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...
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sg-ntu-dr.10356-961332020-03-07T12:10:40Z Acute alcohol produces ataxia and cognitive impairments in aged animals : A comparison between young adult and aged rats Novier, Adelle. Diaz-Granados, Jaime L. Mittleman, Guy. Matthews, Douglas B. Skike, Candice E. Van. School of Humanities and Social Sciences DRNTU::Social sciences::Psychology 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. 2013-12-05T01:30:54Z 2019-12-06T19:26:11Z 2013-12-05T01:30:54Z 2019-12-06T19:26:11Z 2013 2013 Journal Article Novier, A., Skike, C. E. V., Diaz-Granados, J. L., Mittleman, G., & Matthews, D. B. (2013). Acute alcohol produces ataxia and cognitive impairments in aged animals : A comparison between young adult and aged rats. Alcoholism : clinical and experimental research, 37(8), 1317-1324. 0145-6008 https://hdl.handle.net/10356/96133 http://hdl.handle.net/10220/18047 10.1111/acer.12110 en Alcoholism : clinical and experimental research |
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DRNTU::Social sciences::Psychology Novier, Adelle. Diaz-Granados, Jaime L. Mittleman, Guy. Matthews, Douglas B. Skike, Candice E. Van. Acute alcohol produces ataxia and cognitive impairments in aged animals : A comparison between young adult and aged rats |
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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. |
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School of Humanities and Social Sciences |
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School of Humanities and Social Sciences Novier, Adelle. Diaz-Granados, Jaime L. Mittleman, Guy. Matthews, Douglas B. Skike, Candice E. Van. |
format |
Article |
author |
Novier, Adelle. Diaz-Granados, Jaime L. Mittleman, Guy. Matthews, Douglas B. Skike, Candice E. Van. |
author_sort |
Novier, Adelle. |
title |
Acute alcohol produces ataxia and cognitive impairments in aged animals : A comparison between young adult and aged rats |
title_short |
Acute alcohol produces ataxia and cognitive impairments in aged animals : A comparison between young adult and aged rats |
title_full |
Acute alcohol produces ataxia and cognitive impairments in aged animals : A comparison between young adult and aged rats |
title_fullStr |
Acute alcohol produces ataxia and cognitive impairments in aged animals : A comparison between young adult and aged rats |
title_full_unstemmed |
Acute alcohol produces ataxia and cognitive impairments in aged animals : A comparison between young adult and aged rats |
title_sort |
acute alcohol produces ataxia and cognitive impairments in aged animals : a comparison between young adult and aged rats |
publishDate |
2013 |
url |
https://hdl.handle.net/10356/96133 http://hdl.handle.net/10220/18047 |
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1681039074969780224 |