Adolescent environmental enrichment induces social resilience and alters neural gene expression in a selectively bred rodent model with anxious phenotype.

Stress is a major influence on mental health status; the ways that individuals respond to or copes with stressors determine whether they are negatively affected in the future. Stress responses are established by an interplay between genetics, environment, and life experiences. Psychosocial stress is particularly impactful during adolescence, a critical period for the development of mood disorders.

Neurotransmission-related gene expression in the frontal pole is altered in subjects with bipolar disorder and schizophrenia.

The frontal pole (Brodmann area 10, BA10) is the largest cytoarchitectonic region of the human cortex, performing complex integrative functions. BA10 undergoes intensive adolescent grey matter pruning prior to the age of onset for bipolar disorder (BP) and schizophrenia (SCHIZ), and its dysfunction is likely to underly aspects of their shared symptomology. In this study, we investigated the role of BA10 neurotransmission-related gene expression in BP and SCHIZ.

Modeling the daily rhythm of human pain processing in the dorsal horn.

Experimental studies show that human pain sensitivity varies across the 24-hour day, with the lowest sensitivity usually occurring during the afternoon. Patients suffering from neuropathic pain, or nerve damage, experience an inversion in the daily modulation of pain sensitivity, with the highest sensitivity usually occurring during the early afternoon. Processing of painful stimulation occurs in the dorsal horn (DH), an area of the spinal cord that receives input from peripheral tissues via several types of primary afferent nerve fibers.

Inference of cell type content from human brain transcriptomic datasets illuminates the effects of age, manner of death, dissection, and psychiatric diagnosis.

Psychiatric illness is unlikely to arise from pathology occurring uniformly across all cell types in affected brain regions. Despite this, transcriptomic analyses of the human brain have typically been conducted using macro-dissected tissue due to the difficulty of performing single-cell type analyses with donated post-mortem brains. To address this issue statistically, we compiled a database of several thousand transcripts that were specifically-enriched in one of 10 primary cortical cell types in previous publications.

Adolescent sleep patterns in humans and laboratory animals.

This article is part of a Special Issue "Puberty and Adolescence". One of the defining characteristics of adolescence in humans is a large shift in the timing and structure of sleep. Some of these changes are easily observable at the behavioral level, such as a shift in sleep patterns from a relatively morning to a relatively evening chronotype.

The neuroendocrine control of the circadian system: adolescent chronotype.

Scientists, public health and school officials are paying growing attention to the mechanism underlying the delayed sleep patterns common in human adolescents. Data suggest that a propensity towards evening chronotype develops during puberty, and may be caused by developmental alterations in internal daily timekeeping. New support for this theory has emerged from recent studies which show that pubertal changes in chronotype occur in many laboratory species similar to human adolescents.

Changes in circadian rhythms during puberty in Rattus norvegicus: developmental time course and gonadal dependency.

During puberty, humans develop a later chronotype, exhibiting a phase-delayed daily rest/activity rhythm. The purpose of this study was to determine: 1) whether similar changes in chronotype occur during puberty in a laboratory rodent species, 2) whether these changes are due to pubertal hormones affecting the circadian timekeeping system. We tracked the phasing and distribution of wheel-running activity rhythms during post-weaning development in rats that were gonadectomized before puberty or left intact.

Chronotype changes during puberty depend on gonadal hormones in the slow-developing rodent, Octodon degus.

During puberty, human adolescents develop a later chronotype, exhibiting a delay in the timing of rest and activity as well as other daily physiological rhythms. The purpose of this study was to determine whether similar changes in chronotype occur during puberty in a laboratory rodent species, and, if so, to determine whether they are due to pubertal hormones acting on the circadian timekeeping system. To test this hypothesis, we carefully tracked daily activity rhythms across puberty in the slow-developing rodent Octodon degus.