Traffic-related particulate matter affects behavior, inflammation, and neural integrity in a developmental rodent model.

Recent studies indicate that exposure to airborne particulate matter (PM) is associated with cognitive delay, depression, anxiety, autism, and neurodegenerative diseases; however, the role of PM in the etiology of these outcomes is not well-understood. Therefore, there is a need for controlled animal studies to better elucidate the causes and mechanisms by which PM impacts these health outcomes. We assessed the effects of gestational and early life exposure to traffic-related PM on social- and anxiety-related behaviors, cognition, inflammatory markers, and neural integrity in juvenile male rats.

Bedding-generated particulate matter: implications for rodent studies.

Objectives: Rodents used in scientific research are typically housed in cages containing natural bedding materials. Despite extensive evidence of biological harm from inhaled particulate matter (PM), relatively little work has been performed to measure bedding-generated PM exposure in caged animals used in basic science research. Our objectives were to determine whether bedding-generated PM was present in significant concentrations in rodent cages and to identify the main factors affecting the accumulation and attenuation of bedding-generated PM inside cages.

Effects of Brain-Derived IL-2 Deficiency and the Development of Autoimmunity on Spatial Learning and Fear Conditioning.

Interleukin-2 (IL-2) has been implicated in neurological disorders including multiple sclerosis and Alzheimer's disease. Peripheral IL-2 deficiency in gene-deleted mice results in T cell mediated autoimmunity that begins to develop slowly after weaning and progressively increases through adulthood. Loss of brain-derived IL-2 results in neurobiological and behavioral abnormalities, and may contribute to the development of CNS autoimmunity by modifying the neuroimmunological milieu of the brain.

Reversal of Neuronal Atrophy: Role of Cellular Immunity in Neuroplasticity and Aging.

Emerging evidence indicates that neuroimmunological changes in the brain can modify intrinsic brain processes that are involved in regulating neuroplasticity. Increasing evidence suggests that in some forms of motor neuron injury, many neurons do not die, but reside in an atrophic state for an extended period of time. In mice, facial motor neurons in the brain undergo a protracted period of degeneration or atrophy following resection of their peripheral axons.