Reinstating Over-Pouring Behavior: Importance of the Imagined Drinking Context.

BACKGROUND: College students significantly over-pour more than a standard drink in a free-pour simulated alcohol-pouring task. Due to this effect, it is likely that much of the self-report alcohol consumption data incorrectly or underreport actual alcohol consumption. Objective: We sought to determine factors that influence over-pouring. Specifically, in two studies we sought to determine the effect of different factors on the amount of fluid subjects pour in a simulated alcohol-pouring task. Methods: Data were collected from 217 undergraduate students (105 subjects in study 1 and 112 different subjects in study 2). In study one, subjects were asked to pour what they consider to be a standard beer for themselves and an unfamiliar peer. In study two subjects were instructed to pour a beer for themself and the experimenter as if they were at an off-campus party. Results: In study one, we found that size of the cup used to pour into significantly impacted the amount of fluid poured. In addition, subjects poured significantly less for themselves than the unfamiliar peer. In study two, the imagined context in which subjects poured significantly increased the amount of fluid poured demonstrating the importance of imagined contextual cues on alcohol use behavior. Conclusions/Importance: Imagined drinking context, presence of an unfamiliar peer, and cup size affect the amount of fluid poured in a simulated alcohol free pour task. Given the various factors that impact free pouring in college students, self-report alcohol data should be considered with caution.

Differences in Behavioral Responding in Adult and Aged Rats Following Chronic Ethanol Exposure.

BACKGROUND: Research suggests symptoms of chronic alcoholism, and withdrawal may be more severe in elderly compared with younger adults. However, examination of the effects of long-term ethanol (EtOH) consumption and withdrawal is limited in aged rodents. We thus investigated EtOH withdrawal and potential deficits in cognitive and motor behavior in young adult and aged rats. We also examined the effects of acute allopregnanolone as a potential mechanism contributing to age-related differences in EtOH's cognitive-impairing effects. METHODS: Male young adult (postnatal days 70 to 72) and aged (approximately 18 months) Sprague-Dawley rats were treated with liquid EtOH diet in a modified chronic intermittent EtOH (modified-CIE) paradigm. The severity of EtOH withdrawal was determined using a 4-item rating scale, and withdrawal-induced anxiety-like behavior was assessed in the elevated plus maze (EPM) and open field. After a 14-day EtOH-free period, spatial performance was assessed in the Morris water maze (MWM) during sober acquisition and in response to a subsequent EtOH and allopregnanolone challenge. RESULTS: Modified-CIE adults consumed more EtOH during treatment and exhibited robust EtOH withdrawal using a behavioral rating scale compared to aged rats. In the EPM, adult and aged modified-CIE groups spent increased time in the closed arms, while aged animals also made significantly more closed arm entries, fewer open arm entries, and spent less time in the open arms during withdrawal compared to controls. Modified-CIE decreased MWM performance of adult and aged rats, but did not result in motor impairments in either age group. Finally, acute allopregnanolone increased time to the MWM platform in adults but not aged animals. CONCLUSIONS: The elderly may be vulnerable to EtOH withdrawal as modified-CIE aged rats displayed anxiety-like behavior compared to controls during withdrawal despite achieving lower blood EtOH concentrations during treatment than younger adults. Our data also indicate that modified-CIE and EtOH withdrawal cause persistent cognitive impairments in both age groups. The results from this study provide further evidence indicating the elderly may be sensitive to the effects of alcohol.

Chronic intermittent ethanol exposure produces persistent anxiety in adolescent and adult rats.

