Effects of social isolation, re-socialization and age on cognitive and aggressive behaviors of Kunming mice and BALB/c mice.

Both Kunming (KM) mice and BALB/c mice have been widely used as rodent models to investigate stress-associated mental diseases. However, little is known about the different behaviors of KM mice and BALB/c mice after social isolation, particularly cognitive and aggressive behaviors. In this study, the behaviors of KM and BALB/c mice isolated for 2, 4 and 8 weeks and age-matched controls were evaluated using object recognition, object location and resident-intruder tests. The recovery of behavioral deficits by re-socialization was also examined for the isolated mice in adolescence. Our study showed that isolation for 2, 4 and 8 weeks led to cognitive deficits and increased aggressiveness for both KM and BALB/c mice. An important finding is that re-socialization could completely recover spatial/non-spatial cognitive deficits resulted from social isolation for both KM and BALB/c mice. In addition, age only impacted aggressiveness of KM mice. Moreover, isolation duration showed different impacts on cognitive and aggressive behaviors for both KM and BALB/c mice. Furthermore, BALB/c mice showed weak spatial/non-spatial memory and low aggressiveness when they were at the same age and isolation duration, compared to KM mice. In conclusion, KM mice and BALB/c mice behaved characteristically under physiology and isolation conditions.

[The alterations of apoptosis factor Bcl-2/Bax in the early Parkinson's disease rats and the protective effect of scorpion venom derived activity peptide].

OBJECTIVE: To explore the alterations of apoptosis factor Bcl-2/Bax in the early Parkinson's disease (PD) rats and the protective effect of scorpion venom derived bioactive peptide. METHODS: Healthy male SD rats (180-220 g) were randomly divided into 4 groups (n = 10): early PD model group, sham operation group, scorpion venom derived bioactive peptide control group, scorpion venom derived bioactive peptide therapy group. 6-hydroxydopamine (6-OHDA) was used to prepare the early PD rat model. The immunohistochemistry was used to detect the expression of Bax and Bcl-2 and further explore the mechanism of anti-apoptosis regarding the neuroprotective effect of scorpion venom derived bioactive peptide. RESULTS: The results indicated that compared with the control rats, the immunostaining of Bax in the brain increased significantly while that of Bcl-2 decreased significantly in the lesion side of 6-OHDA treated rats. Interestingly, scorpion venom derived bioactive peptide could attenuate the above abnormal changes. CONCLUSION: Up-regulation of Bax and down-regulation of Bcl-2 could participate in the early stage of PD and the anti-apoptotic mechanism could be involved in the neuroprotective effect exerted by scorpion venom derived activity peptide regarding the dopaminergic neuron in the early stage.

Neuroprotection by scorpion venom heat resistant peptide in 6-hydroxydopamine rat model of early-stage Parkinson's disease.

Neuroprotective effect of scorpion venom on Parkinson's disease (PD) has already been reported. The present study was aimed to investigate whether scorpion venom heat resistant peptide (SVHRP) could attenuate ultrastructural abnormalities in mitochondria and oxidative stress in midbrain neurons of early-stage PD model. The early-stage PD model was established by injecting 6-hydroxydopamine (6-OHDA) (20 µg/3 µL normal saline with 0.1% ascorbic acid) into the striatum of Sprague Dawley (SD) rats unilaterally. The rats were intraperitoneally administered with SVHRP (0.05 mg/kg per day) or vehicle (saline) for 1 week. Two weeks after 6-OHDA treatment, the rats received behavior tests for validation of model. Three weeks after 6-OHDA injection, the immunoreactivity of dopaminergic neurons were detected by immunohistochemistry staining, and the ultrastructure of neuronal mitochondria in midbrain was observed by electron microscope. In the meantime, the activities of monoamine oxidase-B (MAO-B), superoxide dismutase (SOD) and content of malondialdehyde (MDA) in the mitochondria of the midbrain neurons, as well as the inhibitory ability of hydroxyl free radical and the antioxidant ability in the serum, were measured by corresponding kits. The results showed that 6-OHDA reduced the optical density of dopaminergic neurons, induced damage of mitochondrial ultrastructure of midbrain neurons, decreased SOD activity, increased MAO-B activity and MDA content, and reduced the antioxidant ability of the serum. SVHRP significantly reversed the previous harmful effects of 6-OHDA in early-stage PD model. These findings indicate that SVHRP may contribute to neuroprotection by preventing biochemical and ultrastructure damage changes which occur during early-stage PD.

