Planta Med 2001; 67(1): 38-42
DOI: 10.1055/s-2001-10631
Original Paper
Pharmacology
© Georg Thieme Verlag Stuttgart · New York

Reversal Caused by n-Butylidenephthalide from the Deficits of Inhibitory Avoidance Performance in Rats

Ming-Tsuen Hsieh1,*, Chi-Rei Wu1 , Li-Wei Lin1 , Chia-Chang Hsieh2 , Chang-Hai Tsai2
  • 1 Institute of Chinese Pharmaceutical Sciences, China Medical College, Taichung, Taiwan, R.O.C.
  • 2 Institute of Medical Sciences, China Medical College, Taichung, Taiwan, R.O.C.
Further Information

Publication History

January 6, 2000

July 2, 2000

Publication Date:
31 December 2001 (online)

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Abstract

The present study was designed to investigate the mechanism of action of n-butylidenephthalide on the deficits of inhibitory avoidance performance induced by drugs in rats with piracetam as a positive control. n-Butylidenephthalide attenuated the scopolamine-induced and mecamylamine-induced acquisition impairment, and also attenuated the acquisition impairment induced by scopolamine plus mecamylamine. Furthermore, scopolamine methylbromide, a peripheral cholinergic muscarinic receptor antagonist, did not block the counteracting effect of n-butylidenephthalide on the scopolamine-induced acquisition impairment. n-Butylidenephthalide attenuated the impairment of inhibitory avoidance performance induced by the central acetylcholinergic neurotoxin AF64A administered intracisternally. From the above results, we suggest that n-butylidenephthalide attenuated the deficits of inhibitory avoidance performance induced by drugs, which are the effects related to activating the central but not the peripheral cholinergic neuronal system via muscarinic and nicotinic receptors.