BACKGROUND: Ethanol (EtOH) dependence and tolerance in the adult are marked by increased function of NMDA receptors and decreased function of GABAA receptors, which coincide with altered receptor subunit expression in specific brain regions. Adolescents often use EtOH at levels greater than adults, yet the receptor subunit expression profiles following chronic intermittent EtOH (CIE) exposure in adolescents are not known. Persistent age-dependent changes in receptor subunit alterations coupled with withdrawal-related anxiety may help explain the increase in alcohol abuse following adolescent experimentation with the drug. METHODS: Adolescent and adult rats received 10 intraperitoneal administrations of 4.0 g/kg EtOH or saline every 48 hours. At either 24 hours or 12 days after the final exposure, anxiety-like behavior was assessed on the elevated plus maze and tissue was collected. Western blotting was used to assess changes in selected NMDA and GABAA receptor subunits in whole cortex and bilateral hippocampus. RESULTS: CIE exposure yields a persistent increase in anxiety-like behavior in both age groups. However, selected NMDA and GABAA receptor subunits were not differentially altered by this CIE exposure paradigm in adolescents or adults. CONCLUSIONS: CIE exposure produced persistent anxiety-like behavior, which has important implications for alcohol cessation. Given the reported behavioral and neuropeptide expression changes in response to this dose of EtOH, it is important for future work to consider the circumstances under which these measures are altered by EtOH exposure.

Age-related effects of alcohol from adolescent, adult, and aged populations using human and animal models.

BACKGROUND: This review incorporates current research examining alcohol's differential effects on adolescents, adults, and aged populations in both animal and clinical models. METHODS: The studies presented range from cognitive, behavioral, molecular, and neuroimaging techniques, leading to a more comprehensive understanding of how acute and chronic alcohol use affects the brain throughout the life span. RESULTS: Age of life is a significant factor in determining the effect of alcohol on brain functioning. Adolescents and aged populations may be more negatively affected by heavy alcohol use when compared to adults. CONCLUSIONS: Investigations limiting alcohol effects to a single age group constrains understanding of differential trajectories and outcomes following acute and chronic use. To meaningfully address the sequencing and interaction effects of alcohol and age, the field must incorporate collaborative and integrated research efforts focused on interdisciplinary questions facilitated by engaging basic and applied scientists with expertise in a range of disciplines including alcohol, neurodevelopment, and aging.

Interaction of age and sex as factors in understanding the anxiolytic effects of alcohol: Unasked questions limiting the understanding of a critical health issue.

Understanding the reasons why people consume alcohol is a critical health issue. Alcohol produces a variety of effects, including a reduction in stress or negative emotional states termed an anxiolytic effect. The anxiolytic effect of alcohol is an often-reported reason for why people begin consuming the drug. However, several factors concerning the stress-reducing effect of alcohol need to be investigated. For example, research has demonstrated that both age and sex are factors that impact alcohol's anxiolytic effect producing differential outcomes in aged female rats compared to aged male rats. In light of these findings, the current commentary highlights critical questions in need of research with the goal of better understanding how age and sex interact to influence the anxiolytic effect of alcohol. For example, the central nucleus of the amygdala has been identified as a critical brain region mediating the anxiolytic effect of drugs, but additional research is needed to understand how aging alters the neurological functioning of the central nucleus of the amygdala in both females and males. Furthermore, specific receptor isoforms, such as GABAA receptor α2, have been shown to be critical for anxiolysis and understanding how aging and sex alter receptor isoform expression by brain region is needed. Finally, age and sex interact to alter allopregnanolone levels in brain and differential neurosteroid levels may mediate alcohol's unique anxiolytic effect in aged female rats compared to aged male rats. Given the increasing age of the population in most countries and the increasing alcohol consumption levels in females compared to males, investigating the interaction of sex and age on alcohol's anxiolytic effect has great promise to discover critical answers to what are currently unasked questions.

Increased anxiolytic effect in aged female rats and increased motoric behavior in aged male rats to acute alcohol administration: Comparison to younger animals.

