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Tyrosine hydroxylase is a key enzyme in dopamine biosynthesis. Change in tyrosine hydroxylase expression in the nigrostriatal system is closely related to the occurrence and development of Parkinson＇s disease. Verbascoside, an extract from Radix Rehmanniae Praeparata has been shown to be clinically effective in treating Parkinson＇s disease. However, the underlying mechanisms remain unclear. It is hypothesized that the effects of verbascoside on Parkinson＇s disease are related to tyrosine hydroxylase expression change in the nigrostriatal system. Rat models of Parkinson＇s disease were established and verbascoside（60 mg/kg） was administered intraperitoneally once a day. After 6 weeks of verbascoside treatment, rat rotational behavior was alleviated; tyrosine hydroxylase m RNA and protein expression and the number of tyrosine hydroxylase-immunoreactive neurons in the rat right substantia nigra were significantly higher than the Parkinson＇s model group. These findings suggest that the mechanism by which verbascoside treats Parkinson＇s disease is related to the regeneration of tyrosine hydroxylase-immunoreactive neurons in the substantia nigra.

Immunohistochemistry （IHC） and semi-quantitative RT-PCR were used to detect the distribution of GnIH in the central nervous system of 30-day-old male Luchuan piglets, which laid a theoretical basis for in-depth research on physiological functions of Gn[H from the perspective of morphology and molecular lev- el. IHC results showed that in central nervous system, GnIH immunoreactive neurons distributed in cerebral cortex, cerebellum, hippocampus, olfactory bulb, ports, midbrain, medulla oblongata and spinal cord of Luchuan piglets, but GnIH-immunoreactive （GnIH-ir） cell bodies employed diversified morphologies with va- rying sizes. The results of semi-quantitative RT-PCR showed that the expression of GnIH mRNA in medulla obhingata was the highest, followed by midbrain, and the expression of GnIH mRNA in olfactory bulb was the lowest, while those in other tissues were medium. The results of IHC and semi-quantitative RT-PCR were coincident, which further confirmed wide distribution of GnIH in the central nervous system of male Luchuan piglets.

In this study, we investigated the effects of streptozotocin-induced type 1 diabetes on antioxi- dant-like protein-1 immunoreactivity, protein carbonyl levels, and malondialdehyde formation, a marker for lipid peroxidation, in the hippocampus. For this study, streptozotocin （75 mg/kg） was intraperitoneally injected into adult rats to induce type 1 diabetes. The three experimental pa- rameters were determined at 2, 3, 4 weeks after streptozotocin treatment. Fasting blood glucose levels significantly increased by 20.7-21.9 mM after streptozotocin treatment. The number of antioxidant-like protein-1 immunoreactive neurons significantly decreased in the hippocampal CA1 region, but not the dentate gyrus, 3 weeks after streptozotocin treatment compared to the control group. Malondialdehyde and protein carbonyl levels, which are modified by oxidative stress, significantly increased with a peak at 3 weeks after malondialdehyde treatment, and then decreased 4 weeks after malondialdehyde treatment. These results suggest that neurons in the hippocampal CA1 region, but not the dentate gyrus, are susceptible to oxidative stress 3 weeks after malondialdehyde treatment.

Cajal-Retzius cells are reelin-secreting neurons in the marginal zone of the neocortex and hippocampus. The aim of this study was to investigate Cajal-Retzius cells in Alzheimer＇s disease pathology. Results revealed that the number of Cajal-Retzius cells markedly reduced with age in both wild type and in mice over-expressing the Swedish double mutant form of amyloid precursor protein 695 （transgenic （Tg） 2576 mice）. Numerous reelin-positive neurons were positive for activated caspase 3 in Tg2576 mice, suggesting that Cajal-Retzius neuronal loss occurred via apoptosis in this Alzheimer＇s disease model. Compared with wild type, the number of Cajal-Retzius cells was significantly lower in Tg2576 mice. Western blot analysis confirmed that reelin levels were markedly lower in Tg2576 mice than in wild-type mice. The decline in Cajal-Retzius cells in Tg2576 mice was found to occur concomitantly with the onset of Alzheimer＇s disease amyloid pathology and related behavioral deficits. Overall, these data indicated that Cajal-Retzius cell loss occurred with the onset and development of Alzheimer＇s disease.

Because neurons are susceptible to oxidative damage and thioredoxin reductase 1 is extensively distributed in the central nervous system and has antioxidant properties, we speculated that the enzyme may be involved in the pathogenesis of Parkinson＇s disease. A Parkinson＇s disease model was produced by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine into C57BL/6 mice. Real-time reverse transcription-PCR, western blot analysis and colorimetric assay showed that the levels of thioredoxin reductase 1 mRNA and protein were decreased, along with a significant reduction in thioredoxin reductase activity, in the midbrain of Parkinson＇s disease mice compared with normal mice. Immunohistochemical staining revealed that the number of thioredoxin reductase 1-positive neurons in the substantia nigra pars compacta of Parkinson＇s disease mice was significantly decreased compared with normal mice. These experimental findings suggest that the expression of thioredoxin reductase 1 in the substantia nigra pars compacta of Parkinson＇s disease mice is significantly decreased, and that the enzyme may be associated with disease onset.

