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The Preventive Effects of Bcl-2 and Bcl-xL on Lovastatin-induced Apoptosis of C6 Glial Cells.

Jae Won CHOI ; Jong Min LEE ; Young Jun OH

The Korean Journal of Physiology and Pharmacology.2002;6(5):235-240.

It has been reported that lovastatin induced cell death and suppressed proliferation in various cell lines. In this study, we examined whether the cytotoxic effects of lovastatin could be prevented by Bcl-2 or Bcl-xL in C6 glial cells. Overexpression of human Bcl-2 or Bcl-xL prevented lovastatin (25microM)- induced changes such as DNA fragmentation, chromatin condensation, disruption of cell membrane, and cleavage of poly (ADP-ribose) polymerase. Lovastatin-induced inhibition of cell proliferation was unaffected by Bcl-2 or Bcl-xL overexpression. These results suggest that Bcl-2 and Bcl-xL can prevent lovastatin-induced apoptosis in C6 glial cells, though the inhibition of proliferation remains unaffected by these proteins.
Apoptosis* ; Cell Death ; Cell Line ; Cell Membrane ; Cell Proliferation ; Chromatin ; DNA Fragmentation ; Humans ; Lovastatin ; Neuroglia*

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Effects of Kanagawa Hemolysin on Blood Pressure and Arterial Tone in Rats.

Young Moon KIM

The Korean Journal of Physiology and Pharmacology.2002;6(4):225-.

Kanagawa hemolysin (KH), an exotoxin produced from Kanagawa phenomenon-positive Vibrio parahemolyticus, has been shown to possess various biological activities including hemolysis, enterotoxicity, cytotoxicity, and cardiotoxicity. The aim of this study was to investigate the effect of KH on the cardiovascular system and its mechanism, employing in vivo and in vitro experiments of the rat. Intracerebroventricular (icv) administration of 100 mHU KH produced a marked and continuous pressor effect (icv KH-pressor effect), and the icv pressor effect was not repeatable. However, intravenous (iv) injection of the same dose of KH induced a prominent depressor effect (iv KH-depressor effect). The icv KH-pressor effect was inhibited by acid-denaturation, while the iv KH-depressor effect was not. Simultaneous icv administration of the three agents (ouabain, diltiazem, or bumetanide: 10ng/kg each) significantly reduced the pressor effect. The icv KH-pressor effect was inhibited by treatment with iv phentolamine or chlorisondamine, but was not affected by iv candesartan. The iv KH-depressor effect was repeatable and was attenuated by treatment with iv NAME or methylene blue. In vitro experiments using isolated thoracic aorta, 10(-6) M phenylephrine (PE) and 50 mM KCl produced a sustained contraction. In rings contracted with either agents, KH showed relaxant responses in a concentration- dependent fashion and the relaxation (KH-vasorelaxation) was not dependent on the existence of the endothelium. The KH-vasorelaxation in the endothelium-intact rings contracted by PE was abolished by methylene blue treatment. In summary, the present findings suggest that in the icv KH-pressor effect the cation leak-inducing action of KH is implicated, which leads to the increased central sympathetic tone, that the iv KH-depressor effect results from the vasorelaxation via NO-guanylate cyclase system, and that the KH-vasorelaxation is independent of the endothelium and the guanylate cyclase system is involved in it. In conclusion, the mechanism of KH producing the icv pressor effect may not be identical to that of KH producing the iv depressor effect.
Animals ; Aorta ; Aorta, Thoracic ; Blood Pressure* ; Bumetanide ; Cardiovascular System ; Chlorisondamine ; Diltiazem ; Endothelium ; Exotoxins ; Guanylate Cyclase ; Hemolysis ; Ion Transport ; Methylene Blue ; Phentolamine ; Phenylephrine ; Rats* ; Relaxation ; Vasodilation ; Vibrio

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Effect of Doxorubicin on Catecholamine Release in the Isolated Perfused Rat Adrenal Gland.

Dong Yoon LIM ; Song Hoon OH ; Yoo Seung SEOH ; Eun Sook LEE ; Il Hwan KIM ; Seong Ho JO ; Soon Pyo HONG

The Korean Journal of Physiology and Pharmacology.2002;6(4):215-224.