The population of most countries in the world is increasing and understanding risk factors that can influence the health of the older population is critical. Older adults consume alcohol often in a risky, binge manner. Previous work has demonstrated that aged rats are more sensitive to many of the effects of acute ethanol. In the current project aged, adult, and adolescent female and male rats were tested on the elevated plus maze and open field following either a 1.0 g/kg alcohol injection or a saline injection. We report sex- and age-dependent effects whereas aged female rats, but not aged male rats, showed an increased anxiolytic effect of alcohol in the elevated plus maze while aged male rats, but not aged female rats, showed increased stimulatory movement in the open field. In addition, significant age effects were found for both female and male rats. It is proposed that the sex- and age-dependent effects reported in the current studies may be due to differential levels of alcohol-induced allopregnanolone for the anxiolytic effects and differential levels of alcohol-induced dopamine for the stimulatory effects. The current work provides insights into factors influencing alcohol consumption in older adults.

Singaporean college students overpour drinks similar to Western populations: influence of peer presence in a simulated alcohol-pouring task.

BACKGROUND: College drinking is a global health concern. However, most studies originate from countries with high alcohol consumption. In the United States, college students overpour a standard alcoholic drink, yet it is unclear if this remains true in countries with low alcohol consumption. Additionally, in college, peer influence is the greatest predictor of drinking behavior, yet it is unknown if social norms affect how students pour drinks. This study examined how male college students, in a country with low alcohol consumption, define standard drinks, and if the presence of an unfamiliar peer affects how students pour during a simulated alcohol-pouring task. METHODS: Male undergraduate students (n = 105) underwent baseline assessments of impulsivity, self-monitoring, religiosity, and drinking characteristics. Participants poured fluid into empty cups of different sizes to equal a standard serving of beer or shot of liquor. There were 2 groups based on gender of experimenter. Within each group, participants were randomly assigned to Alone or Dyad condition. In the Alone condition, students were instructed to pour only for themselves. In the Dyad condition, students were instructed to pour for themselves and the experimenter. The volumes poured by the students were compared with standards used in Singapore and the United States. RESULTS: Collapsed across container size, students overpoured shots by 50% and beer by 100% when compared to the standard drink definition in Singapore. When using a more liberal definition, students overpoured beer by 25%, but did not overpour shots. In the presence of an unfamiliar peer, overpouring decreased by 10% for beer. CONCLUSIONS: The current data show that college students, in a country with low alcohol consumption, overestimate standard alcoholic drinks similar to their Western counterparts and use social norms to determine how much to pour for a drink when confronted with an unfamiliar peer. Efforts toward creating internationally recognized standard drink definitions should be considered.

Acute alcohol produces ataxia and cognitive impairments in aged animals: a comparison between young adult and aged rats.

BACKGROUND: Aging in both humans and rodents appears to be accompanied by physiological changes that increase biologic sensitivity to ethanol (EtOH) intoxication. However, animal models designed to investigate this increased alcohol sensitivity have yet to be established. For this reason, we sought to determine whether acute EtOH administration produces differential effects on motor coordination and spatial cognition in young adult and aged rats. METHODS: Male young adult (postnatal day 70 to 72) and aged (~18 months) Sprague-Dawley rats were assessed on 2 motor tasks (the accelerating rotarod [RR] and the aerial righting reflex [ARR]) and a single cognitive performance task (the Morris water maze [MWM]). Following acute EtOH exposure via intraperitoneal injection, animals' performance was reassessed. RESULTS: Aged rats showed a dramatic increase in EtOH-induced ataxia on the RR and the ARR relative to young adult animals. Similarly, results from the MWM revealed that aged animals had slightly greater EtOH-induced impairments compared with young adult animals. Importantly, the increased impairments produced by EtOH were not due to differential blood EtOH levels. CONCLUSIONS: We demonstrate for the first time that aged rats show greater EtOH-induced deficits compared with young adults in tasks of motor and cognitive performance. The possible role of protein kinase C as a mechanism for increased sensitivity to the motor-impairing effects of EtOH is discussed. Given the high prevalence of alcohol use among the elderly, increased vulnerability to alcohol-induced deficits may have a profound effect on injury in this population.

Using animal models to identify clinical risk factors in the older population due to alcohol use and misuse.

