Bellido Inmaculada, Gomez-Luque Aurelio, Plaza Antonio, Rius Francisca, Ortiz Pablo, Sanchez de la Cuesta Felipe
Department of Pharmacology and Clinical Therapeutics, School of Medicine, University of Malaga, Malaga, Spain.
Neurosci Lett. 2002 Mar 15;321(1-2):110-4. doi: 10.1016/s0304-3940(02)00044-7.
S-adenosyl-L-methionine (SAM) has shown efficacy in speeding the onset of the antidepressant effect of imipramine in depressed patients. This effect may be related to their interactions at the serotonin(1A) (5-HT(1A)) receptors. Acute imipramine up-regulated the frontal cortex 5-HT(1A) receptors (B(max), 51.5 +/- 8.4 fmol/mg protein) vs. saline (B(max), 27.5 +/- 5.9 fmol/mg protein), and did not show antidepressant effect. Acute SAM and imipramine+SAM did not modify frontal cortex 5-HT(1A) receptors, and showed antidepressant effects (decrease of the immobility response of 26%, P<0.01; and 47%, P<0.001) vs. saline. All the chronic treatments showed antidepressant effects and up-regulated the hippocampus 5-HT(1A) receptors. SAM prevents the 5-HT(1A) receptor up-regulation induced by acute imipramine in the frontal cortex. This mechanism may contribute to imipramine's antidepressant effect.
S-腺苷-L-甲硫氨酸（SAM）已显示出能加速丙咪嗪对抑郁症患者抗抑郁作用的起效。这种作用可能与其在5-羟色胺（1A）（5-HT(1A)）受体上的相互作用有关。急性给予丙咪嗪使额叶皮质5-HT(1A)受体上调（Bmax，51.5±8.4 fmol/mg蛋白），而生理盐水组（Bmax，27.5±5.9 fmol/mg蛋白）未上调，且急性给予丙咪嗪未显示出抗抑郁作用。急性给予SAM以及丙咪嗪+SAM未改变额叶皮质5-HT(1A)受体，但与生理盐水相比显示出抗抑郁作用（不动反应分别降低26%，P<0.01；以及47%，P<0.001）。所有慢性治疗均显示出抗抑郁作用且上调了海马体5-HT(1A)受体。SAM可阻止急性丙咪嗪诱导的额叶皮质5-HT(1A)受体上调。这一机制可能有助于丙咪嗪的抗抑郁作用。
