Guo-Dong Gao

Fourth Military Medical University, Xi’an, Liaoning, China

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Publications (72)188.95 Total impact

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    ABSTRACT: Background: The nucleus accumbens (NAcc) has been proven to be associated with drug and food craving. NAcc ablative neurosurgery has been suggested to modulate the balance of the brain reward system and thus alleviate drug dependence in patients. It has been hypothesized that it would also alleviate food craving in patients as well as altering their nutritional status. Aims: This study aimed to estimate the effect of NAcc neurosurgery on drug craving and nutritional status in patients with drug dependence at 5 years postoperatively. Methods: The study included 100 patients with NAcc surgery and 92 patients without surgery. Body mass index (BMI) and body fat percentage (BF%) were examined to assess nutritional status, and questionnaires were administered to assess drug craving. Results: Compared with the nonsurgery group and the relapse patients from the surgery group, the nonrelapse patients from the surgery group had higher BMI and BF% but lower drug craving. There were no significant differences between the nonsurgery group and the relapse patients in BMI, but the relapse patients had higher drug craving than the nonsurgery group. Conclusions: Long-term follow-up suggested that NAcc ablative neurosurgery would alleviate drug craving and yield a better nutritional status if individuals sustained abstinence. It would increase drug craving but would not ruin the nutritional status of patients even when individuals relapsed postoperatively.
    No preview · Article · Jan 2016 · Stereotactic and Functional Neurosurgery
  • Nan Li · Lei Chen · Shun-nan Ge · Xue-lian Wang · Guo-dong Gao

    No preview · Conference Paper · Aug 2015
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    ABSTRACT: Abnormal oscillation in the cortical-basal ganglia loop is involved in the pathophysiology of parkinsonism. High-voltage spindles (HVSs), one of the main type abnormal oscillations in Parkinson's disease, are regulated by dopamine D2-like receptors but not D1-like receptors. However, little is known about how dopamine D2-like receptors regulate HVSs and the role of hyperpolarization-activated cyclic nucleotide-gated2 (HCN2) in HVSs regulation. We simultaneously recorded the local field potential (LFP) in globus pallidus (GP) and electrocorticogram (ECoG) in primary motor cortex (M1) in freely moving 6-hydroxydopamine (6-OHDA) lesioned or control rats. The expression of HCN2 and dopamine D2 receptor in the subthalamic nucleus (STN) was examined by immunochemical staining and western blotting. We also tested the role of HCN2 in HVSs regulation by using pharmacological and shRNA methodology. We found that dopamine D2-like receptor agonists suppressed the increased HVSs in 6-OHDA lesioned rats.HCN2 was co-expressed with dopamine D2 receptor in the STN, and dopamine depletion decreased the expression of HCN2 as well as dopamine D2 receptor which contribute to the regulation of HVSs. HCN2 was down regulated by HCN2 shRNA, which thereby led to an increase in the HVSs in naïve rats while HCN2 agonist reduced the HVSs in 6-OHDA lesioned rats. These results suggest that HCN2 in the STN is involved in abnormal oscillation regulation between M1 cortex and GP. Copyright © 2015. Published by Elsevier B.V.
    No preview · Article · May 2015 · Brain research
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    ABSTRACT: Many studies showed that abnormal oscillations in the cortical-basal ganglia loop is involved in the pathophysiology of Parkinson's disease (PD). In contrast to the well-studied beta synchronization, high-voltage spindles (HVSs), another type of abnormal oscillation observed in PD, are neglected. To explore the role of subthalamic nucleus-deep brain stimulation (STN-DBS) in HVSs regulation, we simultaneously recorded the local field potential (LFP) in the globus pallidus (GP) and electrocorticogram (ECoG) in the primary motor cortex(M1) in freely moving 6-hydroxydopamine (6-OHDA) lesioned or control rats before, during, and after STN-DBS. Consistent with our previous study, HVSs occurrence, duration, and relative power and coherence between the M1 cortex and GP increased in 6-OHDA lesioned rats. We found that high but not low frequency stimulation restored the abnormal HVSs activity and motor deficit. These results suggest that the STN is involved in the abnormal oscillation between the M1 cortex and GP. Copyright © 2015. Published by Elsevier Ireland Ltd.
