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Fei Luo

Publications and source records attributed to Fei Luo.

40 records · Page 3Linked to original sources

Peripheral electric stimulation attenuates the expression of cocaine-induced place preference in rats.

The present study was designed to investigate the effect of peripheral electrical stimulation (PES), with high (100 Hz) or low (2 Hz) frequencies, on the expression of cocaine-induced conditioned place preference (CPP). Rats were trained with cocaine (0.1-10 mg/kg, i.p.) under a biased paradigm in a three-compartment chamber for the development of a CPP. One day following the last conditioning, the total time spent in each compartment was recorded after the deliverance of PES. Naloxone (1, 5, and 10 mg/kg, i.p.) was applied to investigate whether endogenous opioid receptor pathways play any role in the effect of PES. It was found that (1). 1 mg/kg and higher doses of cocaine, but not 0.5 mg/kg, produced significant place preference, (2). cocaine-induced CPP, once developed, maintained for more than 13 days in a cocaine-free state, (3). PES of 100 Hz, but not 2 Hz, significantly attenuated the expression of cocaine-induced CPP (P<0.01), (4). PES per se did not influence the natural place preference in rats, and (5). the inhibition of cocaine CPP induced by 100 Hz PES could be reversed by naloxone pre-treatment at 10 mg/kg, but not at lower doses. These results suggest that PES could inhibits cocaine-induced CPP in a frequency-dependent manner. This effect is probably mediated by an endogenous kappa-opioid mechanism.

Animals↗

Effects of lesions of various brain areas on drug priming or footshock-induced reactivation of extinguished conditioned place preference.

We have previously shown with a model of morphine-induced conditioned place preference (CPP) that a brief exposure to footshock stress or a priming dose of morphine could reactivate drug-seeking behavior after a long drug-free period. The present study was designed to examine the possible role of certain brain areas in such a reactivation. After the rats were successfully trained with morphine (4 mg/kg, i.p.) through a CPP paradigm (10 sessions of daily pairing of morphine with one of the two compartments), different parts of nucleus accumbens (NAc), ventral tegmental area (VTA), and central (Ce) or lateral (La) nucleus of amygdala were lesioned with a DC current passing through the respective location. After a 9-day abstinence period, random intermittent footshock (DC square wave, 0.5 mA, 0.5 s width, off time 10-70 s) or drug priming (morphine 0.25 mg/kg, s.c.) reactivated the place preference in sham lesion rats. However, the effect of drug priming could be completely abolished by lesions placed either at VTA, or the majority or shell part, but not the core of NAc. On the other hand, the effect of footshock stressor could be eliminated by a lesion placed at Ce but not La. These results suggest that, while both drug priming and footshock stress are effective in reactivating drug-seeking behavior, they might work through different neurochemical mechanisms and anatomical pathways.

Amygdala↗

Synergistic effect of cholecystokinin octapeptide and angiotensin II in reversal of morphine induced analgesia in rats.

The aim of this paper is to study the synergistic anti-analgesic effect of angiotensin II (Ang II) plus cholecystokinin octapeptide (CCK-8). Our previous studies have shown that both CCK-8 and Ang II are potent anti-opioid substances. Intracerebroventricular (i.c.v.) injection of CCK-8 or Ang II dose-dependently antagonizes morphine-induced analgesia (MIA). In the present study, we observed the combined effect of CCK-8 and Ang II in antagonizing MIA. CCK-8 and Ang II were injected intracerebroventricularly to rats in various proportions and doses. The results were analyzed with isobolographic analysis. Combined injection of CCK-8 and Ang II in a ratio of 1 ng: 2.5 microg or 1 ng: 5 microg produced significantly greater effect in antagonizing MIA. The ED(50) of the two ratios are only 18.5% and 27.5%, respectively, of the theoretical dose of simple addition. We conclude that CCK-8 and Ang II used in such dose ratios may antagonize MIA synergistically.

Analgesics, Opioid↗