Dringenberg H C, Vanderwolf C H
Neuroscience Program, Siebens-Drake Research Institute, University of Western Ontario, London, Canada.
Brain Res. 1996 Jul 29;728(2):181-7. doi: 10.1016/0006-8993(96)00396-4.
In freely-moving rats treated with a combination of reserpine (10 mg/kg, i.p.) and scopolamine (5 mg/kg, i.p.), neocortical low voltage fast activity (LVFA) associated with continuous multiunit activity (MUA) was abolished and replaced by 2-6 Hz large irregular slow activity (LISA) above 1.5 mV associated with a burst-suppression pattern of MUA. Administration of the monoamine oxidase inhibitor pargyline (50-100 mg/kg, i.p.) completely suppressed 2-6 Hz LISA and restored normal-appearing LVFA and continuous MUA. The 5-hydroxytryptamine (5-HT) receptor agonists quipazine (0.5-20 mg/kg, i.p.), (+/-)-DOI (0.1-5 mg/kg, s.c.), and buspirone (0.1-10 mg/kg, i.p.), but not 8-hydroxy-2-(di-n-propylamine) tetraline (8-OH-DPAT, 0.05-0.8 mg/kg, s.c.) and RU 24969 (1-30 mg/kg, i.p.), produced a partial suppression of 2-6 Hz LISA and restored some lower voltage activity (< 1 mV) above 6 Hz associated with continuous MUA. However, as opposed to pargyline, no receptor agonist tested restored continuous, normal-appearing LVFA. Even though agonists at 5-HT receptors can produce some activation of neocortical slow wave activity after combined cholinergic and serotonergic blockade, this effect is not equivalent to that observed after restoration of endogenous 5-HT transmission.
在用利血平（10毫克/千克，腹腔注射）和东莨菪碱（5毫克/千克，腹腔注射）联合处理的自由活动大鼠中，与持续性多单位活动（MUA）相关的新皮质低电压快活动（LVFA）被消除，并被与MUA爆发抑制模式相关的1.5毫伏以上的2 - 6赫兹大的不规则慢活动（LISA）所取代。给予单胺氧化酶抑制剂帕吉林（50 - 100毫克/千克，腹腔注射）可完全抑制2 - 6赫兹的LISA，并恢复外观正常的LVFA和持续性MUA。5 - 羟色胺（5 - HT）受体激动剂喹哌嗪（0.5 - 20毫克/千克，腹腔注射）、（±）- DOI（0.1 - 5毫克/千克，皮下注射）和丁螺环酮（0.1 - 10毫克/千克，腹腔注射），但不是8 - 羟基 - 2 - （二正丙胺）四氢萘（8 - OH - DPAT，0.05 - 0.8毫克/千克，皮下注射）和RU 24969（1 - 30毫克/千克，腹腔注射），可部分抑制2 - 6赫兹的LISA，并恢复一些与持续性MUA相关的6赫兹以上的较低电压活动（< 1毫伏）。然而，与帕吉林不同，所测试的受体激动剂均未恢复持续性的、外观正常的LVFA。尽管5 - HT受体激动剂在胆碱能和5 - HT能联合阻断后可产生一些新皮质慢波活动的激活，但这种效应与内源性5 - HT传递恢复后观察到的效应并不等同。
