Bowden Larsson (fridaypoison9)

The root mean square (RMS) of the triaxial acceleration vectors in middle-aged rats was higher than that in adult rats. In the treadmill running tests, the RMS observed in middle-aged rats was significantly lower than that observed in adult rats. MCC and PGCC, which indicate movement consistencies, were significantly higher in middle-aged rats than they were in adult rats during the entire running test. However, only the RMS of the adult rats showed a negative correlation with exercise duration. Both MCC and PGCC were positively correlated with exercise duration. By contrast, a similar phenomenon was not found in the changes or differences in hippocampal theta rhythms between these two groups. Therefore, we consider that the MCC and PGCC could distinguish age-related movement differences and indicate coordination/adaptation during exercise. Changes in physical activity and alterations in the hippocampal theta rhythm were not different between the groups. V.Is addiction a medical disorder, and if so, what kind of disorder is it? Addiction is considered a brain disease by NIDA, based on observed brain changes in addicts that are interpreted as brain damage. Critics argue that the brain changes result instead from normal neuroplasticity and learning in response to the intense rewards provided by addictive substances, thus addiction is not a disorder but rather a series of normal-range if problematic choices. Relying on the harmful dysfunction analysis of medical disorder to determine disorder versus nondisorder, I argue that even if one accepts the critics' reinterpretation of NIDA's brain evidence and rejects the brain disease account, the critics' conclusion that addiction is not a medical disorder but is rather a matter of problematic nondisordered choice does not follow. This is because there is a further possible account of addiction, the evolutionary "hijack" view, that holds that addiction is due to the availability of substances and stimuli that were unavailable during human species evolution and that "hijack" certain brain areas concerned with human motivation, creating biologically undesigned peremptory desires. I argue that if the hijack theory is correct, then it opens up the possibility that addiction could be a true motivational medical disorder for which there is no underlying neurological-level dysfunction. Finally, I explore the implications of this account for how we see the social responsibility for addiction and how we attempt to control it. V.Despite the widespread belief that MK-801 induces memory deficits associated with dementia and schizophrenia in animal models, data regarding the impairing effect of MK-801 on aversive memory have been inconclusive. In this study, we investigated the effect of MK-801 on multiple memory stages of the inhibitory avoidance task, as well as its underlying signaling mechanism in the mouse hippocampus. We successfully replicated a previous finding suggesting that systemic injection of MK-801 impaired memory acquisition, but we observed that an intrahippocampal infusion of MK-801 facilitated the same memory process. We also found that both systemic and intrahippocampal administration of MK-801 facilitated memory consolidation and memory retrieval of the inhibitory avoidance task. We demonstrated that MK-801-induced increases in shock sensitivity and locomotor activity in the pre-training regimen confounded MK-801's detrimental effect on memory acquisition, thereby reconciling the inconsistent results in previous studies. In addition, the memory-facilitating effect of MK-801 was found to be dependent on drug doses and shock intensities. We next showed that MK-801 induced a fast-onset increase in the extent of mammalian target of rapamycin (mTOR) phosphorylation in the hippocampus. Finally, we observed that rapamycin, an mTOR inhibitor, blocked both the MK-801-induced increases in phosphorylated mTOR and the MK-801 facilitating effect on memory consolidation. These results indi