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Traumatic brain injury (TBI) is a serious health concern for civilians and military populations, and blast-induced TBI (bTBI) has become an increasing problem for military personnel over the past 10 years. To understand the biological and psychological effects of blast-induced injuries and to examine potential interventions that may help to prevent, attenuate, and treat effects of bTBI, it is valuable to conduct controlled animal experiments. This unit discusses available paradigms to model traumatic brain injury in animals, with an emphasis on the relevance of these various models to study blast-induced traumatic brain injury (bTBI). This paper describes the detailed methods of a blast overpressure (BOP) paradigm that has been used to conduct experiments with rats to model blast exposure. This particular paradigm models the pressure wave created by explosions, including improvised explosive devices (IEDs).

Mild traumatic brain injury, caused by the exposure to single or repeated blast overpressure, is a principal concern due to its pathological complexity and neurobehavioral similarities with posttraumatic stress disorder. In this study, we exposed rats to a single or multiple (five total; administered on consecutive days) mild blasts, assessed their behavior at 1 and 16 days postinjury) and performed histological and protein analyses of brains and plasma at an early (2 h) and a late (22 days) termination time point. One day postinjury, multiple-injured (MI) rats showed the least general locomotion and the most depression- and anxiety-related behaviors among the experimental groups; there were no such differences at 16 days. However, at the later time point, both injured groups displayed elevated levels of select protein biomarkers. Histology showed significantly increased numbers of TUNEL+ (terminal-deoxy-transferase-mediated dUTP nick-end labeling)-positive cells in the dorsal and ventral hippocampus (DHC and VHC) of both injured groups as early as 2 h after injury. At 22 days, the increase was limited to the VHC of MI animals. Our findings suggest that the exposure to mild blast overpressure triggers early hippocampal cell death as well as neuronal, glial, and vascular damage that likely contribute to significant, albeit transient increases in depression- and anxiety-related behaviors. However, the severity of the observed pathological changes in MI rats failed to support the hypothesized cumulative effect of repeated injury. We infer that at this blast frequency, a potential conditioning phenomenon counteracts with and reduces the extent of subsequent damage in MI rats., (© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Context: Mild traumatic brain injury (mTBI) represents a major health problem in civilian populations as well as among the military service members due to (1) lack of effective treatments, and (2) our incomplete understanding about the progression of secondary cell injury cascades resulting in neuronal cell death due to deficient cellular energy metabolism and damaged mitochondria., Aims: The aim of this study was to identify and delineate the mitochondrial targeted genes responsible for altered brain energy metabolism in the injured brain., Settings and Design: Rats were either grouped into naïve controls or received lateral fluid percussion brain injury (2-2.5 atm) and followed up for 7 days., Materials and Methods: Rats were either grouped into naïve controls or received lateral fluid percussion brain injury (2-2.5 atm) and followed for 7 days. The severity of brain injury was evaluated by the neurological severity scale-revised (NSS-R) at 3 and 5 days post TBI and immunohistochemical analyses at 7 days post TBI. The expression profiles of mitochondrial-targeted genes across the hippocampus from TBI and naïe rats were also examined by oligo-DNA microarrays., Results: NSS-R scores of TBI rats (5.4 ± 0.5) in comparison to naïe rats (3.9 ± 0.5) and H and E staining of brain sections suggested a mild brain injury. Bioinformatics and systems biology analyses showed 31 dysregulated genes, 10 affected canonical molecular pathways including a number of genes involved in mitochondrial enzymes for oxidative phosphorylation, mitogen-activated protein Kinase (MAP), peroxisome proliferator-activated protein (PPAP), apoptosis signaling, and genes responsible for long-term potentiation of Alzheimer's and Parkinson's diseases., Conclusions: Our results suggest that dysregulated mitochondrial-focused genes in injured brains may have a clinical utility for the development of future therapeutic strategies aimed at the treatment of TBI.

The author investigated the importance of processing considerations within implicit memory in a developmental design. Second-graders (n = 87) and college students (n = 81) completed perceptual (word stem completion) and conceptual (category generation) implicit memory tests after studying target items either nonsemantically (read) or semantically (generated). In support of previous research, the author found no age differences in priming in the nonsemantic study/perceptual test condition. Age differences in priming were found in the semantic study/conceptual test condition, however, where college students had significantly higher priming scores than did children. These developmental dissociations support the theory that the processing requirements of conceptual implicit memory are similar to those in explicit memory. The author also discusses the contribution of the Transfer Appropriate Processing (TAP; H. L. Roediger, D. A. Gallo, & L. Geraci, 2002) framework to understanding these findings.

Cognitive constructs are explored for clinical psychologists interested in cognitive phenomena in depression. Both traditional and modern memory constructs are outlined and described with attention to their contribution to understanding depression. In particular, the notions of memory construction, self-schemas, and autobiographical memory (per [Conway, M.A. (2001). Sensory-perceptual episodic memory and its context: Autobiographical memory. Philosophical Transactions of the Royal Society of London: Biological Sciences, 356, 1375-1384.]) are discussed. Then, the phenomenon of implicit memory is described as a way to bring these constructs together to understand depression. The Rehm and Naus (1990) [Rehm, L.P., and Naus, M.J. (1990). A memory model of emotion. In Ingram, R.E. (Ed.), Contemporary Psychological Approaches to Depression (pp. 23-35). New York: Plenum Press.] memory model of emotion is updated and expanded to include these cognitive constructs, and depression is viewed from the perspective of understanding interactions between explicit and implicit memory processes.