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© 2015 The Committee on Space Research (COSPAR). Published by Elsevier Ltd. All rights reserved. The space radiation environment includes energetic charged particles that may impact cognitive performance. We assessed the effects of 16O ion irradiation on cognitive performance of C57BL/6J × DBA/2J F1 (B6D2F1) mice at OHSU (Portland, OR) one month following irradiation at Brookhaven National Laboratory (BNL, Upton, NY). Hippocampus-dependent contextual fear memory and hippocampus-independent cued fear memory of B6D2F1 mice were tested. 16O ion exposure enhanced cued fear memory. This effect showed a bell-shaped dose response curve. Cued fear memory was significantly stronger in mice irradiated with 16O ions at a dose of 0.4 or 0.8 Gy than in sham-irradiated mice or following irradiation at 1.6 Gy. In contrast to cued fear memory, contextual fear memory was not affected following 16O ion irradiation at the doses used in this study. These data indicate that the amygdala might be particularly susceptible to effects of 16O ion exposure.

Research suggests that spatial navigation relies on the same neural network as episodic memory, episodic future thinking, and theory of mind (ToM). Such findings have stimulated theories (e.g., the scene construction and self-projection hypotheses) concerning possible common underlying cognitive capacities. Consistent with such theories, autism spectrum disorder (ASD) is characterized by concurrent impairments in episodic memory, episodic future thinking, and ToM. However, it is currently unclear whether spatial navigation is also impaired. Hence, ASD provides a test case for the scene construction and self-projection theories. The study of spatial navigation in ASD also provides a test of the extreme male brain theory of ASD, which predicts intact or superior navigation (purportedly a systemizing skill) performance among individuals with ASD. Thus, the aim of the current study was to establish whether spatial navigation in ASD is impaired, intact, or superior. Twenty-seven intellectually high-functioning adults with ASD and 28 sex-, age-, and IQ-matched neurotypical comparison adults completed the memory island virtual navigation task. Tests of episodic memory, episodic future thinking, and ToM were also completed. Participants with ASD showed significantly diminished performance on the memory island task, and performance was positively related to ToM and episodic memory, but not episodic future thinking. These results suggest that (contra the extreme male brain theory) individuals with ASD have impaired survey-based navigation skills—that is, difficulties generating cognitive maps of the environment—and adds weight to the idea that scene construction/self-projection are impaired in ASD. The theoretical and clinical implications of these results are discussed.

The induction of transcription of the 2'-5'-oligoadenylate (2-5A) synthetase gene by type I (alpha/beta) and type II (gamma) interferons (IFNs) has been studied in wild-type (w.t.) and IFN-resistant Friend leukemia cells (FLC). Following IFN treatment, new complexes are formed in vitro between the IFN-responsive sequence (IRS) of the 2-5A synthetase gene and cellular proteins. Within minutes after IFN-alpha/beta addition to w.t. FLC, an IRS-protein complex, designated F1, is detected, as already observed in several human cell lines. In response to IFN-gamma, a novel complex, designated Fg, is observed in w.t. FLC. The Fg complex appears within 3 h, while an F1-like complex is faintly visible 10 to 24 h later. In the IFN-alpha/beta-resistant FLC, IFN-gamma induces only the Fg complex and fails to induce F1. Fg formation is correlated with the IFN-gamma-induced transcription of the 2-5A synthetase gene and the appearance of the corresponding enzymatic activity in both w.t. and IFN-alpha/beta-resistant FLC. These findings suggest that F1 and Fg represent two distinct effector complexes by which type I and type II IFNs, respectively, induce 2-5A synthetase.

Treatment of Friend erythroleukemia cells (FLC) with gamma interferon (IFN-gamma) in the presence of anti-IFN-beta antibodies reduces the effectiveness of the antiviral state and the induction of 2'-5'-oligoadenylate synthetase activity, indicating that the antiviral activity of IFN-gamma in FLC is in part mediated by the production of IFN-beta. Accordingly, IFN-gamma induces a less pronounced antiviral state in FLC resistant to IFN-alpha/beta than in wild-type cells. Moreover, while results of run-on assays indicate that both IFN-alpha and -beta genes are constitutively transcribed in these cells, FLC treatment with IFN-gamma induces only IFN-beta mRNA accumulation. These results indicate that posttranscriptional mechanisms are involved in the regulation of IFN-beta and -alpha expression by IFN-gamma. The low amounts of the induced IFN-beta synergize with IFN-gamma in mounting the potent antiviral effect.