The present study was undertaken to investigate the effect of doxorubicin (DX) on secretion of catecholamines (CA) evoked by ACh, high K+, DMPP and McN-A-343 from the isolated perfused rat adrenal gland and to establish the mechanism of its action. DX (10(-7)~10(-6) M) perfused into an adrenal vein for 60 min produced relatively dose- and time-dependent inhibition of CA secretory responses evoked by ACh (5.32 X 10(-3) M), DMPP (10(-4) M) and McN-A-343 (10(-4) M). However, lower dose of DX did not affect CA secretion by high K+ (5.6 X 10(-2) M), but its higher doses depressed time-dependently CA secretion evoked by high K+. DX itself did also fail to affect basal CA output. In adrenal glands loaded with DX (3 X 10(-7) M), CA secretory responses evoked by Bay-K-8644, an activator of L-type Ca2+ channels and cyclopiazonic acid, an inhibitor of cytoplasmic Ca2+-ATPase were time-dependently inhibited. Furthermore, daunorubicin (3 X 10(-7) M), given into the adrenal gland for 60 min, attenuated CA secretory responses evoked by ACh, high K+, DMPP and McN-A-343. Taken together, these results suggest that DX causes relatively dose- and time-dependent inhibition of CA secretory responses evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors from the isolated perfused rat adrenal gland. However, lower dose of DX did not affect CA secretion by high K+, and higher doses of DX reduced time-dependently CA secretion of high K+. It is thought that these effects of DX may be mediated by inhibiting both influx of extracellular calcium into the rat adrenomedullary chromaffin cells and intracelluar calcium release from the cytoplasmic store. Also, there was no difference in the mode of action between DX and daunorubicin in rat adrenomedullary CA secretion.
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride ; 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester ; Adrenal Glands* ; Animals ; Calcium ; Catecholamines ; Chromaffin Cells ; Cytoplasm ; Daunorubicin ; Dimethylphenylpiperazinium Iodide ; Doxorubicin* ; Rats* ; Veins

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Influence of Tacrine on Catecholamine Secretion in the Perfused Rat Adrenal Gland.

Seok Jeong JANG ; Won Ho YANG ; Dong Yoon LIM

The Korean Journal of Physiology and Pharmacology.2002;6(4):207-214.

The present study was designed to clarify whether tacrine affects the release of catecholamines (CA) from the isolated perfused model of rat adrenal gland or not and to elucidate the mechanism of its action. Tacrine (3 X 10(-5)~3 X 10(-4) M) perfused into an adrenal vein for 60 min inhibited CA secretory responses evoked by ACh (5.32 X 10(-3) M), DMPP (a selective neuronal nicotinic agonist, 10(-4) M for 2 min) and McN-A-343 (a selective muscarinic M1-agonist, 10(-4) M for 2 min) in relatively dose- and time- dependent manners. However, tacrine failed to affect CA secretion by high K+ (5.6 X 10(-2) M). Tacrine itself at concentrations used in the present experiments did not also affect spontaneous CA output. Furthermore, in the presence of tacrine (10(-4) M), CA secretory responses evoked by Bay-K-8644 (an activator of L-type Ca2+ channels, 10(-4) M), but not by cyclopiazonic acid (an inhibitor of cytoplasmic Ca2+-ATPase, 10(-4) M), was relatively time-dependently attenuated. Also, physostigmine (10(-4) M), given into the adrenal gland for 60 min, depressed CA secretory responses evoked by ACh, McN-A-343 and DMPP while did not affect that evoked by high K+. Collectively, these results obtained from the present study demonstrate that tacrine greatly inhibits CA secretion from the perfused rat adrenal gland evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors, but does fail to affect that by direct membrane-depolarization. It is suggested that this inhibitory effect of tacrine may be exerted by blocking both the calcium influx into the rat adrenal medullary chromaffin cells without Ca2+ release from the cytoplasmic calcium store, that is relevant to the cholinergic blockade. Also, the mode of action between tacrine and physostigmine in rat adrenomedullary CA secretion seems to be similar.
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride ; 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester ; Adrenal Glands* ; Animals ; Calcium ; Catecholamines ; Chromaffin Cells ; Cytoplasm ; Dimethylphenylpiperazinium Iodide ; Neurons ; Nicotinic Agonists ; Physostigmine ; Rats* ; Tacrine* ; Veins

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Neuronal Activity of the Vestibular Nuclei Following Acute Hypotension in Rats.

Byung Rim PARK ; Min Sun KIM ; Kum Hyun BAIK ; Moon Young LEE ; Myung Ae CHOI ; Jae Hyo LEE

The Korean Journal of Physiology and Pharmacology.2002;6(4):199-206.

