Association between the Brain-Derived Neurotropic Factor and Attention Deficit Hyperactivity Disorder

Attention deficit hyperactivity disorder (ADHD) is a common childhood psychiatric disorder. Recently, it has been suggested that brain-derived neurotropic factor (BDNF) may play a role in the pathogenesis of ADHD. Our aim of this review is to understand the physiological functions of BDNF and its potential relationship with ADHD and therapeutic approaches of ADHD. Searches were conducted in Pubmed and Research Information Service System (RISS). In this review, we summarized important literatures for the physiological functions of BDNF in neurodevelopment, change of serum BDNF level in ADHD, association of BDNF polymorphism and ADHD and potential association of treatment of ADHD with serum BDNF level. Further studies are required to more clearly understand the source and the role of BDNF in ADHD and to develop BDNF based-ADHD treatement.

Effects of propofol sedation on BDNF-TrkB/p75 signal and cognitive function in rat hippocampus / 上海交通大学学报（医学版）

Objective • To detect the effects of propofol sedation on cognitive function in rats and its mechanism. Methods • Forty-eight SD rats were randomly divided into three groups, i.e. control group, 100 mg/kg group and 300 mg/kg group. Rats were administrated intraperitoneally with propofol (10 mg/mL, 100 mg/kg or 300 mg/kg). The mRNA levels of brain derived neurotropic factor (BDNF)-TrkB/p75 signal molecules in rat hippocampus were evaluated by realtime PCR 45 min after propofol treatment. Learning and memory ability was examined by inhibitory avoidance (IA) test after propofol treatment. Results • The mRNA levels of BDNF in the hippocampal tissue were (1.20±0.13) fold (P=0.002) and (88±12)% (P=0.044) of that in control group, respectively, in 100 mg/kg group and 300 mg/kg group after injection of propofol. The mRNA levels of TrkB were (1.01±0.11) fold (P=0.982) and (86±11)% (P=0.018) of that in control group, respectively, in 100 mg/kg group and 300 mg/kg group. The mRNA levels of p75 were (1.02±0.10) fold (P=0.778) and (1.59±0.18) fold (P=0.000) of that in control group, respectively, in 100 mg/kg group and 300 mg/kg group. There was no significant difference of the 24 h IA memory retention latency between 100 mg/kg group and control group. The 24 h IA memory retention latency in 300 mg/kg group was significantly decreased compared with control group (P=0.028) and 100 mg/kg group (P=0.020). Conclusion • Propofol dose-dependently regulates the expression of BDNF-TrkB/p75 signal molecules, and high dose propofol may reduce cognitive function via BDNF-TrkB/p75 signal.

Effects of propofol sedation on BDNF-TrkB/p75 signal and cognitive function in rat hippocampus / 上海交通大学学报（医学版）

Objective·To detect the effects of propofol sedation on cognitive function in rats and its mechanism. Methods?·?Forty-eight SD rats were randomly divided into three groups, i.e. control group, 100?mg/kg group and 300?mg/kg group. Rats were administrated intraperitoneally with propofol (10?mg/mL, 100?mg/kg or 300?mg/kg). The mRNA levels of brain derived neurotropic factor (BDNF)-TrkB/p75 signal molecules in rat hippocampus were evaluated by realtime PCR 45 min after propofol treatment. Learning and memory ability was examined by inhibitory avoidance (IA) test after propofol treatment. Results?·?The mRNA levels of BDNF in the hippocampal tissue were (1.20±0.13) fold (P=0.002) and (88±12) % (P=0.044) of that in control group, respectively, in 100?mg/kg group and 300?mg/kg group after injection of propofol. The mRNA levels of TrkB were (1.01±0.11) fold ( P=0.982) and (86±11) % (P=0.018) of that in control group, respectively, in 100?mg/kg group and 300?mg/kg group. The mRNA levels of p75 were (1.02±0.10) fold (P=0.778) and (1.59±0.18) fold (P=0.000) of that in control group, respectively, in 100?mg/kg group and 300?mg/kg group. There was no significant difference of the 24 h IA memory retention latency between 100?mg/kg group and control group. The 24 h IA memory retention latency in 300?mg/kg group was significantly decreased compared with control group (P=0.028) and 100?mg/kg group (P=0.020). Conclusion?·?Propofol dose-dependently regulates the expression of BDNF-TrkB/p75 signal molecules, and high dose propofol may reduce cognitive function via BDNF-TrkB/p75 signal.