    No preview · Article · Apr 2015 · Neuroscience Letters
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    ABSTRACT: Astrocytoma is the most common primary brain tumor and it is associated with poor prognosis. Accumulating evidences suggest that certain molecular abnormalities or genetic mutations are associated with its progression and prognosis. Human transcriptional coactivator 4 (PC4), originally identified as a transcriptional coactivator then as a DNA replication and repair factor has been shown to be involved in chromatin organization. Recently, it is reported to function both as tumor suppressor and promoter depending on the cellular settings. In the present study, we for the first time demonstrated that the expression of PC4 in astrocytoma was upregulated as assessed by western blot and immunohistochemical staining. Moreover, elevated PC4 expression was strongly correlated with the progression of astrocytoma. Furthermore, high PC4 expression was also associated with poor overall survival. Finally, in vitro study demonstrated that siRNA mediated PC4 downregulation significantly inhibited the proliferation and invasiveness of human glioma cells. These results suggested that PC4 might play a role in human astrocytoma progression and may be used as a novel indicator for the prognosis of astrocytoma patient.
    No preview · Article · Sep 2014 · Journal of the Neurological Sciences
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    ABSTRACT: The function of TRPV1 (transient receptor potential vanilloid subfamily, member 1) in the central nervous system is gradually elucidated. It has been recently proved to be expressed in nucleus accumbens (NAc), a region playing an essential role in mediating opioid craving and taking behaviors. Based on the general role of TRPV1 antagonist in blocking neural over-excitability by both pre- and post-synaptic mechanisms, TRPV1 antagonist capsazepine (CPZ) was tested for its ability to prohibit persistent opioid craving in rats. In the present study, we assessed the expression of TRPV1 in nucleus accumbens and investigated the effect of CPZ in bilateral nucleus accumbens on persistent morphine conditioned place preference (mCPP) in rats. We also evaluated the side-effect of CPZ on activity by comparing cross-beam times between groups. We found that morphine conditioned place preference increased the TRPV1 expression and CPZ attenuated morphine conditioned place preference in a dose-dependent and target-specific manner after both short- and long-term spontaneous withdrawal, reflected by the reduction of the increased time in morphine-paired side. CPZ (10 nM) could induce prolonged and stable inhibition of morphine conditioned place preference expression. More importantly, CPZ did not cause dysfunction of activity in the subjects tested, which indicates the inhibitory effect was not obtained at the sacrifice of regular movement. Collectively, these results indicated that injection of TRPV1 antagonist in nucleus accumbens is capable of attenuating persistent morphine conditioned place preference without affecting normal activity. Thus, TRPV1 antagonist is one of the promising therapeutic drugs for the treatment of opioid addiction.
    Preview · Article · Aug 2014 · PLoS ONE
  • Lei Chen · Nan Li · Li Gao · Chen Yang · Wei Fang · Xue-Lian Wang · Guo-Dong Gao
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    ABSTRACT: Purpose: Non-human primate models of deep brain stimulation (DBS) play an increasingly important role in the exploration of DBS mechanisms. The establishment and recognized usefulness of such models depend on the precise positioning of the stimulating targets and electrode implants. The optimal method of targeting remains controversial. Materials and methods: This paper described an improved stereotactic procedure that uses a self-developed adaptor to improve accuracy. This involved: (1) connecting clinical stereotactic devices with the skull of primates using a self-developed adaptor; (2) pre-operation targeting via magnetic resonance imaging (MRI); (3) target re-checking by microelectrode recording (MER); (4) DBS electrode implantation; (5) post-operative MRI verification of electrode placement and (6) positioning confirmation by DBS programming. Results: Use of the adaptor enabled clinical stereotactic surgery, pre-operative MRI targeting, microelectrode mapping and post-operative verification in primate DBS operations. Discrepancies between achieved and predetermined electrode position were around 0.6 mm. DBS programming improved the motor function of the hemiparkinsonism animals and decreased the numbers of rotation induced by apomorphine, indicating the precise positioning of the stimulating target and successful implanting of electrode using this method. Conclusions: An improved stereotactic procedure was performed during a non-human primate DBS operation using a self-developed adaptor. The accuracy of DBS electrode implantation in non-human primates was improved with this method.
