Elucidation of the ‘fear circuit’ has opened exciting avenues for understanding and treating human anxiety disorders. However, the translation of rodent to human studies, and vice versa, depends on understanding the homology in relevant circuits across species. Although abundant evidence indicates that the hippocampal-amygdala circuit mediates contextual fear learning, previous studies indicate that this pathway is more restricted in the primate than in rodent. Moreover, cellular components of the amygdala differ across species. The paralaminar nucleus (PL) of the amygdala, a structure that is closely associated with the basal nucleus, is one example, having no clear homologue in rodents. In both human and nonhuman primates, the PL contains a subpopulation of immature-appearing neurons, which merge into the corticoamygdaloid transition area (CTA). To understand whether immature-appearing neurons are positioned to participate in fear circuitry, we first mapped the hippocampal-amygdala projection in the monkey. We then determined whether immature appearing neurons were targets of this path. Retrograde results show that the hippocampal inputs to the amygdala originate in uncal region (CA1’) and the rostral prosubiculum, consistent with earlier studies. The amygdalohippocampal area, ventral basal nucleus, the medial paralaminar nucleus, and its confluence with the CTA are the main targets of this projection. Immature neurons are prominent in the PL and corticoamygdaloid transition area (CTA), and are overlapped by anterogradely labeled fibers from CA1’, particularly in the medial PL and CTA. Hippocampal inputs to the amygdala are more focused in higher primates compared to rodents, supporting previous anatomic studies and recent data from human functional imaging studies of contextual fear. At the cellular level, a hippocampal interaction with immature neurons in the amygdala suggests a novel substrate for cellular plasticity, with implications for mechanisms underlying contextual learning and emotional memory processes.

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Summary Exposure to traumatic stressors typically causes lasting changes in emotionality and behavior. However, coping strategies have been shown to prevent and alleviate many stress consequences and the biological mechanisms that underlie coping are of great interest. Whereas the laboratory stressor inescapable tail-shock induces anxiety-like behaviors, here we demonstrate that permitting a rat to chew on a wooden dowel during administration of tail-shock prevented the development of anxiety like behaviors in the open field and juvenile social exploration tests. Uncontrollable stressors increase corticosterone and decrease thyroid hormone, and we hypothesized that coping would blunt these changes. While tail-shock did produce these effects, active coping did not alter hormone levels. The dissociation between behavioral resilience and circulating hormones is discussed with regard to the utility of these molecules as biomarkers for psychiatric disease.

IMPORTANCE The study sought to identify a new method for measuring internal nasal valve patency. OBJECTIVE To determine whether intraoperative endoscopic suction-assisted evaluation of the internal nasal valve is a useful technique to assess internal nasal valve area and function. DESIGN, SETTING, AND PARTICIPANTS A study of 20 patients undergoing cosmetic and functional septorhinoplasty from May 1 through October 31, 2012, at a private surgical practice was performed. A follow-up study was performed 3 years postoperatively on 7 patients. A photograph of the internal nasal valve was taken endoscopically with and without suction preoperatively, postoperatively, and at 3-year follow-up. Measurement of the internal nasal valve surface areas was then performed by an evaluator masked to patient groupings. MAIN OUTCOMES AND MEASURES Outcome measures were surface area of the internal nasal valve as measured by standardized, endoscopic photography preoperatively, postoperatively, and at 3 years with and without suction and Nasal Obstruction Symptom Evaluation (NOSE) scale scores at 3 years comparing preoperative and postoperative symptoms. RESULTS Among the 20 patients studied, 13 were female and the mean age was 26 years. No difference was found in the observed static surface area of the internal nasal valve comparing preoperative and postoperative values (72 418 vs 76 973 square pixels, P = .58). No difference was found in the observed static surface area of the internal nasal valve comparing preoperative (56 426 square pixels) and postoperative (60 011 square pixels) values (P = .58). No difference was found in the observed surface area of the internal nasal valve under negative pressure comparing preoperative (54 194 square pixels) and immediate postoperative (58 325 square pixels) values (P = .97). At 3 years, the resting surface area of the internal nasal valve was not increased with an internal nasal valve surface area mean of 56 426 square pixels preoperatively and 84 352 postoperatively (P = .09). The surface area of the internal nasal valve was increased when exposed to negative sniff pressures in the 3-year follow-up by 45% (P = .03). The surface area measured a mean of 47 683 square pixels preoperatively and 85 612 square pixels at the 3-year mark under negative pressure. CONCLUSIONS AND RELEVANCE The study outlines a novel technique for measuring internal nasal valve surface area and compliance preoperatively and postoperatively. Surgery on the internal nasal valve has a greater effect on the dynamic function of the internal nasal valve (ie, stiffness that can be accounted for by a mere increase in nasal valve size when measured endoscopically). The study lays the groundwork for future studies using this technique. LEVEL OF EVIDENCE 4.

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