真空微波工艺条件对香脆鳙鱼片品质的影响

研究了预脱水鱼片含水量、微波功率、真空度对真空微波加工香脆鳙鱼片品质的影响,在此基础上,采用混合正交试验进一步优化了真空微波制备香脆鳙鱼片的工艺条件。研究结果表明,适宜的水分含量和微波功率可以提高鱼片的膨化率和脆度,改善鱼片的感官品质。高真空度可以改善鱼片的膨化作用和脆性,提高微波加热的效率,很大程度上避免了鱼片出现焦黑点。最佳的真空微波加热条件是预脱水鱼片水分质量分数控制在(15.3±1)%(50℃鼓风干燥3.5 h),微波功率设定为高火档(686±3.5)W,在真空度0.095 MPa下加热12 s后,间歇摇匀后再加热10 s。     

The electrophysiological properties of substantia nigra pars compacta neurones recorded from 6-hydroxydopamine lesioned guinea-pigs in vitro

Summary Intracellular recordings were made from substantia nigra pars compacta neurones in vitro from animals with partial unilateral 6-hydroxydopamine lesions of the nigrostriatal tract. Lesions were assessed and grouped according to the severity of the strital dopamine depletion. No differences were seen between neurones from control and lesioned side nigrae as regards their membrane properties, firing rates, burst activity or percentage of quiescent neurones in any of the lesioned categories. It is concluded that following partial lesioning, the remaining substantia nigra zona compacta neurones in vitro, are functioning normally.     

离体肺组织切片的制备和孵育

目的建立一种简便有效的离体肺组织切片孵育方法。方法利用肺组织精细切片技术制备肺组织切片 ,以 0 .5mLKrebs Henseleit(K H)缓冲液作为孵育液 ,在 37℃培养箱内分别孵育 1、2、3、4h ,测定肺片的四甲基偶氮唑盐 (MTT)比色、乳酸脱氢酶 (LDH)释放率和三磷酸腺苷 (ATP)含量 ,以反映肺组织活性。结果肺片在 37℃培养箱内孵育 1、2、3、4h后MTT比色、LDH释放率和ATP含量均无统计学差异 (P >0 .0 5 )。结论应用 0 .5mLKrebs Henseleit(K H)缓冲液作为孵育液、在 37℃培养箱对肺片进行孵育时组织活性没有明显变化 ,可作为一种简便有效的孵育方法用于离体肺片研究     

Alterations of G-protein Coupling Function in Phosphoinositide Signalling Pathways of Rat Hippocampus by Ischaemic Brain Injury

The activation of membrane-associated phospholipase C is rapidly and transiently induced in the central nervous system by a variety of stimuli. Ischaemic brain injury is one of the situations that leads to a dramatic increase in polyphosphoinositide (PPI) turnover. In this study, stimulation of PPI hydrolysis by glutamate (500 μM) was measured in hippocampal slices from rats up to 21 days after an ischaemic insult of 30 min. Ischaemia was induced using the four-vessel occlusion method. PPI hydrolysis elicited by glutamate was significantly increased in the slices prepared from ischaemic rats 24 h after reperfusion, the accumulation of inositol phosphates (InsP_s) and inositol 1,4,5-trisphosphate (InsP₃) was 614±74% ( n = 8) and 182±11% ( n = 9) of the basal level respectively. This potentiation was also observed 21 days after ischaemia. Hyper-responsiveness to glutamate was also accompanied by an increase in AIF⁻₄-stimulated formation of [³H]inositol phosphates. In addition, global ischaemia did not change either high-affinity [³H]glutamate binding in hippocampal membranes or the stimulation of PPI hydrolysis by carbachol or noradrenaline in hippocampal slices. The present results suggest that the increased responsiveness to glutamate is the result, at least in part, of functional changes at the G-protein level, and may contribute to the pathophysiology of ischaemic brain injury or to the regenerative phenomena that accompany ischaemic damage.     

The effect of the synthetic neuroprotective dipeptide noopept on glutamate release from rat brain cortex slices

The level of spontaneous and K⁺-stimulated release of endogenous glutamate was studied in experiments on slices of brain cortex of Wistar rats. Pronounced spontaneous release of the neuromediator and its increase under conditions of stimulation were registered by high-performance liquid chromatography with electrochemical detection. The effect of the nootropic and neuroprotective dipeptide Noopept (GVS-111) on release of glutamate was investigated. The peptide in concentrations of 10^?5 and 10^?6 M caused a statistically significant decrease in spontaneous and K⁺-stimulated glutamate release. This effect could be the basis of the neuroprotective action of the peptide, suggesting that further studies of Noopept as neuroprotector are very promising.     

Effect of Carbamazepine on Dopamine Release and Reuptake in Rat Striatal Slices

Carbamazepine has been shown to enhance dopaminergic agonist behavioral effects, but not to displace [3H]spiroperidol binding. To verify if carbamazepine acts presynaptically on dopaminergic neurons, reuptake and release of [3H]dopamine were measured in rat striatal slices in vitro. It was observed that carbamazepine blocked 20% of the reuptake of [3H]dopamine, while cocaine blocked 82% of the reuptake, compared with control. Carbamazepine released 62% and tyramine released 92% of the accumulated [3H]dopamine, compared with control. It was concluded that carbamazepine acts presynaptically on striatal neurons, mainly through enhancement of dopamine release. This finding can be related to some behavioral effects described for carbamazepine; however, the importance of its effects in epileptic and manic-depressive patients remains to be clarified.     

Gliotoxin non-selectively induces apoptosis in fibrotic and normal livers.