    No preview · Article · Jul 2014 · International Journal of Neuroscience
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    ABSTRACT: Voltage gated calcium channels (VGCC) are sensitive to oxidative stress, and their activation or inactivation can impact cell death. Although these channels have been extensively studied in expression systems, their role in the brain, particularly in the substantia nigra pars compacta (SNc), remain controversial. In this study, we assessed 6-hydroxydopamine (6-OHDA) induced transformation of firing pattern and functional changes of calcium channels in SNc dopaminergic neurons. Application of 6-OHDA (0.5-2mM) evoked a dose-dependent, desensitizing inward current and intracellular free calcium concentration ([Ca(2+)]i) rise. In voltage clamp, ω-Conotoxin-sensitive Ca(2+) current modulation mediated by 6-OHDA reflected an altered sensitivity. Furthermore, we found that 6-OHDA modulated Ca(2+) currents through PKA pathway. These results provided evidence for the potential role of VGCCs and PKA involved in oxidative stress in degeneration of SNc neurons in Parkinson's disease (PD).
    No preview · Article · May 2014 · Neuroscience Letters
  • Yuan Wang · Liang Qu · Xue-Lian Wang · Li Gao · Zhen-Zhen Li · Guo-Dong Gao · Qian Yang
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    ABSTRACT: Dopaminergic (DA) neurons in substantia nigra pars compacta (SNc) are vulnerable to excitotoxicity in Parkinson's disease (PD). Neurotoxic stimuli may alter the firing patterns of DA neurons. However, whether firing pattern change underlies neurotoxic stress-induced death of DA neurons remains unknown. In this study, we established long-term cultures of SNc organotypic slices and used this model to evaluate the neurotoxic effects on firing mode and DA neuronal viability following chronic treatment with neurotoxin 6-hydroxydopamine (6-OHDA). Using whole-cell patch clamp to explore the intrinsic membrane properties and firing mode, we showed that chronic exposure to 6-OHDA raised the resting membrane potential of SNc DA neurons and altered their firing pattern, causing it to switch from a regular rhythmic pacemaking firing to an irregular bursting. This firing pattern change correlated with increased death of SNc DA neurons. The 6-OHDA-induced firing pattern change correlated with an increase in the activity of the small conductance calcium-activated potassium channel (SK channel) and with an increase in both the level and activity of protein phosphatase 2A (PP2A). Activation of the SK channel by its agonist 1-EBIO attenuated 6-OHDA-induced firing irregularity and death, while the SK channel antagonist apamin exacerbated the toxic effects of 6-OHDA. Thus, SK channel current is a substantial element in sustaining the SNc DA neuronal rhythmic pacemaking and homeostasis and perturbing SK channel activity underlies 6-OHDA-induced neurotoxicity.
