Reversibility of object recognition but not spatial memory impairment following binge-like alcohol exposure in rats

Abstract

Excessive alcohol use leads to neurodegeneration in several brain structures including the hippocampal dentate gyrus and the entorhinal cortex. Cognitive deficits that result are among the most insidious and debilitating consequences of alcoholism. The object exploration task (OET) provides a sensitive measurement of spatial memory impairment induced by hippocampal and cortical damage. In this study, we examine whether the observed neurotoxicity produced by a 4-day binge ethanol treatment results in long-term memory impairment by observing the time course of reactions to spatial change (object configuration) and non-spatial change (object recognition). Wistar rats were assessed for their abilities to detect spatial configuration in the OET at 1 week and 10 weeks following the ethanol treatment, in which ethanol groups received 9-15 g/kg/day and achieved blood alcohol levels over 300 mg/dl. At 1 week, results indicated that the binge alcohol treatment produced impairment in both spatial memory and non-spatial object recognition performance. Unlike the controls, ethanol treated rats did not increase the duration or number of contacts with the displaced object in the spatial memory task, nor did they increase the duration of contacts with the novel object in the object recognition task. After 10 weeks, spatial memory remained impaired in the ethanol treated rats but object recognition ability was recovered. Our data suggest that episodes of binge-like alcohol exposure result in long-term and possibly permanent impairments in memory for the configuration of objects during exploration, whereas the ability to detect non-spatial changes is only temporarily affected.

Effects of drugs of abuse on hippocampal plasticity and hippocampus-dependent learning and memory: contributions to development and maintenance of addiction

“…In addition to possible enhancement of hippocampus-dependent learning and memory with low doses of ethanol, studies also showed that prolonged ethanol consumption uniformly resulted in hippocampus-dependent spatial learning deficits (Bond and Di Giusto 1976;Beatty et al 1984;Ehrlich and Humpel 2012), which were shown to be irreversible in some cases (Cippitelli et al 2010). Binge ethanol exposure also results in necrotic cell death and neurodegeneration in the hippocampus (Obernier et al 2002;Hamelink et al 2005).…”

Protection against alcohol-induced neuronal and cognitive damage by the PPARγ receptor agonist pioglitazone

“…Lesion studies have shown that damage of the hippocampal area mostly produces spatial reference deficits (Jarrard, 1993; Morris et al , 1982) whereas damage of the EC may also compromise reversal learning abilities (Eijkenboom et al , 2000; Hagan et al , 1992). However, cognitive impairment resulting from binge alcohol exposure includes reversal learning and object recognition deficits rather than deficits in acquisition of spatial reference memory in navigation or exploration tasks in rats (Cippitelli et al , 2010a; Cippitelli et al , 2010b; Obernier et al , 2002b). In these studies, re-learning deficits observed in binge alcohol treated animals have been closely associated with different navigation or exploratory patterns reflecting increased perseverative behavior as well as decreased cognitive flexibility.…”

“…Six horizontal sections containing the bilateral hippocampi and the respective EC regions were analyzed for degenerating cells between 5.6 to 6.6 mm ventral from bregma. Cell counting was conducted as previously described (Cippitelli et al , 2010a; Cippitelli et al , 2014; Cippitelli et al , 2010b). Degenerating granule cells of the entire DG were measured using the program Image J (Schneider et al , 2012).…”

“…The binge model of human alcoholic neurodegeneration, which mimics a single cycle of binge intoxication in human alcoholics (Braconi et al , 2010), is further validated by the fact that during alcohol intoxication animals reach sustained, high blood alcohol levels (BALs), commonly observed among alcoholics. Furthermore, neuronal deficits in animals treated with this binge alcohol model are associated with significant cognitive dysfunctions, such as learning and memory impairment as well as behavioral deficits including maladaptive perseverant behavior (Cippitelli et al , 2010a; Cippitelli et al , 2010b; Obernier et al , 2002b). …”

Perirhinal Cortex mGlu5 Receptor Activation Reduces Relapse to Methamphetamine Seeking by Restoring Novelty Salience

“…Deficits in novel object recognition, or variants of the task, have been observed after repeated exposure to not only meth (Belcher et al, 2007;Gonzalez et al, 2014;O'Dell et al, 2010;Reichel et al, 2014;Reichel et al, 2012b;Rogers et al, 2008), but also cocaine (Briand et al, 2008), ecstasy (Schenk et al, 2010), and alcohol (Cippitelli et al, 2010;Zhao et al, 2012). A few of these studies implicated certain neural mechanisms within a circuit including the prefrontal cortex (Gonzalez et al, 2014;Kamei et al, 2005), hippocampus and entorhinal cortex (Zhao et al, 2012).…”