Author(s): Takashi Ueno, Takanori Miki, Zhi-Yu Wang, Toshifumi Yokoyama, Kyoung-Youl Lee, Takashi Kusaka, Katsuhiko Warita, Kazunori Sumitani, Yoshiki Matsumoto, Tomiko Yakura, Jun-Qian Liu, Kuldip S. Bedif, Yoshiki Takeuchi
Alcohol ingestion has adverse effects on the central nervous system (CNS). The hippocampus is one of the target sites of ethanol neurotoxicity. We hypothesized that short-term ethanol exposure alters the expression of neurotrophins and their receptors, leading to functional disruption in the CNS. Male BALB/C mice were fed a liquid diet containing 5% (v/v) ethanol. Pair-fed control mice were maintained on an identical liquid diet, except that ethanol was isocalorically substituted with sucrose. The hippocampus of mice exhibiting stages 1-2 of ethanol intoxication signs were used in the present study. Short-term ethanol exposure did not alter the mRNA expression of neurotrophin ligand/receptor (nerve growth factor [NGF]/TrkA and brain-derived neurotrophic factor [BDNF]/TrkB) systems in the hippocampus. Similarly, the expression of the glial-derived neurotrophic factor (GDNF), which is known to be a first-acting agent against ethanol neurotoxicity, and its receptor GFRα1 was not affected by short-term ethanol exposure. The mechanisms involved in the hippocampal neurotrophin responses against ethanol neurotoxicity remain unknown. However, our findings could provide a basis for further studies on the possible alterations in the expression of various neurotrophins related to hippocampal functions.