• The Korean Journal of Nuclear Medicine
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• v.36 no.5
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• pp.277-287
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• 2002

Purpose and Methods: We investigated the effect of ginseng total saponin (GTS) on nicotine-induced dopamine (DA) release in the striatum and nucleus accumbens of freely moving rats using in vivo microdialysis technique. Results: Systemic pretreatment with GTS decreased striatal DA release induced by local infusion of nicotine into the striatum. However, GTS had no effect on the resting levels of extracellular DA in the striatum. GTS also blocked nicotine-induced DA release in the nucleus accumbens. Conclusion: The results of the present study suggest that GTS acts on the DA terminals to prevent DA release induced by nicotine. This may reflect the blocking effect of GTS on behavioral hyperactivity induced by psychostimulants.

• Nuclear Medicine and Molecular Imaging
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• v.41 no.2
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• pp.158-165
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• 2007

Technological advances in molecular imaging made it possible to image synaptic neurotransmitter concentration in living human brain. The dopaminergic system has been most intensively studied because of its importance in neurological as well as psychiatric disorders. This paper provides a brief overview of recent progress in imaging studies of dopamine release induced by pharmacologic and nonpharmacologic stimulations.

• Journal of Acupuncture Research
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• v.20 no.4
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• pp.24-41
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• 2003

Objective: Dopamine activity in thenucleus accumbens is an important neuropharmacological component of morphine reinforcement. In this nucleus a shell and core have been distinguished on the basis of anatomical and neurochemical criteria. Although acupuncture has been standard intervention in many detoxication programs worldwide, the central mechanism by which morphine acts to reinforce behavior remain elusive. The present in vivo microdialysis study was conducted, in freely moving rats, to detect the effects of acupuncture on extracellular dopamine release in the nucleus accumbens. Methods: Male Sprague-Dawley rats received acupuncture for 1 min after injection of morphine hydrochloride (5mg/kg, s.c.). The employed acupuncture needle points corresponded to bilateral Neiguan(PC6) on the pericardium channel, which has been used to treat mental and psychosomatic disorders. Extracellular dopamine and its metabolites were measured every 20 mins for 3 hrs following the subcutaneous morphine injection. Results: Results showed that acupuncture at PC6 significantly attenuated increases in dopamine levels induced by a single acute morphine injection in the nucleus accumbens shell and core, respectively. Conclusions: These results provided strong evidence for acupuncture-mediated reduction in morphine-induced dopamine release in the rat nucleus accumbens.

• Animal cells and systems
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• v.3 no.2
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• pp.103-113
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• 1999

Many in-depth reviews related to regulations of prolactin secretion are available. We will, therefore, focus on controversial aspects using personal opinion in this review. The neuroendocrine control of prolactin secretion from the anterior pituitary gland involves multiple factors including prolactin-release inhibiting factor (PIF) and prolactin releasing factor (PRF). The PIF exerts a tonic inhibitory control in the physiological conditions. The PIF should be able to effectively inhibit prolactin release or a lifetime, but the inhibitory action of dopamine cannot be sustained for a long period of time. Perifusion of a high concentration of dopamine (l ,000 nM) could not sustain inhibitory action on prolactin release but when a small amount of ascorbic acid (0.1 mM) is added in a low concentration of dopamine (3 nM) solution, prolactin release was inhibited for a long period. Ascorbate is essential for dopamine action to inhibit prolactin release. We have, therefore, concluded that the PIF is dopamine plus ascorbate. The major transduction system for dopamine to inhibit prolactin release is the adenylyl cyclase system. Dopamine decreases cyclic AMP concentration by inhibiting adenylyl cyclase, and cyclic AMP stimulates prolactin release. However, the inhibitory mechanism of dopamine on prolactin release is much more complex than simple inhibition of CAMP production. The dopamine not only inhibits cyclic AMP synthesis but also inhibits prolactin release by acting on a link(s) after the CAMP event in a chain reaction for inhibiting prolactin release. Low concentrations of dopamine stimulate prolactin release. Lactotropes are made of several different subtypes of cells and several different dopamine receptors are found in pituitary. The inhibitory and stimulatory actions induced by dopamine can be generated by different subtype of receptors. The GH$_4$ZR$_7$ cells express only the short isoform (D$_{2s}$) of the dopamine receptor, as a result of transfecting the D$_{2s}$ receptors into GH$_4$C$_1$ cells which do not express any dopamine receptors. When dopamine stimulates or inhibits prolactin release in GH$_4$ZR$_7$ cells, it is clear that the dopamine should act on dopamine D$_{2s}$ receptors since there is no other dopamine receptor in the GH$_4$ZR$_7$. Dopamine is able to stimulate prolactin release in a relatively low concentration while it inhibits in a high concentration in GH$_4$ZR$_7$. These observations indicate that the dopamine D$_2$ receptor can activate stimulatory and/or inhibitory transduction system depending upon dopamine concentrations.

