Levosulpiride is the 1evo-enantiomer form of racemic sulpiride, a benzamide derivative selectively inhibiting dopaminergic $D_2$ receptors at the trigger zone both in the central nervous system and in the gastrointestinal tract. The purpose of the present study was to evaluate the bioequiva1ence of two levosulpiride tablets, Levopride (SK Pharmaceutical Co., Ltd.) and Levopid (Dae Won Pharmaceutical Co., Ltd.), according to the guidelines of Korea Food and Drug Administration (KFDA). The levosulpiride release from the two levosulpiride tablets in vitro was tested using KP VII Apparatus II method with various different kinds of dissolution media (pH 1.2, 4.0, 6.8 buffer solution and water). Twenty eight normal male volunteers, $23.82{\pm}3.26$ years in age and $69.13{\pm}8.58$ kg in body weight, were divided into two groups and a randomized $2{\times}2$ cross-over study was employed. After one tablet containing 25 mg of levosulpiride was orally administered, blood was taken at predetermined time intervals and the concentrations of levosulpiride in serum were determined using HPLC method with fluorescence detector. The dissolution profiles of two levosulpiride tablets were very similar at all dissolution media. Besides, the pharmacokinetic parameters such as $AUC_t,\;C_{max}\;and\;T_{max}$ were calculated and ANOVA test was utilized for the statistical analysis of the parameters using logarithmically transformed $AUC_t\;and\;C_{max}$ and untransformed $T_{max}$. The results showed that the differences in $AUC_t,\;C_{max}\;and\;T_{max}$ between two tablets based on the Levopride were -1.17%, 1.20% and -1.09%, respectively. There were no sequence effects between two tablets in these parameters. The 90% confidence intervals using logarithmically transformed data were within the acceptance range of log(0.8) to log(1.25) $(e.g.,\;log(0.93){\sim}log(1.07)\;and\;log(0.90){\sim}log(1.14)\;for\;AUC_t\;and\;C_{max}$, respectively). The 90% confidence interval using untransformed data was within ${\pm}20%$$(e.g.,\;-19.47{\sim}16.20\;for\;T_{max})$. All parameters met the criteria of KFDA guideline for bioequivalence, indicating that Levopid tablet is bioequivalent to Levopride tablet.
Objectives : Phencyclidine(PCP) or PCP-like substances such as ketamine have been known to rekindle the cognitive dysfunction in schizophrenia. The aims of this study were to identify whether PCP-like substances can produce cognitive deficit in schizophrenia, to discuss relation with aging process, and finally to speculate underlying neurochemical mecha-nisms by various drug responses. Methods : In experiment I, radial maze tests were done in 24 Sprague-Dawley rats for 3 days to get baseline data. Being divided into 4 groups(6 rats respectively) of normal aged, normal adult controls, atropine-treated and ketamine-treated, the radial maze tests were repeated on every week for 6 weeks, and then the rats were sacrificed by intracardiac perfusion with phosphate-buffered 10% formaldehyde solution for histology. The brain specimen was stained with hematoxylin-eosin to count cells in the prefrontal cortex and hippocampus. In experiment II, radial maze tests were done for 48 rats before any drug treatment and only after ketamine administration. Thereafter, haloperidol, bromocriptine, clonidine, nimodipine, tacrine, valproic acid, naloxone and fluoxetine were intramuscularly injected on every other day in addition to ketamine. Radial maze tests were repeated on every week for 6 weeks, and then rats were prepared by the same procedure for histology. Results : 1) Reaction times of radial maze tests of atropine-treated rats were significantly prolonged than those of normal aged(p<0.05) or normal adult controls(p<0.05). Cell numbers of prefrontal cortex & hippocampus in ketamine-treated rats were significantly reduced than those in normal aged (p<0.05) or normal adult controls(p<0.005). 2) Reduced cell numbers by ketamine became significantly raised by tacrine administration in prefrontal cortex & hippocampus(p<0.05), while there were no significant changes on radial maze tests. Cell numbers also tended to be raised by nimodipine, fluoxetine and haloperidol administration. Conclusions : In conclusion, the visuospatial memory disorders in ketamine-induced psychotic rats might be partly asso-ciated with aging process. Furthermore, the responses to the various drugs suggested cholinergic system might have an important role in the neurochemical mechanism of the cognitive dysfunction in ketamine-induced psychosis. Otherwise, calcium metabolism as well as serotonergic and dopaminergic systems seemed to be possibly related.
