OBJECTIVES: The purpose of this study was to investigate the deficits in executive function in children with ADHD and anxiety disorder, and further, to characterize executive function deficits among the two groups. METHODS: Subjects consisted of 60 children between the ages of 5 and 14 (16 Normal, 24 ADHD, 20 Anxiety Disorder). Neuropsychological tests (KEDI-WISC, CCTT, STROOP, WCST, ROCF) for assessing cognitive and executive function were individually administered to all subjects. RESULTS: There were no significant differences in FSIQ or PIQ among the three groups. However, the ADHD group tended to score lower on the VIQ and subtest of similarity, vocabulary, and digit span tests. The three groups did not significantly differ with respect to CCTT test results. On the STROOP test, the ADHD group showed poor performance on the word, color, and color-word subtests. The three groups did not exhibit significant differences in WCST test results ; however, the anxiety group performed poorly belonging to below 25 percentile rank on perseverative response. On the ROCF test, the ADHD group performed poorly with respect to their organization score and in particular, regarding copy and immediate recall. The anxiety group also performed poorly with regard to organization ; however, this was limited only to immediate recall. CONCLUSION: Children with ADHD displayed poor inhibition and organizational abilities compared to children with anxiety and normal controls. Further, children with anxiety disorder exhibited low cognitive flexibility and voluntary problem-solving abilities compared to ADHD children and normal controls. Based on these results, we suggest that the characteristics of executive dysfunction in ADHD and anxiety disorder in children are different.
Anxiety ; Anxiety Disorders ; Child ; Coat Protein Complex I ; Executive Function ; Humans ; Memory, Short-Term ; Neuropsychological Tests ; Pliability ; Stroop Test ; Vocabulary

Purpose: Poloxamer-407 (P-407) is used to induce hyperlipidemia. Exercise is effective in improving arteriosclerosis and cognitive impairment. In this research, the effect of treadmill running on short-term memory in the P-407-treated hyperlipidemia rats was studied focusing on neuroinflammation. Methods: Rats were classified in normal group, normal and treadmill exercise group, P-407-treated group, and P-407-treated and treadmill exercise group. Hyperlipidemia rats were made by single intraperitoneal injection with P-407 (500 mg/kg). Treadmill exercise was conducted for 30 minutes once a day, 5 days per week during 28 days. Step-down avoidance task was done to measure short-term memory. Glial fibrillary acidic protein and ionized calcium binding adaptor molecule 1 were assessed by immunohistochemistry. Expression of adhesion molecules and proinflammatory cytokines was determined by western blot analysis. Results: Treadmill exercise alleviated lipid profiles in the P-407-induced hyperlipidemia rats. Treadmill exercise improved short-term memory, inhibited reactive astrogliosis and microglia activation, and suppressed expression of adhesion molecules and proinflammatory cytokines in the hyperlipidemic rats. Conclusions Treadmill exercise exerts alleviating effect on memory deficits by inhibiting hippocampal neuroinflammation in the hyperlipidemia. The current results suggest that treadmill running serves as the treatment strategy for the cognitive dysfunction caused by hyperlipidemia.

Amygdalin is known as vitamain B17, and it was called laetrile. Amygdalin is composed of two molecules of glucose, one molecule of benzaldehyde which induces an analgesic action, and one molecule of hydrocyanic acid which is an anti-neoplastic compound. Amygdalin had been used to treat cancers and relieve pain. In order to evaluate whether the analgesic action of amygdalin is related with descending pain control system, we performed patch clamp study. In the present study, the modulatory effects of amygdalin on glycine- and glutamate-induced ion currents in periaqueductal gray (PAG) neurons were investigated using the nystatin-perforated patch clamp method. Continuous application of lipopolysaccharides (LPS) on PAG neurons resulted in increased glycine-induced ion current, and in decreased glutamate-induced ion current. In contrast, continuous application of amygdalin with LPS resulted in decreased glycine-induced ion current increased by LPS, and increased glutamate- induced ion current decreased by LPS in concentration- and time-dependent fashion. These results demonstrate that amygdalin modulates neuronal activity of PAG by modulation of glycine and glutamate. Based on the present results, it can be suggested that amygdalin participates in the regulation of the descending pain control system in the level of PAG neurons. The present study demonstrated that activation of the descending pain control system is one of the possible analgesic mechanisms of amygdalin.
Amygdalin ; Animals ; Benzaldehydes ; Cyclooxygenase 2 ; Glucose ; Glutamic Acid ; Glycine ; Hydrogen Cyanide ; Lipopolysaccharides ; Neurons ; Periaqueductal Gray ; Rats

