderstandings that are perpetuated when words used for technical terms have other, more widely understood, folk meanings. When a word has both technical and folk meanings, it is the responsibility of the specialist to avoid promoting confusion by either using extremely cautious and precise language when using the term or, in cases when confusion is inevitable, abandoning the term in favor of one without a widely understood folk meaning. The study of heredity is beset by such confusion, and the term heritability appears to be at the heart of some of the confusion. In this article, I discuss both the technical and folk meanings of heritability and examine the bridge between them. By continuing to use the term heritability, we risk promulgating serious misunderstanding about the workings of heredity, therefore I suggest selectability as an alternative term to avoid such pitfalls.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42804/1/10709_2005_Article_BF02259512.pd

Neuroimaging Evidence of Major Morpho-Anatomical and Functional Abnormalities in the BTBR T+TF/J Mouse Model of Autism

BTBR T+tf/J (BTBR) mice display prominent behavioural deficits analogous to the defining symptoms of autism, a feature that has prompted a widespread use of the model in preclinical autism research. Because neuro-behavioural traits are described with respect to reference populations, multiple investigators have examined and described the behaviour of BTBR mice against that exhibited by C57BL/6J (B6), a mouse line characterised by high sociability and low self-grooming. In an attempt to probe the translational relevance of this comparison for autism research, we used Magnetic Resonance Imaging (MRI) to map in both strain multiple morpho-anatomical and functional neuroimaging readouts that have been extensively used in patient populations. Diffusion tensor tractography confirmed previous reports of callosal agenesis and lack of hippocampal commissure in BTBR mice, and revealed a concomitant rostro-caudal reorganisation of major cortical white matter bundles. Intact inter-hemispheric tracts were found in the anterior commissure, ventro-medial thalamus, and in a strain-specific white matter formation located above the third ventricle. BTBR also exhibited decreased fronto-cortical, occipital and thalamic gray matter volume and widespread reductions in cortical thickness with respect to control B6 mice. Foci of increased gray matter volume and thickness were observed in the medial prefrontal and insular cortex. Mapping of resting-state brain activity using cerebral blood volume weighted fMRI revealed reduced cortico-thalamic function together with foci of increased activity in the hypothalamus and dorsal hippocampus of BTBR mice. Collectively, our results show pronounced functional and structural abnormalities in the brain of BTBR mice with respect to control B6 mice. The large and widespread white and gray matter abnormalities observed do not appear to be representative of the neuroanatomical alterations typically observed in autistic patients. The presence of reduced fronto-cortical metabolism is of potential translational relevance, as this feature recapitulates previously-reported clinical observations