κ-Opioid receptors in the substantia nigra pars reticulata mediate the U-50,488-induced locomotor activity of preweanling rats

κ-Opioid receptors in the substantia nigra pars reticulata mediate the U-50,488-induced locomotor activity of preweanling rats
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DOI:
10.1016/s0165-3806(99)00153-4
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发表时间:
2000-01-03
期刊:
DEVELOPMENTAL BRAIN RESEARCH
影响因子:
--
通讯作者:
McDougall, SA
McDougall, SA
中科院分区:
其他
文献类型:
--
作者:
Collins, RL;Zavala, AR;McDougall, SA

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本研究的目的是确定K-阿片受体刺激诱导的运动活动在断奶前大鼠的神经解剖位置。为了证实U-50,488诱导的断奶前大鼠的运动活动是由K-阿片受体介导的,最初向1日龄大鼠注射媒介物或K-阿片受体激动剂U-50,488(5 mg/kg,s.c.)随后,15分钟后,注射K-阿片受体拮抗剂nor-binaltorphimine(nor-BNI; 0、2、4、8或12 mg/kg,s.c.)。在随后的实验中,向18日龄大鼠注射载体或U-50,488(5 mg/kg,s.c.)在双侧给予(每侧0.25或0.5 μ l)nor-BNI(0、5、10或20 μ g)至黑质网状部(SNR)或内侧背侧纹状体(MDS)之前15分钟。在最终实验中,18日龄大鼠接受溶剂或U-50,488(0.0、0.8、1.6或3.2 μ g)双侧给药(每侧0.25 μ l)至SNR。结果显示,全身施用nor-BNI(0-12 mg/kg,s.c.)在U-50,488诱导的断奶前大鼠自发活动中产生剂量依赖性降低。U-50,488的运动激活作用的作用部位似乎是SNR,因为(a)向SNR中双侧给予nor-BNI(5、10或20 μ g)导致U-50,488诱导的运动完全减弱,和(B)向SNR中双侧给予U-50,488导致断奶前大鼠运动活性的剂量依赖性增加。纹状体注射nor-BNI并不影响U-50,488诱导的自发活动。当将这些发现综合考虑时,很明显,刺激SNR中的K-阿片受体对于U-50,488诱导的断奶前大鼠自发活动的发生是必要且充分的。(C)2000 Elsevier Science B. V.保留所有权利。
The purpose of the present study was to determine the neuroanatomical location where K-opioid receptor stimulation induces locomotor activity in the preweanling rat. To confirm that the U-50,488-induced locomotor activity of preweanling rats is mediated by K-opioid receptors, Is-day-old rats were initially injected with vehicle or the K-opioid receptor agonist U-50,488 (5 mg/kg, s.c.) followed, 15 min later, by an injection of the K-opioid receptor antagonist nor-binaltorphimine (nor-BNI; 0, 2, 4, 8, or 12 mg/kg, s.c.). In subsequent experiments, 18-day-old rats were injected with vehicle or U-50,488 (5 mg/kg, s.c.) 15 min prior to bilateral administration (0.25 or 0.5 mu l per side) of nor-BNI (0, 5, 10, or 20 mu g) into the substantia nigra pars reticulata (SNR) or medial dorsal striatum (MDS). In the final experiment, 18-day-old rats received bilateral administration (0.25 mu l per side) of vehicle or U-50,488 (0.0, 0.8, 1.6, or 3.2 mu g) into the SNR. Results showed that systemically administered nor-BNI (0-12 mg/kg, s.c.) produced a dose-dependent reduction in the U-50,488-induced locomotor activity of preweanling rats. The site of action for U-50,488's locomotor-activating effects appeared to be the SNR, because (a) bilateral administration of nor-BNI (5, 10, or 20 mu g) into the SNR caused a complete attenuation of U-50,488-induced locomotion, and (b) bilateral administration of U-50,488 into the SNR caused a dose-dependent increase in the locomotor activity of preweanling rats. Striatal injections of nor-BNI did not affect U-50,488-induced locomotor activity. When these findings are considered together it is apparent that stimulation of K-opioid receptors in the SNR is both necessary and sufficient for the occurrence of U-50,488-induced locomotor activity in the preweanling rat. (C) 2000 Elsevier Science B.V. All rights reserved.