PURPOSE: Rocuronium bromide is a nondepolarizing neuromuscular blocking drug and has been used as an adjunct for relaxation or paralysis of the skeletal muscles, facilitation of endotracheal intubation, and improving surgical conditions during general anesthesia. However, intravenous injection of rocuronium bromide induces injection pain or withdrawal movement. The exact mechanism of rocuronium bromide-induced injection pain or withdrawal movement is not yet understood. We investigated whether rocuronium bromide treatment is involved in the induction of inflammation and pain in vascular endothelial cells. METHODS: For this study, calf pulmonary artery endothelial (CPAE) cells were used, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, Western blot, nitric oxide detection, and prostaglandin E2 immunoassay were conducted. RESULTS: Rocuronium bromide treatment inhibited endothelial nitric oxide synthase and suppressed nitric oxide production in CPAE cells. Rocuronium bromide activated cyclooxygenase-2, inducible nitric oxide synthase and increased prostaglandin E2 synthesis in CPAE cells. CONCLUSIONS: Rocuronium bromide induced inflammation and pain in CPAE cells. Suppressing nitric oxide production and enhancing prostaglandin E2 synthesis might be associated with rocuronium bromide-induced injection pain or withdrawal movement.
Anesthesia, General ; Blotting, Western ; Cyclooxygenase 2 ; Dinoprostone* ; Endothelial Cells* ; Immunoassay ; Inflammation* ; Injections, Intravenous ; Intubation, Intratracheal ; Muscle, Skeletal ; Neuromuscular Blockade ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; Nitric Oxide* ; Paralysis ; Pulmonary Artery ; Relaxation

PURPOSE: Cerebral ischemia leads to neuronal cell death, and eventually causes neurological impairments. Tadalafil is a long-acting phosphodiesterase type-5 (PDE-5) inhibitor, and it has been used for the treatment of erectile dysfunction. In the present study, we investigated whether tadalafil has the protective effect on apoptotic neuronal cell death in the motor cortex following transient global ischemia in gerbils. MATERIALS AND METHODS: For this study, Mongolian gerbils were used for the experimental animals, and transient global ischemia was induced to the gerbils by occlusion of both common carotid arteries for 7 min. Gerbils were randomly divided into five groups (n=8 in each group): the sham-operation group, the cerebral ischemia-induced group, the cerebral ischemia-induced and 0.1 mg/kg tadalafil-treated group, the cerebral ischemia-induced and 1 mg/kg tadalafil-treated group, the cerebral ischemia-induced and 10 mg/kg tadalafil-treated group. Tadalafil-treated groups received tadalafil orally once a day for a 7 consecutive days, starting one day after surgery. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and immunohistochemistry for caspase-3 were performed for the detection of apoptotic neuronal cell death in the motor cortex. RESULTS: The number of TUNEL-positive cells was 21.45+/-3.69/section in the sham-operation group, 771.66+/-97.25/section in the cerebral ischemia-induced group, 688.44+/-81.35/section in the cerebral ischemia-induced and 0.1 mg/kg tadalafil-treated group, 295.66+/-36.34/section in the cerebral ischemia-induced and 1 mg/kg tadalafil-treated group, and 198.47+/-25.25/section in the cerebral ischemia-induced and 10 mg/kg tadalafil-treated group. In the present results, induction of ischemic injury increased apoptotic neuronal cell death in the motor cortex of gerbils. However, tadalafil treatment suppressed the cerebral ischemia-induced apoptotic neuronal cell death in the motor cortex as dose-dependently. CONCLUSIONS: Here in this study, we showed that tadalafil has protective effect on the cerebral ischemia-induced apoptotic neuronal cell death, and thus this drug may facilitate the recovery following ischemic cerebral injury.
Animals ; Apoptosis ; Brain Ischemia ; Carbolines ; Carotid Artery, Common ; Caspase 3 ; Cell Death ; Erectile Dysfunction ; Gerbillinae ; Immunohistochemistry ; Ischemia ; Male ; Motor Cortex ; Neurons ; Polyenes ; Tadalafil

