Blustein J E, Whitehouse W G, Calcagnetti D J, Troisi J R, Margules D L, Bersh P J
Department of Psychology, Beaver College, Glenside, PA 19038.
Physiol Behav. 1992 May;51(5):1075-8. doi: 10.1016/0031-9384(92)90095-j.
Prior research has established that escape impairment resulting from prior inescapable shock (IS) could be reversed by the peripheral administration of the opiate antagonist naltrexone (NTX), but not the quaternary form of naltrexone (QNTX), which when systemically administered, does not readily pass the blood-brain barrier. As it was unclear whether the failure of systemically administered QNTX to reduce shuttle escape deficits following exposure to IS could be attributed to reasons other than the restricted access of QNTX to receptor sites in the brain, rats were affixed with chronic indwelling ventricular cannulae to allow direct brain administration of QNTX. The present experiment found a significant attenuation of the escape deficit produced by prior inescapable shock following the intracerebroventricular (ICV) administration of QNTX (10 micrograms/rat). These data provide further evidence of a mediational role for central opiate receptors in the expression of escape interference following inescapable shock.
先前的研究已证实，先前不可逃避电击（IS）导致的逃避障碍可通过外周给予阿片拮抗剂纳曲酮（NTX）得到逆转，但不能通过纳曲酮的季铵盐形式（QNTX）逆转，因为全身给药时，QNTX不易通过血脑屏障。由于尚不清楚全身给药的QNTX未能减轻暴露于IS后的穿梭逃避缺陷是否可归因于QNTX难以进入脑内受体部位以外的其他原因，因此给大鼠植入慢性留置脑室套管，以便直接向脑内给药QNTX。本实验发现，脑室内（ICV）给予QNTX（10微克/只大鼠）后，先前不可逃避电击产生的逃避缺陷有显著减轻。这些数据进一步证明了中枢阿片受体在不可逃避电击后逃避干扰表达中的中介作用。