Cognitive-Enhancing Effect of Dianthus superbus var. Longicalycinus on Scopolamine-Induced Memory Impairment in Mice

Dianthus superbus (D. superbus) is a traditional crude drug used for the treatment of urethritis, carbuncles and carcinomas. The objective of this study was to confirm the cognitive enhancing effect of D. superbus in memory impairment induced mice and to elucidate the possible potential mechanism. Effect of D. superbus on scopolamine induced memory impairment on mice was evaluated using the Morris water maze and passive avoidance tests. We also investigated acetylcholinesterase (AChE) activity and brain-derived neurotropic factor (BDNF) expression in scopolamine-induced mice. HPLC-DAD analysis was performed to identify active compounds in D. superbus. The results revealed that D. superbus attenuated the learning and memory impairment induced by scopolamine. D. superbus also inhibited AChE levels in the hippocampi of the scopolamine-injected mice. Moreover, D. superbus increased BDNF expression in the hippocampus. Eight compounds were identified using HPLC-DAD analysis. The content of 4-hydroxyphenyl acetic acid was higher than contents of other compounds. These results indicated that D. superbus improved memory functioning accompanied by inhibition of AChE and upregulation of BDNF, suggesting that D. superbus may be a useful therapeutic agent for the prevention or treatment of Alzheimer's disease.

Polymorphisms of BDNF Gene and Autism Spectrum Disorders: Family Based Association Study with Korean Trios

OBJECTIVE: Autism spectrum disorders (ASDs) are a group of early childhood-onset neurodevelopmental disorders characterized by deficits in social interaction and language skills, and repetitive behaviors. Brain-derived neurotrophic factor (BDNF) plays a critical role in the differentiation of normal neuronal cells during embryonic and postnatal neuronal development through its neurotrophic effects. METHODS: In this study, we performed a family-based association test (FBAT) between single nucleotide polymorphisms (SNPs; rs6265, rs11030101, rs7103411, and rs7103873) or haplotypes in the BDNF gene and affection status or several quantitative traits characterized by ADI-R with151 Korean trios, including a child diagnosed as ASDs. RESULTS: While no significant association was found between SNPs or haplotypes and the ASDs disease status, a quantitative transmission disequilibrium test (QTDT) by using quantitative traits identified associations of the SNPs (rs6265 and rs11030101) with a domain score for "Restricted, Repetitive and Stereotyped patterns of behavior" (C domain), especially at the subdomain scores for "encompassing preoccupation or circumscribed pattern of interest" (C1) (rs6265A allele, dominant model, p-value=0.019; rs11030101 A allele, additive model, p-value=0.015) and "preoccupations with part of objects or non-functional elements of material" (C4) (rs11030101 A allele, additive model, p-value=0.015) within the ADI-R diagnostic algorithm. In addition, significant associations were also identified between the haplotypes and these quantitative traits (C1, p-value=0.016; C4, p-value=0.012). CONCLUSION: We conclude that BDNF gene polymorphisms have a possible role in the pathogenesis of ASDs.