PURPOSE: Neurogenic lower urinary tract dysfunction (NLUTD) is a possible consequence of several neurological disorders. NLUTD may produce debilitating symptoms and serious complications, such as chronic renal failure, and recurrent urinary tract infections. Many animal studies of NLUTD symptoms have focused on animal models of cerebral ischemia. In the present study, we investigated the effects of treadmill exercise on memory function and its relation to cell proliferation and apoptosis in the hippocampus, following transient global ischemia in gerbils. METHODS: To induce transient global ischemia in gerbil, both common carotid arteries were occluded for 5 minutes. Gerbils in the exercise groups were forced to run on a treadmill exercise for 30 minutes once a day for 2 weeks. Step-down avoidance task and Y maze task were performed. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-staining, immunohistochemistry for 5-bromo-2'-deoxyridine, doublecortin, caspase-3, and Western blot for brain-derived neurotrophic factor (BDNF), Bax, Bcl-2, cytochrome c, caspase-3 were conducted. RESULTS: Ischemia caused memory impairment with an increase of cell proliferation, BDNF expression, and apoptosis in the hippocampus. Treadmill exercise improved memory function with further increase of cell proliferation and BDNF expression and a decrease of apoptosis. CONCLUSIONS: The animal model that we have developed and our assessment of the relation between exercise and brain function can be useful tools for future investigations of NLUTD symptoms associated with stroke, particularly ischemic stroke. The present study suggests that treadmill exercise promoted the recovery of brain function after cerebral ischemia.
Animals ; Apoptosis* ; Blotting, Western ; Brain ; Brain Ischemia ; Brain-Derived Neurotrophic Factor ; Carotid Artery, Common ; Caspase 3 ; Cell Proliferation* ; Cytochromes c ; Exercise Test ; Exercise* ; Gerbillinae ; Hippocampus* ; Immunohistochemistry ; Ischemia ; Kidney Failure, Chronic ; Memory* ; Models, Animal ; Nervous System Diseases ; Neurons* ; Stroke ; Urinary Tract ; Urinary Tract Infections

PURPOSE: The overactive bladder (OAB) syndrome is characterized by urgency usually with frequency and nocturia. Tamsulosin, alpha1-adrenergic receptor antagonist, is widely used to reduce symptoms of urinary obstruction and prostatic hyperplasia. Tamsulosin can across the blood-brain barrier. We investigated the effects of tamsulosin on the symptoms of OAB in relation to neuronal activity using rats. METHODS: Adult female Sprague-Dawley rats, weighing 250+/-10 g (9 weeks old), were used in this study. The animals were divided into five groups (n=8 in each group): control group, OAB-induced group, OAB-induced and 0.01 mg/kg tamsulosin-treated group, OAB-induced and 0.1 mg/kg tamsulosin-treated group, and OAB-induced and 1 mg/kg tamsulosin-treated group. OAB was induced by intraperitoneal injection of cyclophosphamide (75 mg/kg) every third day for 10 days. The rats in the tamsulosin-treated groups orally received tamsulosin once a day for 14 consecutive days at the respective dose of the groups, starting 1 day after the induction of OAB. Cystometry for bladder pressure determination, immunohistochemistry for c-Fos, nicotinamide adenine dinucleotide phosphate-diaphorase histochemistry for nitric oxide synthase (NOS) in the neuronal voiding centers and western blot for inducible NOS in the bladder were conducted. RESULTS: Cyclophosphamide injection enhanced contraction pressure and time, representing the induction of OAB. Contraction pressure and time were significantly suppressed by tamsulosin treatment. c-Fos and NOS expressions in the neuronal voiding centers were enhanced by induction of OAB. OAB-induced c-Fos and NOS expressions were suppressed by tamsulosin treatment. CONCLUSIONS: Tamsulosin exerts inhibitory effect on neuronal activation in the neuronal voiding centers of OAB. The present results suggest the possibility that tamsulosin is effective therapeutic modality for ameliorating the symptoms of OAB.
Adult ; Animals ; Blood-Brain Barrier ; Blotting, Western ; Contracts ; Cyclophosphamide ; Female ; Humans ; Immunohistochemistry ; Injections, Intraperitoneal ; NAD ; Neurons ; Nitric Oxide Synthase ; Nocturia ; Prostatic Hyperplasia ; Rats ; Rats, Sprague-Dawley ; Sulfonamides ; Urinary Bladder ; Urinary Bladder, Overactive

