Clinical observation of physiological and psychological reactions to electric stimulation of the amygdaloid nucleus and the nucleus accumbens in heroin addicts after detoxification / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Stereotactic surgery has been used to treat heroin abstinence in China since 2000 by ablating the amygdaloid nucleus (AMY) and the nucleus accumbens (NAc), which also provides opportunity to identify the relationship between these nuclei and addiction. Our study aimed to explore the physiological and psychological effects of electrically stimulating the AMY and the NAc in heroin addicts after detoxification by observing changes of heart rate, arterial pressure and occurrence of euphoria similar to heroin induced euphoria.</p><p><b>METHODS</b>A total of 70 heroin addicts after detoxification were recruited, and 61 of them were eligible to be given stereotactic surgery for heroin abstinence. The operation was carried out after determining the coordinates of all target nucleuses, and stimulation was performed at the AMY and the NAc solely or jointly. Heart rate, arterial pressure and occurrence of euphoria similar to heroin induced euphoria were recorded and analyzed.</p><p><b>RESULTS</b>The average heat rate was (66 ± 10) beats/min before electric stimulation, and significantly increased to (84 ± 14) beats/min during stimulation, and changed to (73 ± 12) beats/min 10 minutes after stimulation. There was a significant elevation of the average arterial pressure from 83 mmHg before stimulation to 98 mmHg during the stimulation, and it then decreased to 90 mmHg after stimulation. Forty-three of the 61 patients showed intense euphoria similar to heroin induced euphoria. The largest number (118/186) of euphoric responses occurred when the AMY and the NAc were stimulated at the same time. Odds ratio was 5.4 (95%CI: 2.4 - 11.9, P < 0.0001) to quantify the association. Results from a Logistic regression model showed a positive correlation between unilateral stimulation of either the AMY or NAC and induction of euphoria (OR > 1), especially when the left AMY or left NAc was stimulated (P < 0.05).</p><p><b>CONCLUSIONS</b>Our data are consistent with existing results that the AMY and the NAc are related to addiction. Different roles in drug dependence would be suggested according to the location of the AMY and NAc.</p>

Effects and wavelet spectral entropy analysis of rhubarb extracts rhein on synaptic transmission in rat hippocampal ca1 area in vitro / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>5-dihydroxyanthraquinone-2-carboxylic acid (rhein) inhibits oxidoreduction induced by reducing nicotingamide adenine dinucleotide in the mitochondria and reducing reactive oxygen species, it also suppresses lipid peroxidation in rat brain homogenates. This study was to assess the effects of anthraquinone derivatives, rhein on synaptic transmission in the rat hippocampal CA1 pyramidal cell layer by intracellular recording.</p><p><b>METHODS</b>The excitatory postsynaptic potential (EPSP) evoked by stimulation of the Schaffer collaterals in the presence of bicuculline (15 micromol/L) was depressed by application of rhein (0.3 - 30 micromol/L). The amplitude of the EPSP was restored within 20 minutes after removal of rhein from the supernatant. At a concentration of 30 micromol/L, rhein reduced the amplitude of the EPSP to 42% +/- 3.7% (n = 24) of the control. Subsequently, wavelet spectral entropy was used to analyze the EPSP.</p><p><b>RESULTS</b>A strong positive correlation was observed between the wavelet spectral entropy and other parameters such as amplitude, slope of rising phase and slope of descending phase of the EPSP. The paired-pulse facilitation (PPF) of the EPSP was significantly increased by rhein (30 micromol/L). The inhibitory postsynaptic potential (IPSP) recorded in the presence of CNQX (20 micromol/L) and APV (40 micromol/L) is not altered by rhein (30 micromol/L).</p><p><b>CONCLUSIONS</b>Rhein (30 micromol/L) can decrease the frequency but not the amplitude of the miniature EPSP (mEPSP). It is suggested that rhein inhibits excitatory synaptic transmission by decreasing the release of glutamate in rat hippocampal CA1 pyramidal neurons.</p>

