Anisomycin treatment paradigm affects duration of long-term potentiation in slices of the amygdala.

Okulski P, Hess G, Kaczmarek L.

Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology, Pasteura 3, 02-093 Warsaw, Poland.

Anisomycin has been widely used as an inhibitor of protein synthesis in studies on learning and memory as well as synaptic plasticity. However, its mode of action is complicated. Besides the inhibition of translation, this drug displays other effects, most prominently on mitogen-activated protein kinases. In this report we analyze the effects of anisomycin on the late phase of long-term potentiation (LTP) in amygdala slices. The late phase of LTP was evoked by high-frequency repeated-train stimulation delivered to the external capsule and recorded in the lateral amygdaloid nucleus. In the no-drug condition, stimulation resulted in LTP lasting over 3 h without any sign of decay. Application of the drug 15 min before high-frequency stimulation (HFS) caused LTP decay to baseline within 1 h after induction. However, delivering the drug just after the first train of HFS resulted in LTP that returned to baseline level within 3 h since the onset of stimulation. These results show that the duration of the LTP in the amygdala depends on the anisomycin treatment paradigm and thus special caution should be exercised when interpreting the data obtained with this drug. Copyright 2002 IBRO

PMID: 12207948