PURPOSE: Berberine is a type of isoquinoline alkaloid that has been used to treat various diseases. A neuroprotective effect of berberine against cerebral ischemia has been reported; however, the effects of berberine on apoptosis in relation to reactive astrogliosis and microglia activation under ischemic conditions have not yet been fully evaluated. In the present study, we investigated the effects of berberine on global ischemia-induced apoptosis, and focused on the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway in the hippocampus using gerbils. METHODS: Gerbils received berberine orally once a day for 14 consecutive days, starting one day after surgery. In this study, a step-down avoidance task was used to assess short-term memory. Furthermore, we employed the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay to evaluate DNA fragmentation, immunohistochemistry to investigate glial fibriallary acidic protein, CD11b, and caspase-3, and western blot to assess PI3K, Akt, Bax, Bcl-2, and cytochrome c. RESULTS: Our results revealed that berberine treatment alleviated ischemia-induced short-term memory impairment. Treatment with berbeine also attenuated ischemia-induced apoptosis and inhibited reactive astrogliosis and microglia activation. Furthermore, berberine enhanced phospho-PI3K and phospho-Akt expression in the hippocampus of ischemic gerbils. CONCLUSIONS: Berberine exerted a neuroprotective effect against ischemic insult by inhibiting neuronal apoptosis via activation of the PI3K/Akt signaling pathway. The antiapoptotic effect of berberine was achieved through inhibition of reactive astrogliosis and microglia activation. Berberine may therefore serve as a therapeutic agent for stroke-induced neurourological problems.
Apoptosis* ; Berberine* ; Blotting, Western ; Brain Ischemia ; Caspase 3 ; Cytochromes c ; DNA Fragmentation ; Gerbillinae ; Hippocampus ; Immunohistochemistry ; Memory, Short-Term ; Microglia ; Neurons ; Neuroprotective Agents ; Phosphatidylinositol 3-Kinases ; Phosphotransferases*

This study was conducted to evaluate the effects of vardenafil (Levitra), a phosphodiesterase-5 (PDE-5) inhibitor, on cell proliferation in the hippocampal dentate gyrus and on 5-hyroxytryptamine (5-HT, serotonin) synthesis and tryptophan hydroxylase (TPH) expression in the rat dorsal raphe nucleus. Male Sprague-Dawley rats were divided into 6 groups (n=5 in each group): a control group, a 0.5 mg/kg-1 day vardenafil-treated group, a 1 mg/kg-1 day vardenafil-treated group, a 2 mg/kg-1 day vardenafil-treated group, a 1 mg/kg-3 day vardenafil-treated group, and a 1 mg/kg-7 day vardenafil-treated group. 5-bromo-2'-deoxyuridine (BrdU) immunohistochemistry was then performed to evaluate cell proliferation in the dentate gyrus. In addition, 5-HT and TPH immunohistochemistry was conducted to evaluate serotonin expression in the dorsal raphe. The results revealed that treatment with vardenafil increased cell proliferation in the dentate gyrus and enhanced 5-HT synthesis and TPH expression in the dorsal raphe in a dose- and duration-dependent manner. The findings demonstrate that the increasing effect of vardenafil on cell proliferation is closely associated with the enhancing effect of vardenafil on serotonin expression under normal conditions.
Animals ; Cell Proliferation/*drug effects ; *Dentate Gyrus/cytology/drug effects/metabolism ; Imidazoles/*pharmacology ; Male ; Phosphodiesterase Inhibitors/*pharmacology ; Piperazines/*pharmacology ; *Raphe Nuclei/cytology/drug effects/metabolism ; Rats ; Rats, Sprague-Dawley ; Serotonin/*biosynthesis ; Sulfones/pharmacology ; Triazines/pharmacology ; Tryptophan Hydroxylase/metabolism

Peripheral nerve injuries are a commonly encountered clinical problem and often result in a chronic pain and severe functional deficits. c-Fos expression is sometimes used as a marker of increased neuronal activity. We have developed herbal bath "HAC" for pain control using the following herbs: Harpagophytum procumbens, Atractylodes japonica, and Corydalis tuber. In the present study, we investigated the effects of herbal bath "HAC" on the recovery rate of the locomotor function and the expression of c-Fos in the ventrolateral periaqueductal gray (vlPAG) region of brain following sciatic crushed nerve injury in rats. Walking track analysis for the evaluation of functional recovery and immunohistochemistry for the c-Fos expression were used for this study. In the present results, characteristic gait change with dropping of the sciatic function index (SFI) was observed and c-Fos expression in the vlPAG was suppressed following sciatic crushed nerve injury in rats. Immersion into herbal bath "HAC" enhanced SFI value and restored c-Fos expression in the vlPAG to the control value. These results suggest that herbal bath "HAC" might activate neurons in the vlPAG, and it facilitates functional recovery from peripheral nerve injury. Here we showed that herbal bath "HAC" could be used as a new therapeutic intervention for pain control and functional recovery from peripheral nerve injury.
Animals ; Atractylodes ; Baths ; Brain ; Chronic Pain ; Corydalis ; Gait ; Harpagophytum ; Immersion ; Immunohistochemistry ; Neurons ; Periaqueductal Gray ; Peripheral Nerve Injuries ; Rats ; Track and Field ; Walking