    No preview · Article · May 2014 · Molecular Neurobiology
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    ABSTRACT: Background: Glioblastoma (GBM) is an immunosuppressive tumor whose median survival time is only 12- 15 months, and patients with GBM have a uniformly poor prognosis. It is known that heredity contributes to formation of glioma, but there are few genetic studies concerning GBM. Materials and methods: We genotyped six tagging SNPs (tSNP) in Han Chinese GBM and control patients. We used Microsoft Excel and SPSS 16.0 statistical package for statistical analysis and SNP Stats to test for associations between certain tSNPs and risk of GBM in five different models. ORs and 95%CIs were calculated for unconditional logistic-regression analysis with adjustment for age and gender. The SHEsis software platform was applied for analysis of linkage disequilibrium, haplotype construction, and genetic associations at polymorphism loci. Results: We found rs891835 in CCDC26 to be associated with GBM susceptibility at a level of p=0.009. The following genotypes of rs891835 were found to be associated with GBM risk in four different models of gene action: i) genotype GT (OR=2.26; 95%CI, 1.29-3.97; p=0.019) or GG (OR=1.33; 95%CI, 0.23-7.81; p=0.019) in the codominant model; ii) genotypes GT and GG (OR=2.18; 95%CI, 1.26-3.78; p=0.0061) in the dominant model; iii) GT (OR=2.24; 95%CI, 1.28-3.92; p=0.0053) in the overdominant model; iv) the allele G of rs891835 (OR=1.85; 95%CI, 1.14-3.00; p=0.015) in the additive model. In addition, "CG" and "CGGAG" were found by haplotype analysis to be associated with increased GBM risk. In contrast, genotype GG of CCDC26 rs6470745 was associated with decreased GBM risk (OR=0.34; 95%CI, 0.12-1.01; p=0.029) in the recessive model. Conclusions: Our results, combined with those from previous studies, suggest a potential genetic contribution of CCDC26 to GBM progression among Han Chinese.
    No preview · Article · Apr 2014 · Asian Pacific journal of cancer prevention: APJCP
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    ABSTRACT: Complement activation and inflammation have been suggested in the pathogenesis of stroke; mannose-binding lectin (MBL) was found to have roles during the process. We therefore evaluated the short-term prognostic value of serum MBL in Chinese patients with an acute ischemic stroke (AIS). Consecutive AIS patients admitted to the emergency department were identified. Clinical information was collected. Serum concentration of MBL and NIH Stroke Scale (NIHSS) was measured at the time of admission. Short-term functional outcome was measured by modified Rankin scale (mRS) 90 days after admission. Multivariate analyses were performed using logistic regression models. During the inclusion period, 231 patients were diagnosed with AIS, and 220 completed follow-up. The results indicated that the serum MBL levels were significantly (P = 0.000) higher in acutely ischemic stroke patients as compared with normal controls. MBL was an independent prognostic marker of short-term functional outcome and death (odds ratio (OR) 5.28 (2.88-10.67) and 6.99 (3.55-13.97), respectively, P = 0.000 for both, adjusted for NIHSS, other predictors, and vascular risk factors) in patients with AIS. MBL improved the area under the receiver operating characteristic curve of the NIHSS score for functional outcome from 0.826 (95 % CI 0.773-0.879) to 0.857 (95 % CI 0.808-0.905, P = 0.000) and for mortality from 0.768 (95 % CI 0.682-0.853) to 0.822 (95 % CI 0.747-0.896, P = 0.000). Serum MBL levels are a useful, complementary tool to predict functional outcome and mortality 90 days after stroke.
    No preview · Article · Apr 2014 · Molecular Neurobiology
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    ABSTRACT: Epidemiological studies demonstrate that pain frequently occurs comorbid with depression. Gentiopicroside (Gent) is a secoiridoid compound isolated from Gentiana lutea that exhibits analgesic properties and inhibits the expression of GluN2B-containing N-methyl-D-aspartate (NMDA) receptors in the anterior cingulate cortex of mice. However, the effects of Gent on the reserpine-induced pain/depression dyad and its underlying mechanisms are unclear. Reserpine administration (1 mg/kg subcutaneous daily for 3 days) caused a significant decrease in the nociceptive threshold as evidenced by the reduced paw withdrawal latency in response to a radiant heat source and mechanical allodynia. Behavioral detection indicated a significant increase in immobility time during a forced swim test, as well as decreased time in the central area and total travel distance in an open field test. Furthermore, reserpinized animals exhibited increased oxidative stress. Systemic Gent administration dose-dependently ameliorated the behavioral deficits associated with reserpine-induced pain/depression dyad. At the same time, the decrease in biogenic amine levels (norepinephrine, dopamine, and serotonin) was integrated with the increase in caspase-3 levels and GluN2B-containing NMDA receptors in the amygdala of the reserpine-injected mice. Gent significantly reversed the changes in the levels of biogenic amines, caspase-3, and GluN2B-containing NMDA receptors in amygdala. However, Gent did not affect the expression of GluN2A-containing NMDA receptors. The inhibitory effects of Gent on oxidative stress were occluded by simultaneous treatment of GluN2B receptors antagonist Ro25-6981. Our study provides strong evidence that Gent inhibits reserpine-induced pain/depression dyad by downregulating GluN2B receptors in the amygdala.
