title: Impairment of long-term potentiation in the hippocampus of alcohol-treated OLETF rats.
abstract: Type 2 diabetes and chronic heavy alcohol consumption each have been known to be associated with the impairment of hippocampus-dependent cognitive functions. Although both conditions often coexist clinically and there is accumulated evidence of a relationship between the two, the combined effect on hippocampal long-term potentiation (LTP) has not yet been investigated. We compared the effect of type 2 diabetes itself with that of type 2 diabetes with chronic heavy alcohol consumption on the hippocampal LTP using Otsuka Long-Evans Tokushima Fatty (OLETF) rat model, which resembles the characteristics of human type 2 diabetes. Ten of 16-week-old male OLETF rats were randomized into two treatment groups according to weight: the OLETF-Alcohol (O-A, n=5) and the OLETF-Control (O-C, n=5). The rats in the O-A group were fed Lieber-DeCarli Regular EtOH over a 10-week period and the amount of alcohol consumption was 8.42±2.52g/kg/day. To ensure the effect of poor glycemic control on LTP, intraperitoneal glucose tolerance test was performed after a 10-week treatment. The hippocampal LTP was measured by extracellular field excitatory post-synaptic potentials at Shaffer collateral (SC) synapses in the CA1 region. Although the O-A group showed significantly lower fasting and postprandial glucose (P<0.01 and P=0.02, respectively), the hippocampal LTP was more significantly attenuated in the O-A group than the O-C group (P=0.032). The results of this study suggested that chronic heavy alcohol consumption could potentiate the impairment of hippocampal LTP in individuals with impaired glucose tolerance or early type 2 diabetes, even though it did not aggravate, but did improve glycemic control. Clinical attention to chronic heavy drinking will be required in preventing cognitive impairment in individuals with type 2 diabetes.
authors.affiliation: Department of Psychiatry, Seoul St. Mary's Hospital, The Catholic University of Korea, Seoul, Republic of Korea.
authors.forename: Jung-Ah
authors.initials: JA
authors.lastname: Min
authors.forename: Hye-Ryeon
authors.initials: HR
authors.lastname: Lee
authors.forename: Jae-Ick
authors.initials: JI
authors.lastname: Kim
authors.forename: Anes
authors.initials: A
authors.lastname: Ju
authors.forename: Dai-Jin
authors.initials: DJ
authors.lastname: Kim
authors.forename: Bong-Kiun
authors.initials: BK
authors.lastname: Kaang
mesh_terms: D000437:Alcoholism / Q000150:complications / Q000503:physiopathology*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D056547:CA1 Region, Hippocampal / Q000503:physiopathology*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications / Q000503:physiopathology; D019706:Excitatory Postsynaptic Potentials; D005951:Glucose Tolerance Test; D066298:In Vitro Techniques; D017774:Long-Term Potentiation; D008297:Male; D051381:Rats; D020334:Rats, Inbred OLETF; D013569:Synapses / Q000502:physiology
chemical_list: D001786:Blood Glucose