We measured the developmental increase of tyrosine hydroxylase(TH) activity and dopamine content with high performance liquid chromatography with electrochemical detection(HPLC-EC) in dissociated cultures of fetal rat brainstem(E14). TH activity and dopamine content increased progressively upto 7 days in vitro, when the effects of various drugs on the dopamine contents were studied. ${\alpha}-Methyl-p-tyrosine$, a TH inhibitor and NSD-1015, an inhibitor of aromatic amiono acid decarboxylase effectively depleted dopamine contents. Dopamine contents were depleted by reserpine and increased by pargyline. When cultures grown for 1 week in control medium were then exposed to tetrodotoxin$(0.1\;{\mu}M$) for 7 days, exposure to tetrodotoxin markedly decreased TH activity. All the above results indicate that dopamine metabolism in the cultered cells reflect reliably the property of brain dopamine metabolism. We suggest that measuring TH activity and dopamine content in brainstem culture with HPLC-EC can be useful tool in the study of pharmacology as well as toxicology of the central dopaminergic system.
Parkinson's disease (PD) is a progressive neurodegenerative disease that mainly affects motor system with clinical features such as bradykinesia, rigidity, tremor and abnormal posture. PD is characterized by the death of dopaminergic neurons in the substantia nigra pars compacta, which is associated with accumulation of oxidative stress and dysregulation of intracellular signaling pathway. Quercetin-3-O-glucuronide (Q3GA), a major metabolite of quercetin, has been reported to have neuroprotective effects. In this study, we examined the neuroprotective effect of Q3GA against 1-methyl-4-phenyl pyridinium ($MPP^+$)-induced neurotoxicity of PD and the underlying molecular mechanisms in SH-SY5Y cells. MTT and LDH assay showed that Q3GA significantly decreased $MPP^+$-induced cell death, which is accompanied by a reduction in poly (ADP-ribose) polymerase (PARP) cleavage. Furthermore, it attenuated $MPP^+$-induced intracellular reactive oxygen species (ROS) with the reduction of Bax/ Bcl-2 ratio. Moreover, Q3GA significantly increased the phosphorylation of Akt and cAMP response element binding protein (CREB), but it has no effects on the phosphorylation of extracellular signal-regulated kinase (ERK). Taken together, these results demonstrate that Q3GA significantly attenuates $MPP^+$-induced neurotoxicity through ROS reduction and Akt/CREB signaling pathway in SH-SY5Y cells. Our findings suggest that Q3GA might be one of the potential candidates for the prevention and/or treatment of PD.