BACKGROUND: Liver fibrosis is the common response to chronic liver injury, ultimately leading to cirrhosis. Several lines of evidence indicate that inducing apoptosis of hepatic stellate cells (HSC) may lead to regression of liver fibrosis. Recently, it was shown that gliotoxin (GTX) induces apoptosis of HSC. However, the clinical use of GTX may be limited because of the lack of cell and tissue specificity, causing a high risk of potentially severe adverse effects. The aim of this study, therefore, was to study the effect of GTX on different cells of the liver. METHODS: We used normal and fibrotic precision-cut rat liver slices to study the effect of GTX on the various resident liver cell types. In these slices, the complex cell-cell interactions are preserved, which closely mimics the in vivo situation. RESULTS: GTX exhibited a potent apoptosis-inducing activity in these slices. Both immunohistochemical stainings and real-time mRNA techniques showed that this apoptosis-inducing effect was seen in HSC. However, Kupffer cells and liver endothelial cells were also affected by GTX, whereas hepatocytes were only mildly affected. CONCLUSIONS: This study indicates that the apoptosis-inducing strategy to treat liver fibrosis has high potential, but it will be necessary to develop an HSC-specific therapy to prevent adverse effects.     

Orthograde transport and release of insulin-like growth factor I from the inferior olive to the cerebellum

Insulin-like growth factor I (IGF-I) and its receptor are expressed in functionally related areas of the rat brain such as the inferior olive and the cerebellar cortex. A marked decrease of IGF-I levels in cerebellum is found when inferior olive neurons are lesioned. In addition, Purkinje cells in the cerebellar cortex depend on this growth factor to survive and differentiate in vitro. Thus, we consider it possible that IGF-I forms part of a putative trophic circuitry encompassing the inferior olive and the cerebellar cortex and possibly other functionally connected areas. To test this hypothesis we have studied whether IGF-I may be taken up, transported, and released from the inferior olive to the cerebellum. We have found that ¹²⁵I-IGF-I is taken up by inferior olive neurons in a receptor-mediated process and orthogradely transported to the cerebellum. Thus, radioactivity found in the cerebellar lobe contralateral to the injection site in the inferior olive was immunoprecipitated by an anti-IGF-I antibody, co-eluted with ¹²⁵I-IGF-I in an HPLC column, and co-migrated with ¹²⁵I-IGF-I in an SDS-urea polyacrylamide gel electrophoresis. Time-course studies indicated that orthograde axonal transport is relatively rapid since 30 min after the injection, radiolabeled IGF-I was already detected in the contralateral cerebellum. Furthermore, transport of IGF-i from the inferior olive is specific since when ¹²⁵I-neurotensin was injected in the inferior olive or when ¹²⁵I-IGF-I was injected in the pontine nucleus, no radiactivity was found in the contralateral cerebellum. In addition, no specific transport of ¹²⁵I-IGF-I was found in climbing fiber-deafferented rats or when excess unlabeled IGF-I was co-injected with ¹²⁵I-IGF-I. We next studied whether IGF-I is released by inferior olive neurons. We found that the release of IGF-I from cerebellar slices of normal rats was significantly greater in response to depolarizing stimuli than that from slices obtained of climbing fiber-deafferented animals. Indeed, in vitro release of IGF-I in response to KCI or veratridine was almost completely abolished in the latter. These data suggest that IGF-I is taken up by inferior olive neurons through IGF-I receptors and transported to the cerebellum through their axons without any major modification. Moreover, the release of IGF-I from the cerebellum after depolarization depends on the presence of climbing fiber afferents. Altogether these results indicate that the olivo-cerebellar pathway is able to take up, orthogradely transport, and release IGF-I. Since a similar process has been described in the visual system for basic fibroblast growth factor (bFGF), we propose that IGF-I, bFGF, and possibly other growth factors may constitute afferent trophic signals involved in plastic mechanisms within specific neural circuitries. © 1993 Wiley-Liss, Inc.     

Feedback Stimulation of Somatodendritic Serotonin Release: A 5-HT3 Receptor-Mediated Effect in the Raphe Nuclei of the Rat

Slices from rat midbrain containing the raphe nuclei and from hippocampus were prepared, loaded with [³H]5-HT and superfused and the resting and the electrically stimulated [³H]5-HT release was measured. The 5-HT₃ receptor agonist 2-methyl-5-HT (1 to 10 μmol/l) increased the resting tritium outflow in superfused raphe nuclei slices, EC₅₀ 5.3 μmol/l. The 2-methyl-5-HT-induced increase of tritium outflow was an external Ca²⁺-independent process and was not altered by reserpine pretreatment but it was reversed by addition of the 5-HT uptake inhibitor fluoxetine (1 μmol/l). The 5-HT₃ receptor antagonists ondansetron and GYKI-46 903 (1 μmol/l) did not antagonize the stimulatory effect of 2-methyl-5-HT on resting tritium outflow. 2-Methyl-5-HT in lower concentration increased the electrically induced tritium overflow from raphe nuclei slices (EC₅₀ 0.56 μmol/l) and also from hippocampal slices preloaded with [³H]5-HT. These effects were reversed by 1 μmol/l of ondansetron and GYKI-46903. The 5-HT₃ receptor antagonists (1 μmol/l) were without effects on depolarization-evoked [³H]5-HT release at 2 Hz stimulation, when 10 Hz stimulation was used, ondansetron and GYKI-46 903 reduced the tritium overflow from raphe nuclei slices. These data indicate that 5-HT₃ receptors positively alter depolarization-induced somatodendritic 5-HT release in the raphe nuclei. They also show that 2-methyl-5-HT is able to evoke 5-HT release not only from vesicles but also from cytoplasmic stores via a transporter-dependent exchange process.