Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9415824 | Brain Research | 2005 | 7 Pages |
Abstract
The main goal of the present study was to analyse the effects of (±)-huprine X ((±)-HX) and galantamine (GAL), with potentiating action on nicotinic receptors, and huperzine A (HPA), devoid of nicotinic activity, on [3H]-acetylcholine ([3H]-ACh) release in striatal slices of rat brain. All compounds are non-covalent and reversible inhibitors of AChE. Addition of (±)-HX (0.01 μM), GAL (10 μM) and HPA (0.1 μM) to the superfusion medium decreased the release of the ACh neurotransmitter to a similar extent: 36%, 30% and 34%, respectively (P < 0.01). This effect was reverted in the presence of atropine (ATR; 0.1 μM), which blocks the pre-synaptic muscarinic M2 receptor. After that, a wide range of concentrations of drugs, concomitantly with ATR (0.1 μM), was studied in the presence of haloperidol (HAL; 0.01μM), a dopamine D2 antagonist. In these conditions, a dose-dependent increase of [3H]-ACh release was observed in the presence of (±)-HX, GAL and HPA. To test the role of nicotinic receptors in the drugs' effects on [3H]-ACh release, mecamylamine (MEC) 100 μM was used to block such receptors. MEC alone significantly decreased neurotransmitter release by 18% (P < 0.05), but no change was obtained in the presence of both ATR and MEC. Under these conditions, (±)-HX, GAL and HPA increased the release of [3H]-ACh by 37%, 25% and 38%, respectively (P < 0.01). Taking into account all of these data, the present results suggest that the effects induced by (±)-HX and GAL nicotinic-receptor potentiators seem to be mainly due to their ability in inhibiting acetylcholinesterase activity, but not by interaction on the nicotinic receptors.
Keywords
Related Topics
Life Sciences
Neuroscience
Neuroscience (General)
Authors
S. Roman, A. Badia, P. Camps, D. Muñoz-Torrero, M.V. Clos,