Subjective Experience of Sensation in Anorexia Nervosa.

Subjective experience of sensation in anorexia nervosa.

Behav Res Ther. 2013 Feb 27; 51(6): 256-265
Zucker NL, Merwin RM, Bulik CM, Moskovich A, Wildes JE, Groh J

The nature of disturbance in body experience in anorexia nervosa (AN) remains poorly operationalized despite its prognostic significance. We examined the relationship of subjective reports of sensitivity to and behavioral avoidance of sensory experience (e.g., to touch, motion) to body image disturbance and temperament in adult women currently diagnosed with AN (n = 20), women with a prior history of AN who were weight restored (n = 15), and healthy controls with no eating disorder history (n = 24). Levels of sensitivity to sensation and attempts to avoid sensory experience were significantly higher in both clinical groups relative to healthy controls. Sensory sensitivity was associated with body image disturbance (r(56) = .51, p < .0001), indicating that body image disturbance increased with increased global sensitivity to sensation. Sensory sensitivity was also negatively and significantly correlated with lowest BMI (r(2) = -.32, p < .001), but not current BMI (r(2) = .03, p = .18), and to the temperament feature of harm avoidance in both clinical groups. We discuss how intervention strategies that address sensitization and habituation to somatic experience via conditioning exercises may provide a new manner in which to address body image disturbance in AN. HubMed – eating


Potency Optimization of Huwentoxin-IV on hNav1.7: a Neurotoxic TTX-S Sodium-Channel Antagonist from the Venom of the Chinese Bird-eating Spider Selenocosmia huwena.

Peptides. 2013 Mar 19;
Revell JD, Lund PE, Linley JE, Metcalfe J, Burmeister N, Sridharan S, Jones C, Jermutus L, Bednarek M

The spider venom peptide Huwentoxin-IV (HwTx-IV) 1 is a potent antagonist of hNav1.7 (IC50 determined herein as 17nM±2). Nav1.7 is a voltage-gated sodium channel involved in the generation and conduction of neuropathic and nociceptive pain signals. We prepared a number of HwTx-IV analogs as part of a structure-function study into Nav1.7 antagonism. The inhibitory potency of these analogs was determined by automated electrophysiology and is reported herein. In particular, the native residues Glu(1), Glu(4), Phe(6) and Tyr(33) were revealed as important activity modulators and several peptides bearing mutations in these positions showed significantly increased potency on hNav1.7 while maintaining the original selectivity profile of the wild-type peptide 1 on hNav1.5. Peptide 47 (Gly(1), Gly(4), Trp(33)-HwTx) demonstrated the largest potency increase on hNav1.7 (IC50 0.4nM±0.1). HubMed – eating


Adolescent female C57BL/6 mice with vulnerability to activity-based anorexia exhibit weak inhibitory input onto hippocampal CA1 pyramidal cells.

Neuroscience. 2013 Mar 20;
Chowdhury TG, Wable GS, Sabaliauskas NA, Aoki C

Anorexia nervosa (AN) is an eating disorder characterized by self-imposed severe starvation and often linked with excessive exercise. Activity-based anorexia (ABA) is an animal model that reproduces some of the behavioral phenotypes of AN, including the paradoxical increase in voluntary exercise following food restriction (FR). Although certain rodents have been used successfully in this animal model, C57BL/6 mice are reported to be less susceptible to ABA. We re-examined the possibility that female C57BL/6 mice might exhibit ABA vulnerability during adolescence, the developmental stage/sex among the human population with particularly high AN vulnerability. After introducing the running wheel to the cage for three days, ABA was induced by restricting food access to 1 hour per day (ABA1, N=13) or 2 hours per day (ABA2, N=10). All 23 exhibited increased voluntary wheel running (p<0.005) and perturbed circadian rhythm within two days. Only one out of five survived ABA1 for three days, while ten out of ten survived ABA2 for three days and could subsequently restore their body weight and circadian rhythm. Exposure of recovered animals to a second ABA2 induction revealed a large range of vulnerability, even within littermates. To look for the cellular substrate of differences in vulnerability, we began by examining synaptic patterns in the hippocampus, a brain region that regulates anxiety as well as plasticity throughout life. Quantitative EM analysis revealed that CA1 pyramidal cells of animals vulnerable to the second ABA2 exhibit less GABAergic innervation on cell bodies and dendrites, relative to the animals resilient to the second ABA (p<0.001) or controls (p<0.05). These findings reveal that C57BL/6J adolescent females can be used to capture brain changes underlying ABA vulnerability, and that GABAergic innervation of hippocampal pyramidal neurons is one important cellular substrate to consider for understanding the progression of and resilience to AN. HubMed – eating



HOW YOU LOOK IS NOT WHO YOU ARE: TEENS TALK EATING DISORDERS – In the Mix is the Emmy award winning PBS documentary series for teens A diverse group of girls and boys talk about their eating disorders, their symptoms, th…