The effect of 4-Methylcatechol treatment in chronic constrictive injury of the rat sciatic nerve on the allodynia and spinal neurotrophic factors / 대한마취과학회지

BACKGROUND: The effect of chronic administration of 4-methylcatechol known as a neurotrophic factor inducer on the allodynia and spinal neurotrophic factors was investigated in chronic constrictive injury of sciatic nerve in rats. METHODS: With the Sprague Dawly rat, sciatic nerve was loosely ligated with 4-0 chromic catgut and neuropathic pain model was made. The threshold for tactile allodynia was measured with von Frey hair by up-down method and cold allodynia was measured by dropping 20microliter of 100% acetone on the dorsum of the injured foot. 4-Methylcatechol (100microgram/kg, intraperitoneal) was injected once a day for 14 days and the effect on allodynia was compared with saline injected group. At 3, 7 and 14 days after injection, lumbar spinal cord was harvested and the mRNA content of nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF) was measure by real time PCR. RESULTS: Mechanical and cold allodynia improved from 7 days after 4-methylcatechol administration. NGF and BDNF in spinal cord decreased compared to sham operated group. BDNF in lumbar spinal cord has increased tendency after treatment without statistical significance. CONCLUSIONS: Chronic intraperitoneal administration of 4-methylcatechol may improve tactile and cold allodynia in chronic constrictive injury rat model of neuropathic pain. The BDNF mRNA in spinal cord might increase after 4-methylcatechol treatment.

The Change of Neuropathic Pain and Pain Related Gene Expression following Exposure to Chronic Smoking / 대한마취과학회지

BACKGROUND: Several studies have reported reduced pain and anxiety in smokers, and considerable evidence shows that smoking induces analgesia, which is thought to be nicotine-mediated. We investigated if smoking could reduce the development of neuropathic pain and nociceptive transmission in the spinal cord. METHODS: Sprague Dawley rats weighing 130-150 g were used for this experiment. The Animals were divided into two groups: the smoking group (S group) was exposed to cigarette smoking for 5 hours per day for 6 weeks at self-made smoking chamber: the control group (C group) was exposed to room air. After a 4-week exposure period, neuropathic pain was induced by left L5 spinal nerve ligation (SNL). Mechanical threshold and withdrawal response to 100% acetone were measured throughout the experiment. The changes in the expression of the c-fos and BDNF genes in the spinal cord were compared using real time PCR. RESULTS: Mechanical allodynia was induced after SNL in both groups, but no significant difference was observed between two groups. Cold allodynia after SNL was significantly less in S group than C group. In S group, the expression of c-fos was decreased at 5th day, but that of BDNF expression was significantly elevated at 5th day after SNL compared to C group. CONCLUSIONS: Chronic exposure to cigarette smoke reduced the cold allodynia in neuropathic rats. The decreased expression of c-fos and elevated expression of BDNF in the spinal cord after SNL may contribute to antinociception.

Effects of lysophosphatidic acid on morphology proliferation and brain-derived neurotropic factor expression of olfactory ensheathing cells / 中国矫形外科杂志

[Objective]To investigate the effects of lysophosphatidic acid(LPA) on the morphology,proliferation and brain-derived neurotropic factor(BDNF) expression of olfactory ensheathing cells(OECs) in vitro.[Method]Primary cultures of OECs separated from adult rat olfactory bulbs were purified and cultured.Five experimental cultures were grown for a period of time in media with LPA at different concentrations,namely 1,5,10,20 and 50 ?mol/L,and the control culture was grown in the medium without LPA.Immunofluorescent staining was used to identify OECs and to observe their morphological changes.The proliferation of OECs was measured by MTT assay.Western blotting was used to detect the protein expression of BDNF.[Result]Exposure to LPA in medium induced the switch in the dominant morphology of OECs from process-bearing to flat morphology.This shift in morphology was reversed when LPA was removed from media.LPA at concentrations from 1 ?mol/L to 50 ?mol/L enhanced OECs proliferation,especially at the concentration of 10 ?m/L.Proliferation of OECs in all experimental cultures reached their respective significant peaks after 60 h of LPA treatment.There were significant upregulations in BDNF expression of OECs treated with LPA(1~50 ?m/L) compared with those in the control culture.[Conclusion]A reversible change from process-bearing to flat in morphology of OECs can be induced by LPA.LPA stimulates OECs proliferation in a time-and concentration-dependent manner.LPA upregulates BDNF expression of OECs.