The number of people over the age of 65 years old is increasing and understanding health risks associated with the aged population is important. Recent research has revealed that alcohol (ethanol) consumption levels in older demographics remains elevated and often occurs in a dangerous binge pattern. Given ethical constraints on investigating high level or binge pattern alcohol consumption in humans, animal models are often used to study the effects of ethanol. The current review highlights ongoing work revealing that aged rats are often more sensitive to the effects of acute ethanol compared to younger rats. Specifically, aged rats are more sensitive to the motor impairing, hypnotic, hypothermic, and often the cognitive effects of ethanol compared to younger rats. In addition, the development of ethanol tolerance following chronic exposure may have a different temporal pattern in aged rats compared to younger rats. However, the neurobiological mechanisms that cause the increased sensitivity to ethanol in aged animals have yet to be identified. Furthermore, the differential age effects of ethanol highlight clinical risk factors for alcohol misuse in the older human population. Future work is needed to determine underlying CNS mechanisms producing altered effects of ethanol in aged subjects and also the development of educational material concerning ethanol's effects across ages for health care providers working with the aged population.

Chronic intermittent ethanol exposure during adolescence produces sex- and age-dependent changes in anxiety and cognition without changes in microglia reactivity late in life.

Binge-like ethanol exposure during adolescence has been shown to produce long lasting effects in animal models including anxiety-like behavior that can last into young adulthood and impairments in cognition that can last throughout most of the lifespan. However, little research has investigated if binge-like ethanol exposure during adolescence produces persistent anxiety-like behavior and concomitantly impairs cognition late in life. Furthermore, few studies have investigated such behavioral effects in both female and male rats over the lifespan. Finally, it is yet to be determined if binge-like ethanol exposure during adolescence alters microglia activation in relevant brain regions late in life. In the present study female and male adolescent rats were exposed to either 3.0 or 5.0 g/kg ethanol, or water control, in a chronic intermittent pattern before being tested in the elevated plus maze and open field task over the next ∼18 months. Animals were then trained in a spatial reference task via the Morris water maze before having their behavioral flexibility tested. Finally, brains were removed, sectioned and presumptive microglia activation determined using autoradiography for [3H]PK11195 binding. Males, but not females, displayed an anxiety-like phenotype initially following the chronic intermittent ethanol exposure paradigm which resolved in adulthood. Further, males but not females had altered spatial reference learning and impaired behavioral flexibility late in life. Conversely, [3H]PK11195 binding was significantly elevated in females compared to males late in life and the level of microglia activation interacted as a function of sex and brain regions, but there was no long-term outcome related to adolescent alcohol exposure. These data further confirm that binge-like ethanol exposure during adolescence produces alterations in behavior that can last throughout the lifespan. In addition, the data suggest that microglia activation late in life is not exacerbated by prior binge-like ethanol exposure during adolescence but the expression is sex- and brain region-dependent across the lifespan.

Calcium mediates glomerular filtration through calcineurin and mTORC2/Akt signaling.

Alterations to the structure of the glomerular filtration barrier lead to effacement of podocyte foot processes, leakage of albumin, and the development of proteinuria. To better understand the signaling pathways involved in the response of the glomerular filtration barrier to injury, we studied freshly isolated rat glomeruli, which allows for the monitoring and pharmacologic manipulation of early signaling events. Administration of protamine sulfate rapidly damaged the isolated glomeruli, resulting in foot process effacement and albumin leakage. Inhibition of calcium channels and chelation of extracellular calcium reduced protamine sulfate-induced damage, suggesting that calcium signaling plays a critical role in the initial stages of glomerular injury. Calcineurin inhibitors (FK506 and cyclosporine A) and the cathepsin L inhibitor E64 all inhibited protamine sulfate-mediated barrier changes, which suggests that calcium signaling acts, in part, through calcineurin- and cathepsin L-dependent cleavage of synaptopodin, a regulator of actin dynamics. The mTOR inhibitor rapamycin also protected glomeruli, demonstrating that calcium signaling has additional calcineurin-independent components. Furthermore, activation of Akt through mTOR had a direct role on glomerular barrier integrity, and activation of calcium channels mediated this process, likely independent of phosphoinositide 3-kinase. Taken together, these results demonstrate the importance of calcium and related signaling pathways in the structure and function of the glomerular filtration barrier.