Purpose: It has been postulated that dopamine release in the striatum underlies the reinforcing properties of nicotine. Substantial evidence in the animal studies demonstrates that nicotine interacts with dopaminergic neuron and regulates the activation of the dopaminergic system. The aim of this study was to visualize the dopamine release by smoking in human brain using PET scan with $[^{11}C]raclopride$. Materials and Methods: Five male non-smokers or ex-smokers with an abstinence period longer than 1 year (mean age of $24.4{\pm}1.7$ years) were enrolled in this study $[^{11}C]raclopride$, a dopamine D2 receptor radioligand, was administrated with bolus-plus-constant infusion. Dynamic PET was performed during 120 minutes ($3{\times}20s,\;2{\times}60s,\;2{\times}120s,\;1{\times}180s\;and\;22{\times}300s$). following the 50 minute-scanning, subjects smoked a cigarette containing 1 mg of nicotine while in the scanner. Blood samples for the measurement of plasma nicotine level were collected at 0, 5, 10, 15, 20, 25, 30, 45, 60, and 90 minute after smoking. Regions for striatal structures were drawn on the coronal summed PET images guided with co-registered MRI. Binding potential, calculated as (striatal-cerebellar)/cerebellar activity, was measured under equilibrium condition at baseline and smoking session. Results: The mean decrease in binding potential of $[^{11}C]raclopride$ between the baseline and smoking in caudate head, anterior putamen and ventral striatum was 4.7%, 4.0% and 7.8%, respectively. This indicated the striatal dopamine release by smoking. Of these, the reduction in binding potential in the ventral striatum was significantly correlated with the cumulated plasma level of the nicotine (Spearman's rho=0.9, p=0.04). Conclusion: These data demonstrate that in vivo imaging with $[^{11}C]raclopride$ PET could measure nicotine-induced dopamine release in the human brain, which has a significant positive correlation with the amount or nicotine administered bt smoking.
Kim, Tae Hyun;Kim, Do Hoon;Lee, Sang Kyu;Son, Bong Ki;Jung, Jun Sub
Korean Journal of Biological Psychiatry
/
v.14
no.4
/
pp.232-240
/
2007
Objectives : Vascular endothelial growth factor(VEGF), one of potent cytokines, and its receptors were related with various biological functions and pathological conditions. The purpose of this study was to investigate the changes of serum level of free VEGF, soluble VEGFR-1, and soluble VEGFR-2 after treatment with atypical antipsychotic drug in schizophrenia. Method : The schizophrenic patients were diagnosed with DSM-IV and were prospectively followed up for 4 and 8 weeks. Thirteen schizophrenic patients were evaluated their clinical assessment with serum levels of free VEGF, sVEGFR-1, sVEGFR-2, and positive and negative symptom scale(PANSS) at baseline, 4 weeks, and 8 weeks after treatment with atypical antipsychotic drug. Thirteen normal control subjects were recruited and matched with the patient group by age and sex. Result : The serum level of free VEGF($295.2{\pm}43.7$pg/ml)and sVEGFR-2($8259{\pm}336.7$) at baseline(before treatment) in schizophrenic patients were not significantly different, compared with the control group($199.0{\pm}28.8$ and $8481{\pm}371.9$) respectively. However, the serum level of sVEGFR-1($86.2{\pm}10.3$, p<0.05) was significantly increased in the schizophrenic patients compared with the control group($59.0{\pm}6.4$). After treatment with antipsychotic drug, the serum levels of free VEGF at 4 weeks($338.9{\pm}56.5$) and 8 weeks($309.5{\pm}58.7$) were not significantly, different compared with baseline. But the serum levels of sVEGFR-1 was significantly decreased at 8 weeks ($57.3{\pm}6.3$, p<0.05) after antipsychotic drug treatment. The serum levels of sVEGFR-2 were decreased at 4 weeks ($7761{\pm}403.0$, p<0.05) and 8 weeks($7435{\pm}333.5$, p<0.05) compared with baseline. Conclusion : The decreased serum level of sVEGFR-1 and sVEGFR-2 might be affected by dopaminergic system which was influenced by antipsychotic drug.
