Alcohol self-administration in two rat lines selectively bred for extremes in anxiety-related behavior

According to the tension reduction hypothesis, individuals with art elevated anxiety level may be more sensitive to the anxiolytic effects of alcohol and may, therefore, have a higher predisposition to consume alcohol. To examine this hypothesis, we studied the drinking behavior as well as the sensitivity to the anxiolytic effect of alcohol in two rat lines that were bred and selected for differences in anxiety-related behavior on the elevated plus-maze: the extremely anxious HAB (high anxiety-related behavior) and the non-anxious LAB (low anxiety- related behavior) lines. Alcohol self-administration and the occurrence of an alcohol deprivation effect were studied in female and male HAB and LAB rats in a free-choice, 4-bottle home cage paradigm. The sensitivity of HAB and LAB rats to the anxiolytic effect of alcohol was assessed by testing their behavior oil the elevated plus-maze after an acute application of ethanol. During the first days of voluntary ethanol drinking, the ethanol intake and preference of female LABs was significantly higher than that of female HABs. Although not statistically significant, the same trend could be seen in male LABs. Moreover, male as well as female LAB but not HAB rats showed a significant alcohol deprivation effect after abstinence. There were no differences when saccharin was presented to naive animals, indicating that the different ethanol drinking behavior of HAB and LAB rats does not represent a general difference in the consumption of new liquids. Application of ethanol resulted in an anxiolytic effect in HAB but not in LAB rats oil the elevated plus-maze. In summary, increased inborn anxiety and voluntary ethanol consumption of HAB and LAB rats were correlated to some extent; however, this relationship was a negative one. It is concluded that, although such a relationship knight exist in solve individuals, increased levels of inborn anxiety and alcohol consumption are not necessarily related, (C) 2002 American College of Neuropsychopharmacology. Published by Elsevier Science In

Accumulated hippocampal formaldehyde induces age-dependent memory decline

Aging is an important factor in memory decline in aged animals and humans and in Alzheimer's disease and is associated with the impairment of hippocampal long-term potentiation (LTP) and down-regulation of NR1/NR2B expression. Gaseous formaldehyde exposure is known to induce animal memory loss and human cognitive decline; however, it is unclear whether the concentrations of endogenous formaldehyde are elevated in the hippocampus and how excess formaldehyde affects LTP and memory formation during the aging process. In the present study, we report that hippocampal formaldehyde accumulated in memory-deteriorating diseases such as age-related dementia. Spatial memory performance was gradually impaired in normal Sprague-Dawley rats by persistent intraperitoneal injection with formaldehyde. Furthermore, excess formaldehyde treatment suppressed the hippocampal LTP formation by blocking N-methyl-d-aspartate (NMDA) receptor. Chronic excess formaldehyde treatment over a period of 30 days markedly decreased the viability of the hippocampus and down-regulated the expression of the NR1 and NR2B subunits of the NMDA receptor. Our results indicate that excess endogenous formaldehyde is a critical factor in memory loss in age-related memory-deteriorating diseases