The role of peripheral vestibular receptors in acute hypotension was investigated in anesthetized rats. Acute hypotension was induced by either intravenous infusion of sodium nitroprusside (SNP) or by experimental hemorrhage, and electrical activity and expression of cFos-like immunoreactive (cFL) protein were measured in the medial vestibular nuclei (MVN). Blood pressure decreased proportionately to the does of intravenous SNP and to the volume of the hemorrhage. Blood pressure decreased 10, 30, 50% for the 5, 10, 15ng/kg SNP injection, respectively, and also decreased 30 and 50% after 1- and 2-ml blood loss, respectively, due to hemorrhage. In animals with intact labyrinths, acute hypotension induced by either intravenous infusion of SNP or hemorrhage produced different electrical activities with three different patterns in type I and II neurons of MVN. The responses of type I neurons showed excitatory in 2/3 of recorded neurons and inhibitory or no change in 1/3 of neurons, while the responses of type II neurons showed inhibitory in 2/3 of recorded neurons and excitatory or no change in 1/3 of neurons. In unilateral labyrinthectomized animals, 2/3 of type I neurons ipsilateral to the lesion showed an inhibitory response, and 2/3 of contralateral type I neurons showed an excitatory response after the induction of acute hypotension. The response patterns of type II neurons were opposite from those of the type I neurons. After 30% decrease in blood pressure, cFL protein expressed in the bilateral vestibular nuclei of control animals with intact labyrinths. Expression of cFL protein increased significantly proportionately to the reduction of blood pressure. The unilateral labyrinthectomized animals with acute hypotension produced expression of cFL neurons in contralateral vestibular nuclei to the lesion side, but not in ipsilateral vestibular nuclei. However, cFL protein was not expressed in bilateral vestibular nuclei after acute hypotension in bilateral labyrinthectomized animals. These results suggest that the peripheral vestibular receptors might play a significant role in controlling blood pressure following acute hypotension via activation of type I neurons and inhibition of type II neurons in the vestibular nuclei.
Animals ; Blood Pressure ; Ear, Inner ; Hemorrhage ; Hypotension* ; Infusions, Intravenous ; Neurons* ; Nitroprusside ; Rats* ; Vestibular Nuclei*

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Responses of Inferior Olive Neurons to Stimulation of Semicircular Canals.

Sah Hoon PARK ; Jong Seong PARK ; Min Su LEE ; Jung Woo SHIN

The Korean Journal of Physiology and Pharmacology.2002;6(4):193-198.

In spite of abundant anatomical evidences for the fiber connection between vestibular nuclei and inferior olivary (IO) complex, the transmission of vestibular information through the vestibulo- olivo-cerebellar climbing fiber pathway has not been physiologically established. The aims of the present study were to investigate whether there are IO neurons specifically responding to horizontal rotation and also in which subregions of IO complex these vestibularly-activated neurons are located. The extracellular recording was made in 68 IO neurons and responses of 46 vestibularly-activated cells were analyzed. Most of the vestibularly-activated IO neurons responded to signals of vertical rotation (roll), while a small number (13/46) of recorded cells were activated by horizontal canal signal (yaw). Regardless of yaw-sensitive or roll-sensitive, vestibular IO neurons were excited, when the animal was rotated to the side contralateral to the recording side. The gain and excitation phase were very similar to otolithic or vertical-canal responses. Histologic identification of recording sites showed that most of vestibular IO neurons were located in beta subnucleus. Electrical stimulation of a HSC evoked an inhibitory effect on the excitability of the ipsilateral IO neurons. These results suggest that IO neurons mainly in the beta subnucleus receive vestibular signals from semicircular canals and otolithic organs, encode them, and transmit vestibular information to the cerebellum.
Animals ; Cerebellum ; Electric Stimulation ; Neurons* ; Olea* ; Otolithic Membrane ; Semicircular Canals* ; Vestibular Nuclei

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Role of Calmodulin in the Generation of Reactive Oxygen Species and Apoptosis Induced by Tamoxifen in HepG2 Human Hepatoma Cells.

Yong Soo LEE

The Korean Journal of Physiology and Pharmacology.2002;6(4):187-192.

