Evaluation of Touchscreen Chambers To Assess Cognition in Adult Mice: Effect of Training and Mild Traumatic Brain Injury.

Cognitive impairments are often experienced after a mild traumatic brain injury (mTBI). In the clinical arena, neuropsychological assessments are used frequently to detect cognitive deficits. Animal models of mTBI, however, rely on an assortment of behavioral tasks to assess cognitive outcome.

Greater neurobehavioral deficits occur in adult mice after repeated, as compared to single, mild traumatic brain injury (mTBI).

Mild traumatic brain injury (mTBI) accounts for the majority of all brain injuries and affected individuals typically experience some extent of cognitive and/or neuropsychiatric deficits. Given that repeated mTBIs often result in worsened prognosis, the cumulative effect of repeated mTBIs is an area of clinical concern and on-going pre-clinical research. Animal models are critical in elucidating the underlying mechanisms of single and repeated mTBI-associated deficits, but the neurobehavioral sequelae produced by these models have not been well characterized.

NF-κB mediates Gadd45β expression and DNA demethylation in the hippocampus during fear memory formation.

Gadd45-mediated DNA demethylation mechanisms have been implicated in the process of memory formation. However, the transcriptional mechanisms involved in the regulation of Gadd45 gene expression during memory formation remain unexplored. NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) controls transcription of genes in neurons and is a critical regulator of synaptic plasticity and memory formation.