Zhu H, Paul I A, McNamara M, Redmond A, Nowak G, Piletz J E
Department of Psychiatry, University of Mississippi Medical Center, Jackson 39216-4505, USA.
Neurochem Int. 1997 Jan;30(1):101-7. doi: 10.1016/s0197-0186(96)00043-5.
A low density of brain IR2-imidazoline receptive sites has previously been linked to depression. In this study we evaluated brain IR2-binding sites in a rat model of depression, olfactory bulbectomy, and determined the effects of chronic imipramine treatment in vivo on these sites. Compared with sham-operated controls, adaptation to olfactory bulbectomy had no effect on either the density (Bmax) or affinity (KD) of [3H]-idazoxan binding to brain IR2 sites. However, 25 days of imipramine treatment (i.p., 20 mg/kg/day) enhanced significantly the density of IR2 binding sites, with no change in affinity in both the model and the control group. These results indicate that the brain IR2-imidazoline receptive sites might be a target for antidepressants.
先前已发现脑内IR2-咪唑啉受体位点密度较低与抑郁症有关。在本研究中，我们评估了抑郁症大鼠模型——嗅球切除术大鼠脑内的IR2结合位点，并确定了体内慢性丙咪嗪治疗对这些位点的影响。与假手术对照组相比，适应嗅球切除术对[3H]-伊达唑胺与脑IR2位点结合的密度（Bmax）或亲和力（KD）均无影响。然而，丙咪嗪治疗25天（腹腔注射，20mg/kg/天）显著提高了IR2结合位点的密度，模型组和对照组的亲和力均无变化。这些结果表明，脑内IR2-咪唑啉受体位点可能是抗抑郁药的作用靶点。