Chronic Intermittent Ethanol Administration during Adolescence Produces Sex Dependent Impairments in Behavioral Flexibility and Survivability.

Chronic intermittent ethanol exposure during adolescence produces behavioral impairments and neurobiological changes that can last into young adulthood. One such behavioral impairment is reduced behavioral flexibility, a behavioral impairment that has been correlated with the risk for increased ethanol intake. In the current study, we investigated if chronic intermittent ethanol exposure during adolescence alters cognition, including behavioral flexibility, over a 22-month testing period. Female and male rats were treated with either 3.0 g/kg or 5.0 g/kg ethanol via gavage in a chronic intermittent fashion during adolescence and then tested every 4 to 5 months on a series of cognitive measures in the Morris water maze. Chronic intermittent ethanol selectively impaired behavioral flexibility in both female and male rats, although the pattern of results was different as a function of sex. In addition, female, but not male, rats were impaired in a short-term relearning test. Finally, male rats administered ethanol during adolescence were significantly more likely to not survive the 22-month experiment compared to female rats administered ethanol during adolescence. The current results demonstrate that adolescence is a unique period of development where chronic intermittent ethanol exposure produces long-lasting, selective cognitive impairments across the lifespan.

Chronic Intermittent Ethanol Exposure Alters Behavioral Flexibility in Aged Rats Compared to Adult Rats and Modifies Protein and Protein Pathways Related to Alzheimer's Disease.

Repeated excessive alcohol consumption increases the risk of developing cognitive decline and dementia. Hazardous drinking among older adults further increases such vulnerabilities. To investigate whether alcohol induces cognitive deficits in older adults, we performed a chronic intermittent ethanol exposure paradigm (ethanol or water gavage every other day 10 times) in 8-week-old young adult and 70-week-old aged rats. While spatial memory retrieval ascertained by probe trials in the Morris water maze was not significantly different between ethanol-treated and water-treated rats in both age groups after the fifth and tenth gavages, behavioral flexibility was impaired in ethanol-treated rats compared to water-treated rats in the aged group but not in the young adult group. We then examined ethanol-treatment-associated hippocampal proteomic and phosphoproteomic differences distinct in the aged rats. We identified several ethanol-treatment-related proteins, including the upregulations of the Prkcd protein level, several of its phosphosites, and its kinase activity and downregulation in the Camk2a protein level. Our bioinformatic analysis revealed notable changes in pathways involved in neurotransmission regulation, synaptic plasticity, neuronal apoptosis, and insulin receptor signaling. In conclusion, our behavioral and proteomic results identified several candidate proteins and pathways potentially associated with alcohol-induced cognitive decline in aged adults.

Expanding laparoscopic cholecystectomy to rural Mongolia.

