Olfactory exposure to males, including men, causes stress and related analgesia in rodents.

We found that exposure of mice and rats to male but not female experimenters produces pain inhibition. Male-related stimuli induced a robust physiological stress response that results in stress-induced analgesia. This effect could be replicated with T-shirts worn by men, bedding material from gonadally intact and unfamiliar male mammals, and presentation of compounds secreted from the human axilla. Experimenter sex can thus affect apparent baseline responses in behavioral testing.

Male-Specific Conditioned Pain Hypersensitivity in Mice and Humans.

Pain memories are hypothesized to be critically involved in the transition of pain from an acute to a chronic state. To help elucidate the underlying neurobiological mechanisms of pain memory, we developed novel paradigms to study context-dependent pain hypersensitivity in mouse and human subjects, respectively. We find that both mice and people become hypersensitive to acute, thermal nociception when tested in an environment previously associated with an aversive tonic pain experience. This sensitization persisted for at least 24 hr and was only present in males of both species. In mice, context-dependent pain hypersensitivity was abolished by castrating male mice, pharmacological blockade of the hypothalamic-pituitary-adrenal axis, or intracerebral or intrathecal injections of zeta inhibitory peptide (ZIP) known to block atypical protein kinase C (including the protein kinase Mζ isoform). In humans, men, but not women, self-reported higher levels of stress when tested in a room previously associated with tonic pain. These models provide a new, completely translatable means for studying the relationship between memory, pain, and stress.

Perception of recovery after pediatric mild traumatic brain injury is influenced by the "good old days" bias: tangible implications for clinical practice and outcomes research.

Recovery from mild traumatic brain injury (mTBI) is primarily based on the resolution of post-concussive symptoms back to a premorbid level. However, the "good old days" bias means fewer premorbid symptoms are retrospectively recalled, thus skewing the determination of recovery relative to pre-injury. The objectives of this study were to investigate the "good old days" bias in pediatric mTBI and demonstrate the implications of this bias on perceived recovery. Children and adolescents 2-18 years old (mean = 10.9, SD = 4.4, N = 412) were recruited after sustaining an mTBI. Ratings of premorbid symptoms were provided: (a) in the Emergency Department (ED; by parents), (b) retrospectively at a 1-month follow-up (by parents and adolescents), and (c) retrospectively at a 3-month follow-up (by parents and adolescents). Parent ratings of premorbid symptoms decreased by 80% from the ED to 1-month post-injury (p < .001) but were stable from 1 to 3 months post-injury (p < .05). Adolescents premorbid ratings declined from 1 to 3 months post-injury. Slow recovery did not have a differential impact on premorbid reporting. Using premorbid ratings obtained in the ED, instead of retrospective symptom reporting at the time of follow-up, suggests that a significant minority of patients believed to be "not recovered" actually have the "same or lower" symptom ratings at 1 (29%) and 3 months (41%) post-injury compared with before the injury. The "good old days" bias is present in pediatric mTBI by 1-month post-injury, influences retrospective symptom reporting, and has measureable implications for determining recovery in research and clinical practice.