    No preview · Article · Mar 2014 · Neuromolecular medicine
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    ABSTRACT: Glioblastoma (GBM), a deadly brain tumor, is the most malignant glioma. It mainly occurs in adults and occurs significantly more in males than in females. We genotyped 19 tag single nucleotide polymorphisms (tSNPs) from 13 genes in a case–control study of the Han Chinese population to identify genetic factors contributing to the risk of GBM. These tSNPs were genotyped by Sequenom MassARRAY RS1000. Statistical analysis was performed using χ 2 test and SNPStats, a website software. Using χ 2 test, we found that the distribution of two tSNPs (rs2267130 in checkpoint kinase 2 (CHEK2), p = 0.040; rs1695 in GSTP1, p = 0.023) allelic frequencies had significant difference between cases and controls. When we analyzed all of the tSNPs using the SNPStats software, we found that rs1695 in GSTP1 decreased the risk of GBM in log-additive model (OR = 0.56, 95 % CI, 0.34–0.94, p = 0.022). Besides, we found that there is an interaction between rs3212986 in excision repair cross-complementing group 1 (ERCC1) and gender under codominant and recessive models. The gene polymorphisms in CHEK2, GSTP1, and ERCC1 may be involved in GBM in the Han Chinese population. Since our sample size is small, further investigation needs to be performed.
    No preview · Article · Feb 2014 · Tumor Biology
  • Jian-Ping Deng · Jiang Li · Tao Zhang · Jia Yu · Zhen-Wei Zhao · Guo-Dong Gao
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    ABSTRACT: Dural arteriovenous fistula (DAVF) of the anterior cranial fossa is usually treated by surgical disconnection or endovascular embolization via the ophthalmic artery. The middle meningeal artery is a rarely used approach. This study investigated the safety and efficacy of embolization of DAVF of the anterior cranial fossa with Onyx through the middle meningeal artery. A retrospective review of a prospective cerebral vascular disease database was performed. Patients with DAVF of the anterior cranial fossa managed with embolization through the middle meningeal artery with Onyx were selected. Information on demography, symptoms and signs, angiographic examinations, interventional treatments, angiographic and clinical results, and follow-up was collected and analyzed. Five patients were included in this study, four of whom had hemorrhage. All fistulas were fed by the bilateral ethmoidal arteries arising from the ophthalmic artery and by the anterior branch of the middle meningeal artery. The abnormal shunt unilaterally drained into the superior sagittal sinus with interposition of the cortical veins all five patients. All endovascular treatments were successful with evidence of an angiographic cure. No complications occurred, and all patients recovered uneventfully without neurologic deficits. There were nearly no symptoms among the patients during follow-up. Embolization of DAVF of the anterior cranial fossa via the middle meningeal artery with Onyx is safe, effective, and a good choice for management of DAVF. More cases are needed to verify these findings.