In view of the facts that dopamine (DA) when given directly into a lateral ventricle (i.c.v.) of the rabbit brain induces antidiuresis and that haloperidol, a non-specific antagonist of DA receptors, produces anti-diuresis in smaller doses and diuresis and natriuresis in larger doses, the present study was undertaken to delineate the roles of various DA receptors involved in the center-mediated regulation of renal function. Bromocriptine (BRC), a relatively specific agonist of D-2 receptors and at the same time a D-,1 antagonist, elicited natriuresis and diuresis when given i.c.v. in doses ranging from 20 to 600 {\mu}g/kg$, roughly in dose-related fashion, while the renal perfusion and glomerular filtration progressively decreased with doses, indicating that the diuretic, natriuretic action resides in the tubules, not related to the hemodynamic effects. These diuresis and natriuresis were most marked with 200 ${\mu}g/kg$, with the fractional sodium excretion reaching about 10%. With 600 ${\mu}g/kg$, however, the diuretic, natriuretic action was preceded by a transient oliguria resulting from severe reduction of renal perfusion, concomitant with marked but transient hypertension. When given intravenously, however, BRC produced antidiuresis and antinatriuresis along with decreases in renal hemodynamics associated with systemic hypotension, thus indicating that the renal effects produced by i.c.v. BRC is not caused by a direct renal effects of the agent which might have reached the systemic circulation. In experiments in which DA was given i.c.v. prior to BRC, 150 ${\mu}g/kg$ DA did not affect the effects of BRC (200 ${\mu}g/kg$), while 500 ${\mu}g/kg$ DA abolished the BRC effect. In rabbits treated with reserpine, 1 mg/kg i.v.,24 h prior to the experiment, i.c.v. BRC could unfold its renal effects not only undiminished but rather exaggerated and more promptly. In preparations in which one kidney is deprived of nervous connection, the denervated kidney responded with marked diuresis and natriuresis, whereas the innervated, control kidney exhibited antidiuresis. These observations suggest that i.c.v. BRC influences the renal function through release of some humoral natriuretic factor as well as by increasing sympathetic tone, and that various DA receptors might be involved with differential roles in the center-mediated regulation of the renal function.
Kim, Bom-Sahn;Jang, Sung-June;Eo, Jae-Seon;Park, Eun-Kyung;Kim, Yu-Kyeong;Kim, Jong-Min;Lee, Won-Woo;Kim, Sang-Eun
Nuclear Medicine and Molecular Imaging
/
v.41
no.4
/
pp.272-279
/
2007
Purpose: The aim of this study was to evaluate the discriminating nature of $^{123}I-FP-CIT$ SPECT in patients with parkinsonism. Methods: $^{123}I-FP-CIT$ SPECT images acquired from the 18 normal controls; NC ($60.4{\pm}10.0$ yr) and 237 patients with parkinsonism ($65.9{\pm}9.2$ yr) were analyzed. From spatialIy normalized images, regional counts of the caudate, putamen, and occipital lobe were obtained using region of interest method. Binding potential (BP) was calculated with the ratio of specific to nonspecific binding activity at equilibrium. Additionally, the BP ratio of putamen to caudate (PCR) and asymmetric Index (ASI) were measured. Results: BPs of NC $3.37{\pm}0.57,\; 3.10{\pm}0.41,\; 3.23{\pm}0.48$ for caudate, putamen, whole striatum, respectively) had no significant difference with those of essential tremor; ET ($3.31{\pm}0.64,\; 3.06{\pm}0.61,\; 3.14{\pm}0.63$) and Alzheimer's disease; AD (3.33 $\pm$0.60, 3.29$\pm$0.79, 3.31$\pm$0.70), but were higher than those of Parkinson's disease; PD (1.92$\pm$0.74, 1.39$\pm$0.68, 1.64$\pm$0.68), multiple system atrophy; MSA (2.36$\pm$1.07, 2.16$\pm$0.91, 2.26$\pm$0.96), and dementia with Lewy body; DLB (1.95$\pm$0.72, 1.64$\pm$0.65, 1.79$\pm$0.66)(p<0.005). PD had statisticalIy lower values of PER and higher values of ASI than those of NC (p<0.005). And PD had significantIy lower value of PCR, higher ASI and lower BP in the putamen and whole striatum than MSA (p<0.05). Conclusion: Dopamine transporter image of $^{123}I-FP-CIT$ SPECT was a good value in differential diagnosis of parkinsonism.