Mice carrying mutant amyloid precursor protein and presenilin-1 genes （APP/PS1 double trans- genic mice） have frequently been used in studies of Alzheimer＇s disease; however, such studies have focused mainly on hippocampal and cortical changes. The severity of Alzheimer＇s disease is known to correlate with the amount of amyloid-13 protein deposition and the number of dead neurons in the locus coeruleus. In the present study, we assigned APP/PS1 double transgenic mice to two groups according to age： young mice （5-6 months old） and aged mice （16-17 months old）. Age-matched wild-type mice were used as controls. Immunohistochemistry for tyrosine hydroxylase （a marker of catecholaminergic neurons in the locus coeruleus） revealed that APP/PS1 mice had 23% fewer cells in the locus coeruleus compared with aged wild-type mice. APP/PS1 mice also had increased numbers of cell bodies of neurons positive for tyrosine hydroxylase, but fewer tyrosine hydroxylase-positive fibers, which were also short, thick and broken. Quantitative analysis using unbiased stereology showed a significant age-related increase in the mean volume of tyrosine hy- droxylase-positive neurons in aged APP/PS1 mice compared with young APP/PS1 mice. Moreover, the mean volume of tyrosine hydroxylase-positive neurons was positively correlated with the total volume of the locus coeruleus. These findings indicate that noradrenergic neurons and fibers in the locus coeruleus are predisposed to degenerative alterations in APP/PS1 double transgenic mice.

A bilateral spared dorsal root ganglion model was established in healthy adult cats by bilateral resection of L1-5 and L7-S2 dorsal root ganglia. L6 dorsal root ganglia were spared. Zusanfi （ST36） and Xuanzhong （BL39） or Futu （ST32） and Sanyinjiao （SP6） were alternatively electro-stimulated on the right leg. Immunohistochemical staining of anti-serum platelet-derived growth factor demonstrated that the number of total neurons and medium-small sized platelet-derived growth factor positive neurons was significantly decreased on the 7~ day following injury. After 7 days of acupuncture, the total number of positive and large neurons staining for platelet-derived growth factor on the acupuncture side significantly increased compared to the non-acupuncture side. After acupuncture for 14 days, the total positive and medium-small sized neurons significantly increased compared with the non-acupuncture side. Results indicate that acupuncture promoted the synthesis of platelet-dedved growth factor in spared dorsal root ganglia.

This study examined the isolation and differentiation of dorsal root ganglion progenitor cells for therapeutic use in neurodegenerative diseases. Rat embryonic dorsal root ganglia progenitors were isolated and purified using the differential adhesion method combined with cytosine arabinoside treatment. After culture in serum-free medium supplemented with B27, basic fibroblast growth factor and epidermal growth factor, these cells remained viable and survived for more than 18 months in vitro. Most cells differentiated to neurons that were immunoreactive for gamma-aminobutyric acid and choline acetyltransferase as detected by immunohistochemical staining. In addition, nerve growth factor and neurotrophic tyrosine kinase receptor expression were also observed in dorsal root ganglion progenitors and differentiated cells. K252a, an inhibitor that blocks nerve growth factor-induced signaling, inhibited cell survival, suggesting the possible existence of a nerve growth factor autocrine loop in these proliferating cells.

Aim： To trace the origin of abundant vesicular glutamate transporter 1-like immunoreactive （VGIuT1-LI） axon terminals in the dorsal division of the principal sen- sory trigeminal nucleus （Vpd） and the relationships between VGIuT1-LI, as well as the glutamic acid decarboxylase （GAD）-LI axon terminals, and phosphateactivated glutaminase （PAG）-LI thalamic projecting neurons in the Vpd. Methods： Following unilateral trigeminal rhizotomy, triple-immunofluorescence histochemistry for VGIuT1, GAD and PAG and the immunogold-silver method for VGIuT1 or GAD, combined with the immunoperoxidase method for PAG were performed, respectively. Results： After unilateral trigeminal rhizotomy, the density of VGluT1-like immunoreactivity （1R） in the Vpd on the lesion side was reduced compared to its contralateral counterpart. Under the confocal laser-scanning microscope, the VGIuT1-LI or GAD-LI axon terminals were observed to be in close apposition to the PAG-LI thalamic projecting neuronal profiles, and further electron microscope immunocytochemistry confirmed that VGIuT1- and GAD-LI axon terminals made asymmetrical and symmetrical synapses upon the PAG-LI neuronal structures. Conclusion： The present results suggest that the VGIuT1-LI axon terminals, which mainly arise from the primary afferents of the trigeminal ganglion, along with the PAG-LI neuronal profiles, form the key synaptic connection involved in sensory signaling.