    No preview · Article · Feb 2014 · Clinical neurology and neurosurgery
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    ABSTRACT: Quercetin has been demonstrated to play an important role in altering the progression of ischemic brain injuries and neurodegenerative diseases by protecting against oxidative stress. The effects of quercetin on brain damage after subarachnoid hemorrhage (SAH), however, have not been investigated. This study was designed to explore the effects of quercetin on oxidative stress and brain edema after experimental SAH using four equal groups (n = 16) of adult male Sprague-Dawley (SD) rats, including a sham group, an SAH + vehicle group, an SAH + quercetin10 group, and an SAH + quercetin50 group. The rat SAH model was induced by injection of 0.3 ml of non-heparinised arterial blood into the prechiasmatic cistern. In the SAH + quercetin10 and SAH + quercetin50 groups, doses of 10 mg/kg and 50 mg/kg quercetin, respectively, were directly administered by intraperitoneal injection at 30 min, 12 h, and 24 h after SAH induction. Cerebral tissue samples were extracted for enzymatic antioxidant determination, lipid peroxidation assay, caspase-3 activity and water content testing 48 h after SAH. Treatment with a high dose (50 mg/kg) of quercetin markedly enhanced the activities of copper/zinc superoxide dismutase (CuZn-SOD) and glutathione peroxidase (GSH-Px), and treatment with this dose significantly reduced the level of malondialdehyde (MDA). Caspase-3 and brain edema was ameliorated and neurobehavioral deficits improved in rats that received the high dose of quercetin. The findings suggest that the early administration of optimal dose of quercetin may ameliorate brain damage and provide neuroprotection in the SAH model, potentially by enhancing the activity of endogenous antioxidant enzymes and inhibiting free radical generation.
    Preview · Article · Jan 2014 · International journal of medical sciences
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    ABSTRACT: Efflux of monocaroxylates like lactate, pyruvate, and ketone bodies from astrocytes through monocarboxylate transporter 4 (MCT4) supplies the local neuron population with metabolic intermediates to meet energy requirements under conditions of increased demand. Disruption of this astroglial-neuron metabolic coupling pathway may contribute to epileptogenesis. We measured MCT4 expression in temporal lobe epileptic foci excised from patients with intractable epilepsy and in rats injected with pilocarpine, an animal model of temporal lobe epilepsy (TLE). Cortical MCT4 expression levels were significantly lower in TLE patients compared with controls, due at least partially to MCT4 promoter methylation. Expression of MCT4 also decreased progressively in pilocarpine-treated rats from 12 h to 14 days post-administration. Underexpression of MCT4 in cultured astrocytes induced by a short hairpin RNA promoted apoptosis. Knockdown of astrocyte MCT4 also suppressed excitatory amino acid transporter 1 (EAAT1) expression. Reduced MCT4 and EAAT1 expression by astrocytes may lead to neuronal hyperexcitability and epileptogenesis in the temporal lobe by reducing the supply of metabolic intermediates and by allowing accumulation of extracellular glutamate.
    No preview · Article · Jan 2014 · Molecular Neurobiology
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    ABSTRACT: Several recent studies have showed that the n-myc downstream regulated gene 2 (NDRG2) is a new tumor suppressor gene, and that it plays an important role in tumor suppression in several cancers or cancer cell lines. However, few studies focused on its function in neuroblastoma cells. In the present investigation, we demonstrated that NDRG2 overexpression inhibited their proliferation. Using a cDNA microarray, we found that overexpression of NDRG2 inhibited the expression of cysteine-rich protein 61 (CYR61), a proliferation related gene. From our research, CYR61 may partially hinder NDRG2-mediated inhibition of cell proliferation. Overexpression of NDRG2 resulted in accumulation of cells in the G1 phase, which was accompanied by upregulation of p21 and p27 and downregulation of CDK4 and cyclin D1. Taken together, these data indicate that NDRG2 inhibits the proliferation of neuroblastoma cells partially through suppression of CYR61. Our findings offer novel insights into the physiological roles of NDRG2 in neuroblastoma cell proliferation, and NDRG2 may prove to be effective candidate for the treatment of children with neuroblastoma.
