“A Massive Long Way”: Interconnecting Histories, a “Special Child,” ADHD, and Everyday Family Life

Focusing on one family from a study of dual-earner middle-class families carried out in Los Angeles, California, this article draws on interview and video-recorded data of everyday interactions to explore illness and healing as embedded in the microcultural context of the Morris family. For this family, an important aspect of what is at stake for them in their daily lives is best understood by focusing on 9-year-old Mark, who has been diagnosed with attention-deficit/hyperactivity disorder (ADHD). In this article, we grapple with the complexity of conveying some sense of how Mark’s condition is experienced and relationally enacted in everyday contexts. Through illuminating connections between lives as lived and lives as told, we explore the narrative structuring of healing in relation to Mark’s local moral world with the family at its center. We examine how his parents understand the moral consequences of the child’s past for his present and future, and work to encourage others to give due weight to his troubled beginnings before this child joined the Morris family. At the same time, we see how the Morris parents act to structure Mark’s moral experience and orient to a desired future in which Mark’s “success” includes an appreciation of how he is accountable to others for his actions. Through our analyses, we also seek to contribute to discussions on what is at stake in everyday life contexts for children with ADHD and their families, through illuminating aspects of the cultural, moral and relational terrain that U.S. families navigate in contending with a child’s diagnosis of ADHD. Further, given that ADHD is often construed as a “disorder of volition,” we seek to advance anthropological theorizing about the will in situations where volitional control over behavior is seen to be disordered

Control of interneuron dendritic growth through NRG1/erbB4-mediated kalirin-7 disinhibition.

Neuregulin 1 (NRG1) is a secreted trophic factor that activates the postsynaptic erbB4 receptor tyrosine kinase. Both NRG1 and erbB4 have been repeatedly associated with schizophrenia, but their downstream targets are not well characterized. ErbB4 is highly abundant in interneurons, and NRG1-mediated erbB4 activation has been shown to modulate interneuron function, but the role for NRG1-erbB4 signaling in regulating interneuron dendritic growth is not well understood. Here we show that NRG1/erbB4 promote the growth of dendrites in mature interneurons through kalirin, a major dendritic Rac1-GEF. Recent studies have shown associations of the KALRN gene with schizophrenia. Our data point to an essential role of phosphorylation in kalirin-7's C terminus as the critical site for these effects. As reduced interneuron dendrite length occurs in schizophrenia, understanding how NRG1-erbB4 signaling modulates interneuron dendritic morphogenesis might shed light on disease-related alterations in cortical circuits

What is psychiatry? Co-producing complexity in mental health

What is psychiatry? Such a question is increasingly important to engage with in light of the development of new diagnostic frameworks that have wide-ranging and international clinical and societal implications. I suggest in this reflective essay that ‘psychiatry' is not a singular entity that enjoins consistent forms of critique along familiar axes; rather, it is a heterogeneous assemblage of interacting material and symbolic elements (some of which endure, and some of which are subject to innovation). In underscoring the diversity of psychiatry, I seek to move towards further sociological purchase on what remains a contested and influential set of discourses and practices. This approach foregrounds the relationships between scientific knowledge, biomedical institutions, social action and subjective experience; these articulations co-produce both psychiatry and each other. One corollary of this emphasis on multiplicity and incoherence within psychiatric theory, research and practice, is that critiques which elide this complexity are rendered problematic. Engagements with psychiatry are, I argue, best furthered by recognising its multifaceted nature

The history of attention deficit hyperactivity disorder

The contemporary concept of attention deficit hyperactivity disorder (ADHD) as defined in the DSM-IV-TR (American Psychiatric Association 2000) is relatively new. Excessive hyperactive, inattentive, and impulsive children have been described in the literature since the nineteenth century. Some of the early depictions and etiological theories of hyperactivity were similar to current descriptions of ADHD. Detailed studies of the behavior of hyperactive children and increasing knowledge of brain function have changed the concepts of the fundamental behavioral and neuropathological deficits underlying the disorder. This article presents an overview of the conceptual history of modern-day ADHD

Coordinated Nuclear and Synaptic Shuttling of Afadin Promotes Spine Plasticity and Histone Modifications

The ability of a neuron to transduce extracellular signals into long lasting changes in neuronal morphology is central to its normal function. Increasing evidence shows that coordinated regulation of synaptic and nuclear signaling in response to NMDA receptor activation is crucial for long term memory, synaptic tagging, and epigenetic signaling. Although mechanisms have been proposed for synapse-to-nuclear communication, it is unclear how signaling is coordinated at both subcompartments. Here, we show that activation of NMDA receptors induces the bi-directional and concomitant shuttling of the scaffold protein afadin from the cytosol to the nucleus and synapses. Activity-dependent afadin nuclear translocation peaked 2 h post-stimulation, was independent of protein synthesis, and occurred concurrently with dendritic spine remodeling. Moreover, activity-dependent afadin nuclear translocation coincides with phosphorylation of histone H3 at serine 10 (H3S10p), a marker of epigenetic modification. Critically, blocking afadin nuclear accumulation attenuated activity-dependent dendritic spine remodeling and H3 phosphorylation. Collectively, these data support a novel model of neuronal nuclear signaling whereby dual-residency proteins undergo activity-dependent bi-directional shuttling from the cytosol to synapses and the nucleus, coordinately regulating dendritic spine remodeling and histone modifications