BACKGROUND: Although laparoscopic cholecystectomy was first introduced in Mongolia in 1994, the benefits of the laparoscopic approach have been largely unavailable to the majority of the population. The burden of gallbladder disease in Mongolia is significant. Despite the barriers to expanding laparoscopic surgery in Mongolia (lack of physical resources and adequate training opportunities, a difficult political situation, and an austere environment), the Health Sciences University of Mongolia (HSUM) began looking for ways to further the development of laparoscopy for the entire country, including the rural areas where half the population resides. METHODS: Combined didactic and practical training courses lasting 2 weeks were developed collaboratively by a private nongovernmental organization and HSUM. The courses were taught at tertiary care centers in the capital city (Ulaanbaatar) and in a smaller, rural city (Erdenet), the regional northern referral center. Demographic data, preoperative diagnosis, ultrasound and operative findings, operative times, length of hospital stay, and intraoperative and postoperative complication rates were compared from 2007-2008 from hospitals in Ulaanbaatar and Erdenet. RESULTS: A total of 36 surgeons participated in the training classes, and a total of 410 laparoscopic cholecystectomies were performed. Ultrasound was used as a diagnostic tool in all cases. There was no significant difference in intraoperative or postoperative complications between hospitals in the capital, where the procedures were performed by skilled laparoscopic surgeons, and in Erdenet, where the training courses first introduced laparoscopic cholecystectomy. Neither were there differences in complication rates between cases during the teaching and nonteaching periods. CONCLUSIONS: Laparoscopic cholecystectomy can be expanded safely to the regional diagnostic referral centers in rural Mongolia through short-term training courses as a method to markedly improve access and outcomes for the 50% of the country previously denied the benefits of minimally invasive surgery.

Homeostatic role of transforming growth factor-beta in the oral cavity and esophagus of mice and its expression by mast cells in these tissues.

Transforming growth factor-beta (TGF-beta) is a pleiotropic growth factor; its overexpression has been implicated in many diseases, making it a desirable target for therapeutic neutralization. In initial safety studies, mice were chronically treated (three times per week) with high doses (50 mg/kg) of a murine, pan-neutralizing, anti-TGF-beta antibody. Nine weeks after the initiation of treatment, a subset of mice exhibited weight loss that was concurrent with decreased food intake. Histopathology revealed a unique, nonneoplastic cystic epithelial hyperplasia and tongue inflammation, as well as dental dysplasia and epithelial hyperplasia and inflammation of both the gingiva and esophagus. In an effort to determine the cause of this site-specific pathology, we examined TGF-beta expression in these tissues and saliva under normal conditions. By immunostaining, we found higher expression levels of active TGF-beta1 and TGF-beta3 in normal tongue and esophageal submucosa compared with gut mucosal tissues, as well as detectable TGF-beta1 in normal saliva by Western blot analysis. Interestingly, mast cells within the tongue, esophagus, and skin co-localized predominantly with the TGF-beta1 expressed in these tissues. Our findings demonstrate a novel and restricted pathology in oral and esophageal tissues of mice chronically treated with anti-TGF-beta that is associated with basal TGF-beta expression in saliva and by mast cells within these tissues. These studies illustrate a previously unappreciated biological role of TGF-beta in maintaining homeostasis within both oral and esophageal tissues.

Behavioral effects of ethanol in cerebellum are age dependent: potential system and molecular mechanisms.

BACKGROUND: Adolescent rats are less sensitive to the motor-impairing effects of ethanol than adults. However, the cellular and molecular mechanisms underlying this age-dependent effect of ethanol have yet to be fully elucidated. METHOD: Male rats of various ages were used to investigate ethanol-induced ataxia and its underlying cellular correlates. In addition, Purkinje neurons from adolescent and adult rats were recorded both in vivo and in vitro. Finally, protein kinase C (PKCγ) expression was determined in 3 brain regions in both adolescent and adult rats. RESULTS: The present multi-methodological investigation confirms that adolescents are less sensitive to the motor-impairing effects of ethanol, and this differential effect is not because of differential blood ethanol levels. In addition, we identify a particular cellular correlate that may underlie the reduced motor impairment. Specifically, the in vivo firing rate of cerebellar Purkinje neurons recorded from adolescent rats was insensitive to an acute ethanol challenge, while the firing rate of adult cerebellar Purkinje neurons was significantly depressed. Finally, it is demonstrated that PKCγ expression in the cortex and cerebellum mirrors the age-dependent effect of ethanol: adolescents have significantly less PKCγ expression compared to adults. CONCLUSIONS: Adolescents are less sensitive than adults to the motor-impairing effects of ethanol, and a similar effect is seen with in vivo electrophysiological recordings of cerebellar Purkinje neurons. While still under investigation, PKCγ expression mirrors the age effect of ethanol and may contribute to the age-dependent differences in the ataxic effects of ethanol.