[Establishing the model of kappaB-decoy inhibiting the activity of NF-kappaB in PC12 cells].

OBJECTIVE: Observing the time course and establishing the model of kappaB-decoy oligodeoxynucleotides (rcB-decoy) inhibiting the activity of NF-kappaB in the PC12 cells. METHODS: PC12 cells cultivating in the 6 wells plate were divided into 3 groups, experimental group: adding kappaB-decoy complex (6 microg DNA/well), the control group: adding scrambled-decoy complex, the normal group: adding lipid-Lipofectamine 2000, transfer and cultivate 48 h, then lipopolysaccharide (LPS, 200 ng/ml) was added in the cells for 0.5-4 h. The immunocytochemistry and Western blot were used to measure the expression or the activity of NF-kappaB in PC12 cells. RESULTS: In PC12 cells, compared with normal group, the expression of NF-kappaB enhanced obviously with the time of the stimulation of LPS in scrambled-decoy treated control group (P < 0.01), in 2-4 h the level reached the peak; the expression of NF-kappaB showed the stable level with the time of the stimulation of LPS in kappaB-decoy treated experimental group, compared with the control group, the expression levels were obviously lower than the respective time point of control groups (P < 0.01). CONCLUSION: kappaB-decoy could reduce the expression of NF-kappaB in the normal PC12 cells and inhibit the activity of NF-cB in the pathologic PC12 cells.

[Effects of scorpion venom heat-resistant protein on kainic acid induced-damage of cultured primitive rat hippocampal neuropeptide Y-nergic neurons].

AIM: To investigate the effects of scorpion venom heat-resistant protein (SVHRP) on kainic acid induced-damage of cultured primitive rat hippocampal neuropeptide Y-nergic neurons. METHODS: We observed morphological changes, celluar vigor, NPY-immunoreactivity and NPY mRNA expression by means of Thionine staining, MTT assay, immunocytochemistry and RT-PCR, respectively, on the primitively cultured Sprague-Dawley rat hippocampal neuron treated with KA and SVHRP for 24 h. RESULTS: MTT assay and morphologic analysis showed that SVHRP markedly increased neuron survival-rate, and protected them from kA-induced damage. The expression of NPY-immunoreactivity and NPY mRNA in SVHRP group increased obviously compared with other groups. CONCLUSION: SVHRP protected the primitively cultured hippocampal neurons from KA-induced neuroexcitotoxicity and promoted the expression of NPY.

[The protective effect of nicotine on dopaminergic neuron of Parkinson's disease mice].

AIM: To investigate the protective effect of nicotine on dopaminergic neurons and its mechanisms in mice with Parkinson's disease (PD) induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). METHODS: C57BL/6J mice were injected with MPTP for 8 days to establish PD model. Nicotine was given for 10 days in the pretreatment group. Animals were examined behaviorally with the pole test and traction test. Tyrosine hydroxylase (TH) and gamma-aminobutyric acid (GABA) were investigated by the immunocytochemistry (ICC) method. The ultrastructural changes of caudate nucleus(CN) were observed by electron microscope. RESULTS: The results showed that pretreatment nicotine could improve the dyskinesia of PD mice markedly. Simultaneously, TH (P < 0.01) neurons and GABA (P < 0.05) neurons were much more in the pretreatment group when compared with those in the model group. The ultrastructural injury of the pretreatment group was also ameliorated. CONCLUSION: Nicotine has a protective effect on the dopaminergic neurons in the MPTP-treated mice.