BLOCKADE OF PREFRONTO-CORTICAL ALPHA-1-ADRENERGIC RECEPTORS PREVENTS LOCOMOTOR HYPERACTIVITY INDUCED BY SUBCORTICAL D-AMPHETAMINE INJECTION
BLOCKADE OF PREFRONTO-CORTICAL ALPHA-1-ADRENERGIC RECEPTORS PREVENTS LOCOMOTOR HYPERACTIVITY INDUCED BY SUBCORTICAL D-AMPHETAMINE INJECTION
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DOI：
10.1111/j.1460-9568.1994.tb00272.x
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发表时间：
1994-03-01
影响因子：
3.4
通讯作者：
TASSIN, JP
中科院分区：
文献类型：
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作者：
BLANC, G;TROVERO, F;TASSIN, JP
皮层多巴胺能Dl受体的刺激可以抵消d -安非他明在伏隔核应用引起的运动活动增加（Vezina et al., Eur.）。j . >。， 3, 1001 - 1007, 1991)。此外，一种阿尔法1拮抗剂，吡唑嗪，可以防止由腹侧被盖区电解损伤引起的运动亢进（Trovero等人，神经科学，47,69 - 76,1992）。因此，我们试图观察阻断大鼠前额皮质α 1-肾上腺素能受体是否能减少d -安非他明诱发的伏隔核运动活动。在大鼠的内侧前额叶皮层和伏隔核中长期和双侧植入导管，并在圆形走廊中监测运动活动。初步实验表明，腹腔注射0.06 mg/kg吡唑嗪可减轻外周给药d -安非他明（0.75 mg/kg）所致的运动多动。当通过腹腔注射东莨菪碱（0.8 mg/kg）获得运动亢进时，未观察到普拉唑嗪的这种作用。双侧伏隔核注射d -安非他明（4.0 nmol/侧）在30分钟内显著增加运动活动。事先（20分钟）双侧向内侧前额皮质注射哌唑嗪或WB-4101 （0.16 pmol）可消除伏隔核d -安非他明诱发的反应。伏隔核d -安非他明诱发反应的恢复与吡唑嗪的用量密切相关，高剂量时（160 pmol）可观察到极长时间的抑制作用（160 pmol）。相比之下，无论wb - 4101的用量是多少(0。16 ~ 160 pmol)， 3天内恢复。这提示皮质α 1-肾上腺素能受体的阻断促进了局部多巴胺能Dl的传递。后一种作用可能抵消d -安非他明应用于伏隔核引起的运动活动增加。
The stimulation of cortical dopaminergic Dl receptors can counteract the increased locomotor activity evoked by D-amphetamine application in the nucleus accumbens (Vezina et al., Eur. J. Neurosci., 3, 1001 - 1007, 1991). Moreover, an alpha1 antagonist, prazosin, prevents the locomotor hyperactivity induced by electrolytic lesions of the ventral tegmental area (Trovero et al., Neuroscience, 47, 69 - 76, 1992). Attempts were thus made to see whether blockade of alpha1-adrenergic receptors in the rat prefrontal cortex could reduce nucleus accumbens D-amphetamine-evoked locomotor activity. Rats implanted chronically and bilaterally with cannulae into the medial prefrontal cortex and the nucleus accumbens were used for this purpose and locomotor activity was monitored in circular corridors. Preliminary experiments indicated that intraperitoneal injection of prazosin (0.06 mg/kg) reduces the locomotor hyperactivity induced by the peripheral administration Of D-amphetamine (0.75 mg/kg). This effect of prazosin was not observed when locomotor hyperactivity was obtained by an intraperitoneal injection of scopolamine (0.8 mg/kg). Bilateral nucleus accumbens injections Of D-amphetamine (4.0 nmol/side) markedly increased locomotor activity, as estimated in a 30 min period. Prior (20 min) bilateral injections of either prazosin or WB-4101 (0.16 pmol) into the medial prefrontal cortex abolished the nucleus accumbens D-amphetamine-evoked response. The recovery of the nucleus accumbens D-amphetamine-evoked response was closely dependent on the amount of prazosin used, very prolonged inhibitory effects of the drug being seen with a high amount (> 4 days with 160 pmol). In contrast, whatever the amount of WB-41 01 used (0. 1 6 - 160 pmol), recovery occurred within 3 days. It is suggested that the blockade of cortical alpha1-adrenergic receptors facilitates locally dopaminergic Dl transmission. This latter effect may counteract the increased locomotor activity induced by the application Of D-amphetamine into the nucleus accumbens.