Orphan glutamate receptor delta1 subunit required for high-frequency hearing.

The function of the orphan glutamate receptor delta subunits (GluRdelta1 and GluRdelta2) remains unclear. GluRdelta2 is expressed exclusively in the Purkinje cells of the cerebellum, and GluRdelta1 is prominently expressed in inner ear hair cells and neurons of the hippocampus. We found that mice lacking the GluRdelta1 protein displayed significant cochlear threshold shifts for frequencies of >16 kHz. These deficits correlated with a substantial loss of type IV spiral ligament fibrocytes and a significant reduction of endolymphatic potential in high-frequency cochlear regions. Vulnerability to acoustic injury was significantly enhanced; however, the efferent innervation of hair cells and the classic efferent inhibition of outer hair cells were unaffected. Hippocampal and vestibular morphology and function were normal. Our findings show that the orphan GluRdelta1 plays an essential role in high-frequency hearing and ionic homeostasis in the basal cochlea, and the locus encoding GluRdelta1 represents a candidate gene for congenital or acquired high-frequency hearing loss in humans.

Impact of acute ethanol exposure on body temperatures in aged, adult and adolescent male rats.

The mean population age of the United States continues to increase, and data suggest that by the year 2060 the population of people over the age of 65 will more than double, providing a potentially massive strain on health care systems. Research demonstrates individuals 65 and older continue to consume ethanol, often at high levels. However, preclinical animal models are still being developed to understand how ethanol might interact with the aged population. The current experiments investigated differential body temperature responses in aged rats compared to adult rats and adolescent rats. Aged (19 months of age), adult (70 days of age), or adolescent (30 days of age) male Sprague Dawley rats were administered 1.0 g/kg, 2.0 g/kg, or 3.0 g/kg ethanol, intraperitoneally (i.p.), in a balanced Latin square design. Prior to ethanol administration, a core body temperature via an anal probe was obtained, and then repeatedly determined every 60 min following ethanol exposure for a total of 360 min. In addition, a blood sample was obtained from a tail nick 60, 180, and 300 min following the ethanol injection to investigate the relationship of ethanol levels and body temperature in the same animals. Aged rats had significantly greater reductions in body temperature compared to either adult or adolescent rats following both the 2.0 g/kg and 3.0 g/kg ethanol injection. Additionally, adolescent rats cleared ethanol significantly faster than aged or adult animals. These experiments suggest body temperature regulation in aged rats might be more sensitive to acute ethanol compared to adult rats or adolescent rats. Future studies are needed to identify the neurobiological effects underlying the differential sensitivity in aged rats to ethanol.

Acute ethanol administration produces larger spatial and nonspatial memory impairments in 29-33 month old rats compared to adult and 18-24 month old rats.

The average age of the population in many countries is continuing to increase. Older people continue to consume alcohol, often in a binge like fashion. Previous research has demonstrated that older human subjects and aged animal subjects have an increased sensitivity to the effects of ethanol on a variety of behaviors. However, it has yet to be determined if acute ethanol exposure impairs spatial and/or nonspatial memory to a greater extent in aged rats compared to adult rats. In the current studies we trained male rats ranging in age from young adult (2 months of age) to aged rats (29-33 months of age) in the standard nonspatial task followed by the standard spatial task in the Morris water maze. Only animals deemed "cognitively-spared", that is aged animals that learn as well as young animals, were administered one of two doses of moderate ethanol and had their memory tested 30 min later. Acute ethanol administration produced similar performance impairments in spatial and nonspatial memory in all cognitively-spared animals except for the 29-33 month old animals which showed a significantly greater cognitive impairment in both tasks. In addition, blood ethanol levels were similar across all ages. The present work adds to the growing literature on the selective effects of acute ethanol exposure in aged animals.