Tamoxifen, an antiestrogen, has previously been shown to induce apoptosis in HepG2 human hepatoblastoma cells through activation of the pathways independent of estrogen receptors, i.e., intracellular Ca2+ increase and generation of reactive oxygen species (ROS). However, the mechanism of tamoxifen to link increased intracellular Ca2+ to ROS generation is currently unknown. Thus, in this study we investigated the possible involvement of calmodulin, a Ca2+ activated protein, and Ca2+/ calmodulin-dependent protein kinase II in the above tamoxifen-induced events. Treatment with calmodulin antagonists (calmidazolium and trifluoroperazine) or specific inhibitors of Ca2+/calmodulin-dependent protein kinase II (KN-93 and KN-62) inhibited the tamoxifen-induced apoptosis in a dose-dependent manner. In addition, these agents blocked the tamoxifen-induced ROS generation in a concentration-dependent fashion, which was completely suppressed by intracellular Ca2+ chelation. These results demonstrate for the first time that, despite of its well-known direct calmodulin-inhibitory activity, tamoxifen may generate ROS and induce apoptosis through indirect activation of calmodulin and Ca2+/calmodulin-dependent protein kinase II in HepG2 cells.
Apoptosis* ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calmodulin* ; Carcinoma, Hepatocellular* ; Estrogen Receptor Modulators ; Hep G2 Cells ; Hepatoblastoma ; Humans* ; Protein Kinases ; Reactive Oxygen Species* ; Receptors, Estrogen ; Tamoxifen*

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Effect of Berberine on Depression- and Anxiety-Like Behaviors and Activation of the Noradrenergic System Induced by Development of Morphine Dependence in Rats.

Bombi LEE ; Bongjun SUR ; Mijung YEOM ; Insop SHIM ; Hyejung LEE ; Dae Hyun HAHM

The Korean Journal of Physiology and Pharmacology.2012;16(6):379-386. doi:10.4196/kjpp.2012.16.6.379

The purpose of this study was to evaluate whether berberine (BER) administration could attenuate depression- and anxiety-like behaviors and increase corticotrophin-releasing factor (CRF) and tyrosine hydroxylase (TH) expression following chronic morphine withdrawal in rats. Male rats were exposed to chronic, intermittent, escalating morphine (10~50 mg/kg) for 10 days. After the last morphine injection, depression- and anxiety-like beahvior associated with morphine discontinuation persisted for at least three days during withdrawal without any change in ambulatory activity. Daily BER administration significantly decreased immobility in the forced swimming test and increased open-arm exploration in the elevated plus maze test. BER administration also significantly blocked the increase in hypothalamic CRF expression and TH expression in the locus coeruleus (LC) and the decrease in hippocampal brain-derived neurotrophic factor (BDNF) mRNA expression. Taken together, these findings demonstrated that BER administration significantly reduced morphine withdrawal-associated behaviors following discontinuation of repeated morphine administration in rats, possibly through modulation of hypothalamic CRF and the central noradrenergic system. BER may be a useful agent for treating or alleviating complex withdrawal symptoms and preventing morphine use relapses.
Animals ; Berberine ; Brain-Derived Neurotrophic Factor ; Depression ; Humans ; Locus Coeruleus ; Male ; Morphine ; Morphine Dependence ; Rats ; Recurrence ; RNA, Messenger ; Substance Withdrawal Syndrome ; Swimming ; Tyrosine 3-Monooxygenase

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Synaptic Plasticity in Mouse Models of Autism Spectrum Disorders.

Leeyup CHUNG ; Alexandra L BEY ; Yong Hui JIANG

The Korean Journal of Physiology and Pharmacology.2012;16(6):369-378. doi:10.4196/kjpp.2012.16.6.369

Analysis of synaptic plasticity together with behavioral and molecular studies have become a popular approach to model autism spectrum disorders in order to gain insight into the pathosphysiological mechanisms and to find therapeutic targets. Abnormalities of specific types of synaptic plasticity have been revealed in numerous genetically modified mice that have molecular construct validity to human autism spectrum disorders. Constrained by the feasibility of technique, the common regions analyzed in most studies are hippocampus and visual cortex. The relevance of the synaptic defects in these regions to the behavioral abnormalities of autistic like behaviors is still a subject of debate. Because the exact regions or circuits responsible for the core features of autistic behaviors in humans are still poorly understood, investigation using region-specific conditional mutant mice may help to provide the insight into the neuroanatomical basis of autism in the future.
Animals ; Autistic Disorder ; Child ; Autism Spectrum Disorder ; Hippocampus ; Humans ; Mice ; Plastics ; Visual Cortex

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Retraction: A Novel Carbamoyloxy Arylalkanoyl Arylpiperazine Compound (SKL-NP) Inhibits Hyperpolarization-Activated Cyclic Nucleotide-Gated (HCN) Channel Currents in Rat Dorsal Root Ganglion Neurons.

Gehoon CHUNG ; Tae Hyung KIM ; Hyewon SHIN ; Eunhee CHAE ; Hanju YI ; Hongsik MOON ; Hyun Jin KIM ; Joong Soo KIM ; Sung Jun JUNG ; Seog Bae OH

The Korean Journal of Physiology and Pharmacology.2012;16(5):367-367. doi:10.4196/kjpp.2012.16.5.367

No abstract available.

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