    No preview · Article · Jan 2014 · Asian Pacific journal of cancer prevention: APJCP
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    ABSTRACT: Although many pathogenic copy number variations (CNVs) are associated with neuropsychiatric diseases, few of them have been functionally characterised. Here we report multiple schizophrenia cases with CNV abnormalities specific to unc-51-like kinase 4 (ULK4), a novel serine/threonine kinase gene. Deletions spanning exons 21-34 of ULK4 were present in 4 out of 3,391 schizophrenia patients from the International Schizophrenia Consortium, but absent in 3,181 controls. Deletions removing exons 33 and 34 of the large splice variant of ULK4 also were enriched in Icelandic schizophrenia and bipolar patients compared to 98,022 controls (P=0.0007 for schizophrenia plus bipolar disorder). Combining the two cohorts gives a p value less than 0.0001 for schizophrenia, or for schizophrenia plus bipolar disorder. The expression of ULK4 is neuron-specific and developmentally regulated. ULK4 modulates multiple signalling pathways including ERK, p38, PKC, and JNK, which are involved in stress responses and implicated in schizophrenia. Knockdown of ULK4 disrupts the composition of microtubules and compromises neuritogenesis and cell motility. Targeted Ulk4 deletion causes corpus callosum agenesis in mice. Our findings indicate that ULK4 is a rare susceptibility gene for schizophrenia.
    Full-text · Article · Nov 2013 · Journal of Cell Science
  • Dong Jia · Li-Jun Heng · Rui-Hua Yang · Guo-Dong Gao
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    ABSTRACT: Previous research has demonstrated that diabetes induces learning and memory deficits. However, the mechanism of memory impairment induced by diabetes is poorly understood. Dietary fatty acids, especially polyunsaturated fatty acids, have been shown to enhance learning and memory and prevent memory deficits in various experimental conditions. The present study investigated the effects of fish oil supplementation on the lipid peroxidation, inflammation and neuron apoptosis in the hippocampus of streptozotocin (STZ)-induced diabetes rats. The effects of diabetes and fish oil treatment on the spatial learning and memory were also evaluated using the Morris Water Maze. STZ-induced diabetes impaired spatial learning and memory of rats, which was associated with the inflammation, oxidative stress and apoptosis of hippocampal neurons. Fish oil administration ameliorated cognitive deficit, reduced oxidative stress and TNF-α, protected the hippocampal neurons by increasing AKT phosphorylation and decreasing caspase-9 expression. These results suggested that the principle mechanisms involved in the antidiabetic and neuroprotective effect of fish oil were its antioxidant, anti-inflammatory and anti-apoptosis potential, supporting a potential role for fish oil as an adjuvant therapy for the prevention and treatment of diabetic complications.
    No preview · Article · Nov 2013 · Neuroscience
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    ABSTRACT: Relapse is a major clinical problem and remains a major challenge in the treatment of drug addiction. There is strong evidence that the endocannabinoid system of the nucleus accumben core (NAcc) is involved in drug-seeking behavior, as well as in the mechanisms that underlie relapse to drug use. To reveal the mechanism that underlies this finding, we examined the expression pattern of the cannabinoid receptor 1 (CB1-R) in the NAcc of SD rats that had been undergoing morphine withdrawal (MW) for 1 day, 3 days and 3 weeks (acute, latent and chronic phases, respectively). Morphine exposure induced conditioned place preference (CPP) in rats. Significant increase of CB1-R expression in NAcc was observed in animals in the 1 day, 3 days and 3 weeks morphine withdrawal compare to the control group. Immunofluorescence labeling showed axonal fibers or terminals by fluorescence microscope observation. Immunoelectron microscopy detection showed silver-gold particles located in the presynaptic membranes that mainly give rise to symmetrical synapses. Quantitative electron microscopy showed an increase in number of CB1-R-positive terminals in the morphine withdrawal groups and the number of immunogold particles was significantly increased at these inhibitory terminals. We also confirmed that infusions of the CB1-R antagonist rimonabant into the NAcc attenuated the CPP during morphine withdrawal. Our present data have thus indicated that increasing pattern of CB1-R expression in the NAcc during above morphine withdrawal phases, which might underlie the relapse associated drug seeking behavior after morphine withdrawal.
    No preview · Article · Aug 2013 · Brain research

Publication Stats

497 Citations
188.95 Total Impact Points


  • 2005-2016
    • Fourth Military Medical University
      • Department of Biochemistry and Molecular Biology
      Xi’an, Liaoning, China
  • 2011
    • Peking Union Medical College Hospital
      Peping, Beijing, China