McRee R C, Terry-Ferguson M, Langlais P J, Chen Y, Nalwalk J W, Blumenstock F A, Hough L B
Behavioral Neurobiology Section, Department of Psychology, San Diego State University, 6363 Alvarado Ct., Suite 237, San Diego, CA 92182, USA.
Brain Res. 2000 Mar 10;858(2):227-36. doi: 10.1016/s0006-8993(99)02309-4.
The current study examined the possible role of increased histamine release and granulocyte activity in the vascular changes that precede the onset of necrotic lesions with the thalamus of the pyrithiamine-induced thiamine deficiency (PTD) rat model of Wernicke's encephalopathy (WE). An increase in histamine release and the number of granulocytes was observed in lateral thalamus on day 9 and in medial thalamus on day 10 of PTD treatment, a duration of thiamine deficiency associated with perivascular edema in this brain region. Within the hippocampus, histamine release was significantly increased on day 9, declined to control levels on days 10-12, and was significantly elevated on days 12-14. No granulocytes were observed in hippocampus of either PTD or control rats. These observations suggest that the release of histamine from nerve terminals and histamine and other vasoactive substances from granulocytes may be responsible for thiamine deficiency-induced vascular breakdown and perivascular edema within thalamus.