Purpose: Attention deficit hyperactivity disorder (ADHD) has been known as psychiatric disorder in childhood associated with dopamine dysregulation. In present study, we investigated changes in dopamine transporter (DAT) density of the basal ganglias using I-123 N-(3-iodopropen-2-yl) -2-carbomethoxy-3beta-(4-chlorophenyl) tropane [I-123 IPT] SPECT in children with ADHD before and after methylphenidate treatment. Materials and Method: Nine drug-naive children with ADHD and seven normal children were included in the study. We peformed brain SPECT two hours after the intravenous administration of I-123 IPT and made both quantitative and qualitative analyses using the obtained SPECT data, which were reconstructed for the assessment of soecific/nonspecific DAT binding ratios in the basal ganglia. All children with ADHD reperformed [123I]IPT SPECT after treatment with methylphenidate(0.7mg/kg/d) during about 8 weeks. SPECT data reconstructed for the assessment of specific/nonspecific DAT binding ratio of the basal ganglia were compared between before and after treatment methylphenidate. We investigated correlation between the change of ADHD symptom severity assessed with ADHD rating scale-IV and specific/nonspecific DAT binding ratio of basal ganglia. Results: Children with ADHD had a significantly greater specificinonspecific DAT binding ratio of the basal ganglia comparing to normal children(Right : z = 2.057, p = 0.041 : Left : z : 2.096, p = 0.032). Under treatment with methylphenidate in all children with ADHD, specificinonspecific DAT binding ratio of both basal ganglia decreased significantly greater than before treatment with methylphenidate (Right : t = 3.239, p = 0.018 ; Left : t = 3.133, p = 0.020). However, no significant correlation between the change of ADHD symptom severity scores and specific/nonspecific DAT binding ratio of the basal ganglia were found. Conclusions: These findings support the complex dysregulation of the dopaminergic neurotransmitter system in children with ADHD.
Purpose: We investigated quantification of dopaminergic transporter (DAT) and serotonergic transporter (SERT) on $^{123}I$-FP-CIT SPECT for differentiating between multiple systemic atrophy (MSA) and idiopathic Parkinson's disease (IPD). Materials and Methods: N-fluoropropyl-$2{\beta}$-carbomethoxy-$3{\beta}$-4-[$^{123}I$]-iodophenylnortropane SPECT ($^{123}I$-FP-CIT SPECT) was performed in 8 patients with MSA (mean age: $64.0{\pm}4.5yrs$, m:f=6:2), 13 with early IPD (mean age: $65.5{\pm}5.3yrs$, m:f=9:4), and 12 healthy controls (mean age: $63.3{\pm}5.7yrs$, m:f=8:4). Standard regions of interests (ROls) of striatum to evaluate DAT, and hypothalamus and midbrain for SERT were drawn on standard template images and applied to each image taken 4 hours after radiotracer injection. Striatal specific binding for DAT and hypothalamic and midbrain specific binding for SERT were calculated using region/reference ratio based on the transient equilibrium method. Group differences were tested using ANOVA with the postHoc analysis. Results: DAT in the whole striatum and striatal subregions were significantly decreased in both patient groups with MSA and early IPD, compared with healthy control (p<0.05 in all). In early IPD, a significant increase in the uptake ratio in anterior and posterior putamen and a trend of increase in caudate to putamen ratio was observed. In MSA, the decrease of DAT was accompanied with no difference in the striatal uptake pattern compared with healthy controls. Regarding the brain regions where $^{123}I$-FP-CIT binding was predominant by SERT, MSA patients showed a decrease in the binding of $^{123}I$-FP-CIT in the pons compared with controls as well as early IPD patients (MSA: $0.22{\pm}0.1$ healthy controls: $0.33{\pm}0.19$, IPD: $0.29{\pm}0.19$), however, it did not reach the statistical significance. Conclusion: In this study, the differential patterns in the reduction of DAT in the striatum and the reduction of pontine $^{123}I$-FP-CIT binding predominant by SERT could be observed in MSA patients on $^{123}I$-FP-CIT SPECT. We suggest that the quantification of SERT as well as DAT using $^{123}I$-FP-CIT SPECT is helpful to differentiate parkinsonian disorders in early stage.
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