Two electrophysiological studies tested the hypothesis that operant conditioning of mu rhythms via neurofeedback training can renormalize mu suppression, an index of mirror neuron activity, and improve behavior in children diagnosed with autism spectrum disorders (ASD). In Study 1, eight high-functioning ASD participants were assigned to placebo or experimental groups before 10 weeks of training of the mu frequency band (8-13 Hz). Following training, experimental participants showed decreased mu power and coherence, increased sustained attention ability, and improved scores on subscales of the ATEC compared to the placebo group. Both groups showed improvement in imitation ability. In Study 2, 19 high-functioning ASD children underwent a similar procedure with verified diagnoses, a modified double-blind protocol, and training of the high mu band (10-13 Hz). The results showed decreases in amplitude but increases in phase coherence in mu rhythms and normalization of mu rhythm suppression in experimental participants compared to placebo. Furthermore, like Study 1, participants showed improvements in sustained attention and in ATEC scores but no improvements in imitation following training. This suggests that training of the mu rhythm can be effective in producing changes in EEG and behavior in high-functioning ASD children, but does not affect imitation behavior per se.

Although imitation impairments are often reported in individuals with autism spectrum disorders (ASD), previous work has not yet determined whether these impairments are significant, specific to ASD, and present across the entire spectrum. This report of 53 studies on imitation in ASD seeks to determine whether individuals with ASD show significant imitation deficits, the magnitude of these deficits, and whether they are specific to ASD. Using standard meta-analytic techniques in a random-effects model, the data reviewed suggest that individuals with ASD show deficits in imitation, performing on average 0.81 SDs below individuals without ASD on imitation tasks. This deficit was specific to the condition of having ASD. Moderator analyses revealed that the average Autism Diagnostic Observation Schedule (ADOS) scores of groups of ASD participants were significantly and strongly negatively associated with the imitation abilities of these subjects, but average participant IQ was not associated with imitation abilities. Study setting, novelty of actions, format of imitation tasks (live vs. not), number of actions to imitate, or verbal prompts were not found to significantly affect the sizes of the imitation differences between individuals with and without ASD. The manner in which imitation was operationalized, however, had significant effects on whether imitation deficits were found between individuals with and without ASD. In tests that measured imitation of both form and end points, participants with ASD showed significant deficits compared with those without ASD; on tests of end point emulation only, individuals with ASD showed no deficits.

Explaining how genes influence behavior is important to many branches of psychology, including development, behavior genetics, and evolutionary psychology. Presented here is a developmental model linking the immediate consequence of gene activity (transcription of messenger RNA molecules from DNA sequences) to behavior through multiple molecular, cellular, and physiological levels. The model provides a level of detail appropriate to theories of behavioral development that recognizes the molecular level of gene action, dispensing with the metaphorical use of such terms as blueprints, plans, or constraints that has obscured much previous discussion. Special attention is paid to the possible role of immediate-early genes in initiating developmental responses to experience, adding specificity to the claim that neither genes nor experience act alone to shape development.The question of how genes affect behavior has been a longstanding focus of both controversy and research within the behavioral and social sciences. It is most directly of concern to the study of behavioral development (Gottlieb, 1998;Wahlsten, 1999) but is also important for behavior genetics (McClearn, Plomin, GoraMaslak, & Crabbe, 1991;Plomin & Rutter, 1998;Turkheimer, 1998) and evolutionary psychology (Buss, 1994;Lloyd, 1999). Although no one today seriously doubts that behavior is influenced in some way by genetic constitution, a general understanding of the mechanisms by which genes exert their influence is still far away. The immediate effect of genes is to specify, through the intermediate stage of messenger RNA (mRNA) synthesis, the polypeptide sequences of various proteins, including those involved in brain structure and function and thus presumably in the organization of behavior. It is, however, a very long step from polypeptide sequences to behavior-a step, moreover, that covers much incompletely understood territory. The aim of this article is to provide a map of that territory, in the form of a model that incorporates genetic influences into a conceptually rigorous account of the development of behavior.This article focuses on the development of behavior. However, genetic activity is involved not only in the developmental transitions between conception and maturity but also in the processes of learning and behavioral plasticity that occur throughout the life span (Robertson, 1992;Tischmeyer & Grimm, 1999). Any account of genetic influences on behavior must include an analysis of the different "causal pathway[s] through which the gene influences the phenotype" (McClearn, et al., 1991, p. 223). Although the techniques of behavioral genetic analysis permit the identification of individual genes with significant effects on behavior (Wahlsten, 1999), understanding how genes influence behavior requires an analysis of the various processes underlying behavioral changes (Gottlieb, 1995).Our analysis extends ideas proposed in earlier articles (Johnston, 1987(Johnston, , 1988 and builds on work done by other developmental theorists working within ...

ABSTRACT-Grapheme-color synaesthesia is a neurological phenomenon in which particular graphemes, such as the numeral 9, automatically induce the simultaneous perception of a particular color, such as the color red. To test whether the concurrent color sensations in graphemecolor synaesthesia are treated as meaningful stimuli, we recorded event-related brain potentials as 8 synaesthetes and 8 matched control subjects read sentences such as ''Looking very clear, the lake was the most beautiful hue of 7.'' In synaesthetes, but not control subjects, congruous graphemes, compared with incongruous graphemes, elicited a more negative N1 component, a less positive P2 component, and a less negative N400 component. Thus, contextual congruity of synaesthetically induced colors altered the brain response to achromatic graphemes beginning 100 ms postonset, affecting pattern-recognition, perceptual, and meaning-integration processes. The results suggest that grapheme-color synaesthesia is automatic and perceptual in nature and also suggest that the connections between colors and numbers are bidirectional.