Influence of ACh on the level of protein kinase C, intracellular free Ca(2+) and cyclic AMP/cyclic GMP of cultured human pituitary adenoma cells / 生理学报

We found previously that ACh can significantly inhibit the proliferation of cultured human pituitary adenoma cells. In order to make a further investigation of the mechanism of the inhibitory effect of ACh on the proliferation of pituitary adenoma cells, we observed the levels of protein kinase C (PKC), [Ca(2+)](i) and cAMP/cGMP in cultured pituitary adenoma cells after treatment with ACh. The results demonstrate that (1) compared with control, PMA, a PKC activator, increased the activity of cytoplasm, membrane and total PKC in human pituitary adenoma cells. However, after a 15-min treatment with ACh (10 micromol/L), a significant reduction of the activity of cytoplasm, membrane and total PKC in human pituitary adenoma cells was observed, and the reduction effect could be blocked by atropine. (2) The level of [Ca(2+)](i) of single adenoma cells was found to decrease immediately on the addition of ACh (10 micromol/L), which could also be blocked by atropine. (3) ACh increased the amount of cAMP in the cytoplasm of human pituitary adenoma cells, but had no effect on that of cGMP. These data provide an important clue to explore the molecular mechanisms of the inhibitory effect of ACh on the proliferation of pituitary adenoma cells, and suggest that the modulating effect of ACh on the proliferation of pituitary adenoma cells results from the interactions of several cellular signaling pathways.

Protective effect of Rheum tanguticum polysaccharides (RTP) on traumatic brain injury in rats / 中国中药杂志

<p><b>OBJECTIVE</b>To evaluate protective effects of Rheum tanguticum polysaccharides (RTP) on traumatic brain injury (TBI) in rats.</p><p><b>METHOD</b>The polysaccharides (RTP) were extracted from Tanguficum Maxim. 120 rats were divided into 15 groups, with 8 rats in each group. RTP at 100, 200 and 400 mg x kg(-1) were administrated orally once a day for five days, and model of brain injury was made by dropping weight method.</p><p><b>RESULT</b>RTP reduced water content and malondialdehyde (MDA) levels, and increased total SOD activity and Na+-K+ ATPase activity after injuried.</p><p><b>CONCLUSION</b>The polysaccharides may be one of the effective comptents in Rheum tanguticum, showing significant neuroprotective effects.</p>

The effect of acetylcholine on the proliferation and apoptosis of three kinds of cultured human pituitary adenoma cells / 生理学报

In order to elucidate the effect of acetylcholine (ACh) on the occurrence and development of human pituitary adenoma, it was firstly observed whether there exists choline acetyl transferase (ChAT) which is necessary for the synthesis of acetylcholine in the cells of human pituitary adenoma, and then MTT method, (3)H TdR incorporation, cell cycle analysis and TUNEL were employed to estimate the influence of ACh on the proliferation, DNA synthesis and apoptosis of three kinds of human pituitary adenoma (human prolactinoma, somatotropinoma and non-functional tumor) cells cultured in vitro. The results showed that (1) the positive staining of ChAT was obviously observed in the cells of the three kinds of human pituitary adenoma, however, it was lower than that in normal human pituitary gland; (2) ACh had a similar effect on the proliferation of the three kinds of human pituitary adenoma cells. ACh at 0.1-10 micromol/L decreased the (3)H TdR incorporation and the MTT A value in a dose-dependent manner. At the same time, ACh decreased the ratio of S or G(2) phase pituitary adenoma cells significantly, but increased the ratio of G(1) phase pituitary tumour cells markedly; (3) the effect of acetylcholine on the proliferation of human pituitary adenoma cells was inhibited by atropine, but not by tubocurarine; (4) ACh had no effect on the apoptosis of human pituitary adenoma cells cultured in vitro. These data suggest that ACh may have a significant modulating effect on the proliferation of pituitary adenoma cells by means of paracrine or autocrine, and the effect is mediated by muscarinic receptor.