Perry D C, Getz R, Lee I Y, Panchison D, Okuda Y, Miller L P
Department of Pharmacology, George Washington University Medical Center, Washington, DC 20037.
Brain Res. 1993 Jul 23;617(2):296-302. doi: 10.1016/0006-8993(93)91097-c.
Transient forebrain ischemia was produced in gerbils by short-term occlusion of the common carotid arteries under halothane anesthesia. Histological analysis of brains 7 days post-ischemia demonstrated characteristic destruction of CA1 pyramidal cells. lambda Opiate binding (measured with [3H]naloxone in the presence of 300 nM diprenorphine) at 7 days post-ischemia was significantly increased in the stratum lucidum of the hippocampus (the mossy fiber layer), but not in any other region measured, including other hippocampal regions, cortex, amygdala, caudate putamen, thalamus, and hypothalamus. The increase in mossy fiber lambda binding was slow to develop (no increase detected up to 48 h post-ischemia), and long-lasting (binding remained elevated at 32 days post-ischemia). While MK-801 significantly inhibited CA1 pyramidal cell destruction when administered 20 min prior to ischemia, the increase in mossy fiber lambda binding was still evident. None of seven different opioid agonists and antagonists examined had an effect on either the pyramidal cell damage or increased mossy fiber lambda binding seen 7 days after ischemia.
在氟烷麻醉下，通过短期阻断沙鼠的颈总动脉来制造短暂性前脑缺血。缺血7天后对大脑进行组织学分析，结果显示CA1锥体细胞出现典型性破坏。缺血7天后，海马体透明层（苔藓纤维层）的λ阿片受体结合（在300 nM二丙诺啡存在的情况下用[³H]纳洛酮测量）显著增加，但在其他测量区域，包括其他海马区域、皮质、杏仁核、尾状壳核、丘脑和下丘脑，均未增加。苔藓纤维λ结合的增加发展缓慢（缺血后48小时内未检测到增加），且持续时间长（缺血32天后结合仍保持升高）。虽然在缺血前20分钟给予MK - 801可显著抑制CA1锥体细胞破坏，但苔藓纤维λ结合的增加仍然明显。所检测的七种不同阿片类激动剂和拮抗剂均未对缺血7天后出现的锥体细胞损伤或苔藓纤维λ结合增加产生影响。
