Acute ethanol administration decreases GAP-43 and phosphorylated-GAP-43 in the rat hippocampus

• Published in: Brain research Vol. 1112; no. 1; pp. 16 - 25
• Main Authors: Kim, Hyun Joon, Choi, Kyung Mi, Ku, Bo Mi, Mun, Jihye, Joo, Yeon, Han, Jae Yoon, Kim, Young Hee, Roh, Gu Seob, Kang, Sang Soo, Cho, Gyeong Jae, Choi, Wan Sung
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 27.09.2006; Amsterdam Elsevier; New York, NY
• Subjects: Alcoholism and acute alcohol poisoning; Analysis of Variance; Animals; Biological and medical sciences; Blotting, Western - methods; Central Nervous System Depressants - administration & dosage; Central Nervous System Depressants - blood; Ethanol; Ethanol - administration & dosage; Ethanol - blood; GAP-43; GAP-43 Protein - genetics; GAP-43 Protein - metabolism; Gene Expression Regulation - drug effects; Hippocampus; Hippocampus - drug effects; Immunohistochemistry - methods; LTP; Male; Medical sciences; p-GAP-43; Phosphorylation - drug effects; Protein Kinase C - metabolism; Rats; Rats, Sprague-Dawley; RNA, Messenger - metabolism; Time Factors; Toxicology; dg; CA3p; Ethanol; GAP-43; BALs; Iml; LTP; CA3sr; i.p; p-GAP-43; Hippocampus; Potentiation; p-GAP-43 LTP; Phosphorylation; Growth associated protein 43; Rat; Acute; Rodentia; Central nervous system; Electrophysiology; Long term; Encephalon; Vertebrata; Mammalia; Animal
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2006.07.018

Acute alcohol ingestion is well known to have deleterious effects on memory and also known to inhibit long-term potentiation, a putative cellular substrate of memory. In this study, we for the first time revealed that growth-associated protein 43 (GAP-43), which is well known as a presynaptic substrate of protein kinase C and one of the major synaptic plasticity-related genes, was down regulated by single ethanol administration (2.5 g/kg, 15% in saline, i.p.) in the rat hippocampus. Using real-time PCR, we confirmed that GAP-43 mRNA level is significantly decreased 2 h after ethanol administration. GAP-43 and p-GAP-43 (Ser 41) immunoreactivities in the hippocampus were also reduced 4 h after ethanol administration. Immunohistochemical study showed that the reduction of GAP-43 and p-GAP-43 expression was associated with the perforant and mossy fibers pathways. These results suggest that the reduction of GAP-43 in the hippocampus might be, at least in part, a cause of memory impairment after acute ethanol ingestion.