The effect of home or novel environment on the facilitation of passive avoidance by post-training ethanol

Passive avoidance behavior of mice is improved when mice are injected with ethanol immediately after footshock training. Further study has shown that avoidance can be affected by ethanol injections given within 1 h, but not at 90 or 180 min, after training. The present study was conducted to investigate the possibility that events which occur in the homecage during this sensitive period may influence the effect of ethanol on subsequent avoidance. Male Swiss-Webster mice were housed either singly in a novel environment for 90 min or returned to their (group) homecage following one-trial, step-through, passive avoidance training (0.1 mA footshock) and intraperitoneal injection of 3.0 g/kg ethanol (15% v/v) or saline. As in previous studies, when ethanol-treated mice were returned to their homecage, avoidance was significantly increased at 24 h compared to the behavior of saline-treated mice. However, when mice were isolated in the novel environment for 90 min immediately following treatment, the memory facilitating effects of ethanol were not observed. The avoidance behavior of mice injected with saline was the same regardless of their post-training environment. Also, the number of mice (6 or 10) housed per homecage did not significantly influence the effects of ethanol or post-training environment on avoidance. These findings indicate that environmental factors may interact with the effects of ethanol to modify avoidance behavior. The possible influence of variables such as aggression, thermoregulation, and behavioral arousal on the effects of ethanol in this paradigm are discussed.     

A Meta-Analysis of Structural and Functional Brain Imaging in Dementia of the Alzheimer's Type: A Neuroimaging Profile

We conducted a quantitative review of the imaging literature using meta-analytic methodology to characterize further the magnitude of hippocampal deficit in probable Alzheimer's disease (AD) and to determine whether other neuroanatomic structures in AD can better discriminate the disease from normal aging. Additionally, we parceled the discriminability of neuroanatomic structures by duration of disease to determine those structures most sensitive to AD in its early and late stages. One hundred twenty-one studies published between 1984 and 2000 met criteria for inclusion in the present analysis. In total, structural (i.e., CT and MRI) and functional (i.e., SPECT and PET) neuroimaging results from 3511 patients with AD, and 1632 normal healthy controls were recorded across meta-analyses. Our results include neuroimaging profiles for both early onset and longer duration patients with AD. In sum, these profiles yield a signature of diagnostic markers in both cortical and subcortical neuroanatomic areas. This signature is consistent with the clinical phenomenology of Alzheimer's dementia and should aid in the positive identification of AD.     

Quantitative evidence for distinct cognitive impairment in anorexia nervosa and bulimia nervosa

It is generally agreed that at least some aspects of abnormal eating behaviour is indeed due in part to disordered cognition. The accumulated literature illustrates cognitive impairment in patients with anorexia nervosa (AN) and bulimia nervosa (BN). Yet beyond being inconsistent, these independent studies also do not reveal the magnitude of impairment within and across studies and fail to give due consideration to the magnitude of impairment so as to understand the severity and breadth of impairment and/or differences in cognitive profiles between patients with AN and BN. Hence, the present review on the subject sought to articulate the magnitude of cognitive impairment in patients with AN and BN by quantitatively synthesizing the existing literature using meta-analytic methodology. The results demonstrate modest evidence of cognitive impairment specific to AN and BN that is related to body mass index in AN in terms of its severity, and is differentially impaired between disorders. Together, these results suggest that disturbed cognition is figural in the presentation of eating disorders and may serve to play an integral role in its cause and maintenance. Implications of these findings with respects to future research are discussed.