• Natural Product Sciences
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• v.12 no.4
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• pp.217-220
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• 2006

The effects of $(1R,9S)-\beta-hydrastine$ hydrochloride (BHSH) on $Ca^{2+}$ transport in rat pheochromocytoma PC12 cells were investigated. In the presence of external $Ca^{2+}$, BHSH at $100{\mu}M$ inhibited $K^+$ (56mM)-induced dopamine release, and $K^+-induced$ $Ca^{2+}$ influx and a sustained rise of $[Ca^{2+}]_i$. In addition, BHSH at 100 f.!M reduced the sustained rise of $[Ca^{2+}]_i$ elicited by 20 mM caffeine, but not by $1{\mu}M$ thapsigargin, in presence of external $Ca^{2+}$. These results suggest that BHSH inhibited $K^+-induced$ dopamine release and $[Ca^{2+}]_i$ influx, and store-operated $Ca^{2+}$ channels activated by caffeine, but not by thapsigargin, in PC12 cells.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.04a
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• pp.179-179
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• 1996

The involvement of the cyclic AMP (cAMP) effector system in the release of endogenous dopamine and acetylcholine from the rat neostriatum was assessed. Forskolin, an activator of adenylate cyclase, was used to enhance CAMP production, and the consequence of this enhancement on the spontaneous and potassium stimulated release of dopamine and acetylcholine was evaluated. Neostriatal slices were prepared from Fischer 344 rats and after a preincubation period the release of each endogenous neurotransmitter was measured from the same slice preparation. To measure acetylcholine release the slice acetylcholinesterase (AChE) activity was inhibited with physostigmine, but the release from slices with intact AChE activity was also determined (choline, instead of acetylcholine was detected in the medium). Under both conditions forskolin induced a significant dose-dependent increase in the potassium-evoked release of dopamine. In the same tissue preparations the release of neither acetylcholine (AChE inhibited) nor choline (AChE intact) was affected by forskolin. The results indicate that the cAMP second messenger system is involved ill neuronal mechanisms that enhance neuronal dopamine release, but stimulation of this second messenger by forskolin does not further enhance neostriatal acetylcholine release.

• Biomolecules & Therapeutics
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• v.10 no.3
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• pp.152-158
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• 2002

The present study elucidated the effect of $\beta$-carbolines (harmaline and harmalol) on brain mitochondlial dysfunction caused by the tyrosinase-induced oxidation of dopamine. Harmaline, harmalol and antioxidant enzymes (SOD and catalase) attenuated the dopamine-induced alteration of membrane potential, cytochrome c release and thiol oxidation in mitochondria. In contrast, antioxidant enzymes failed to reverse mitochondrial dysfunction induced by dopmnine plus tyrosinase. $\beta$-Carbolines decreased the damaging effect of dopamine plus tyrosinase against mitochondria, except no effect of harmalol on thiol oxidation. Antioxidant enzymes decreased the melanin formation from dopamine in the reaction mixture containing mitochondria but did not reduce the formation of dopamine quinone caused by tyrosinase. Both harmalol and harmaline inhibited the formation of reactive quinone and melanin. Harmalol being more effective for quinone formation and vise versa. The results indicate that compared to MAO-induced dopamine oxidation, the toxic effect of dopamine in the presence of tyrosinase against mitochondria may be accomplished by the dopamine quinone and toxic substances other than reactive oxygen species. $\beta$-Carbolines may decrease the dopamine plus tyrosinase-induced brain mitochondrial dysfunction by inhibition of the formation of reactive quinone and the change in membrane permeability.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.5
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• pp.1149-1154
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• 2006

Repeated administration of all addictive drugs, including nicotine, can produce sensitization of extracellular dopamine levels in the nucleus accumbens and behavioral sensitization in rat, as evidenced by an enhanced locomotor response and increased dopamine release in brain to a subsequent injection of the drug. In order to investigate the effect of Zizyphus jujuba extract on repeated nicotin-induced sensitization, rats were given repeated injection of saline or nicotine (0.4 mg/kg s.c., twice a day for 7 d), followed by one challenge injection on the 4th day after the last daily injection. Systemic challenge with nicotine (0.4 mg/kg s.c.) and a direct local challenge of 3 mM a larger increase in locomotor activity and extracellular dopamine release in the nucleus accumbens in nicotine-pretreated rats than in saline-pretreated rats, respectively. Zizyphus jujuba extract significantly decreases locomotor activitiy and dopamine release in the nucleus accumbens induced by a nicotine challenge. These results suggest that Zizyphus jujuba extract may attenuate nicotine-induced neurochemical and behavioral sensitization and may be effective in suppressing compulsive nicotine-seeking behavior.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.97.2-97.2
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• 2003

(1R,9S)-(${\beta}$)-Hydrastine (HS) at 10-50 ${\mu}$M has been proven to have an inhibitory effect on dopamine biosynthesis in PC12 cells by the inhibition of tyrosine hydroxylase (TH) activity and TH gene expression. In the present study, therefore, the effects of HS on the basal and K$\^$+/-induced dopamine release, and Ca$\^$2+/ influx induced by high K$\^$+/ and caffeine in PC12 cells were investigated. The dopamine release by high K$\^$+/ (56 mM) was inhibited by co-incubation of 20 ${\mu}$M HS. Application of HS also significantly reduced the magnitude of the maintained Ca$\^$2+/ influx induced by K$\^$+/ depolarization. (omitted)

• Archives of Pharmacal Research
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• v.18 no.4
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• pp.271-276
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• 1995

Changes in the distribution of dopamine and its metabolites, activities of monoamine oxidase, and dopamine uptake were studied inhyperglycemic rat striatum. The hyperglycemia was induced by the administration of streptozotocin (STZ, 40 mg/kg, i.p. for 3 days.). The levels of dihydroxyphenylacetic acid (DOPAC) and homovanillic acid were significantly decreased without change in dopamine level in the synatic cleft 14 days after STZ treatment. In the synaptosome, the dopamine level, however, was significanly increased after the treatment. But the DOPAC level in the synaptosome was decreased 14 days after the treatment. The affinity of dopamine uptake was significantly decreased without changes in the velocity 14 days after the treatment. However the response to uptqke inhibitor was unchanged. The striatal monoamine oxidase activities were also decreased in the hyperglycemic state. These results indicate that various parameters of striatal dopamine activities were decreased in the hyperglycemic rats. Furthermore, it suggests that the increase in dopamine level of synaptosome might be due to the decrease in the release of dopaine in hyperglycemic state.