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  • 1
    Electronic Resource
    Electronic Resource
    Mechanism of Sympathoinhibition by Imidazolines (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 763 (1995), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1995.tb32449.x
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of Cannabinoids on Dopamine Release in the Corpus Striatum and the Nucleus Accumbens In Vitro (1999)
    Oxford UK : Blackwell Science Ltd
    Journal of neurochemistry 73 (1999), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract : Cannabinoid receptors are widely distributed in the nuclei of the extrapyramidal motor and mesolimbic reward systems ; their exact functions are, however, not known. The aim of the present study was to characterize the effects of cannabinoids on the electrically evoked release of endogenous dopamine in the corpus striatum and the nucleus accumbens. In rat brain slices dopamine release elicited by single electrical pulses was determined by fast cyclic voltammetry. Dopamine release was markedly inhibited by the OP2 opioid receptor agonist U-50488 and the D2/D3 dopamine receptor agonist quinpirole, indicating that our method is suitable for studying presynaptic modulation of dopamine release. In contrast, the CB1/CB2 cannabinoid receptor agonists WIN55212-2 (10-6M) and CP55940 (10-6-10-5M) and the CB1 cannabinoid receptor antagonist SR141716A (10-6M) had no effect on the electrically evoked dopamine release in the corpus striatum and the nucleus accumbens. The lack of a presynaptic effect on terminals of nigrostriatal and mesolimbic dopaminergic neurons is in accord with the anatomical distribution of cannabinoid receptors : The perikarya of these neurons in the substantia nigra and the ventral tegmental area do not synthesize mRNA, and hence protein, for CB1 and CB2 cannabinoid receptors. It is therefore unlikely that presynaptic modulation of dopamine release in the corpus striatum and the nucleus accumbens plays a role in the extrapyramidal motor and rewarding effects of cannabinoids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1999.0731084.x
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  • 3
    Electronic Resource
    Electronic Resource
    SHORT COMMUNICATION Inhibition of GABAergic neurotransmission in the ventral tegmental area by cannabinoids (2002)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 15 (2002), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: It was shown recently that Δ9-tetrahydrocannabinol, like several other drugs eliciting euphoria, stimulates dopaminergic neurons projecting from the ventral tegmental area (VTA) to the nucleus accumbens. The aim of the present work was to clarify the mechanism of this stimulatory effect. Our hypothesis was that cannabinoids depress the GABAergic inhibition of dopaminergic neurons in the VTA. Electrophysiological properties of VTA neurons in rat coronal midbrain slices were studied with the patch-clamp technique. GABAA receptor-mediated inhibitory postsynaptic currents (IPSCs) were evoked by electrical stimulation in the vicinity of the recorded neurons. The amplitude of IPSCs was depressed by the synthetic mixed CB1/CB2 cannabinoid receptor agonist WIN55212-2 (10−6 and 10−5 m). The CB1 cannabinoid receptor antagonist SR141716A (10−6 m) prevented the inhibition produced by WIN55212-2 (10−5 m). Two observations showed that IPSCs were depressed with a presynaptic mechanism. WIN55212-2 (10−5 m) did not change the amplitude of miniature IPSCs recorded in the presence of tetrodotoxin. Currents evoked by pressure ejection of muscimol from a pipette were also not changed by WIN55212-2 (10−5 m). The results indicate that activation of CB1 cannabinoid receptors inhibits GABAergic neurotransmission in the VTA with a presynaptic mechanism. Depression of the GABAergic inhibitory input of dopaminergic neurons would increase their firing rate in vivo. Accordingly, dopamine release in the projection region of VTA neurons, the nucleus accumbens, would also increase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.2002.02041.x
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  • 4
    Electronic Resource
    Electronic Resource
    Analysis of the function of GABAB receptors on inhibitory afferent neurons of Purkinje cells in the cerebellar cortex of the rat (2002)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 15 (2002), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Purkinje cells, the output neurons of the cerebellar cortex, receive inhibitory input from basket, stellate and neighbouring Purkinje cells. The aim of the present study was to clarify the role of GABAB receptors on neurons giving inhibitory input to Purkinje cells. In sagittal slices prepared from the cerebellar vermis of the rat, the GABAB receptor agonist baclofen lowered the frequency and amplitude of spontaneous inhibitory postsynaptic currents (IPSCs) recorded in Purkinje cells. These effects were prevented by the GABAB receptor antagonist CGP 55845. Two mechanisms were involved in the depression of the inhibitory input to Purkinje cells. The first mechanism was suppression of the firing of basket, stellate and Purkinje cells. The second mechanism was presynaptic inhibition of GABA release from terminals of the afferent axons. This was indicated by the finding that baclofen decreased the amplitude of IPSCs occurring in Purkinje cells synchronously with action potentials recorded in basket cells. A further support for the presynaptic inhibition is the observation that baclofen decreased the amplitude of autoreceptor currents which are due to activation of GABAA autoreceptors at axon terminals of basket cells by synaptically released GABA. The presynaptic inhibition was partly due to direct inhibition of the vesicular release mechanism, because baclofen lowered the frequency of miniature IPSCs recorded in Purkinje cells in the presence of cadmium and in the presence of tetrodotoxin plus ionomycin. The results show that activation of GABAB receptors decreased GABAA receptor-mediated synaptic input to cerebellar Purkinje cells both by lowering the firing rate of the inhibitory input neurons and by inhibiting GABA release from their axon terminals with a presynaptic mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.2002.01997.x
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  • 5
    Electronic Resource
    Electronic Resource
    Role of Calcium Loading in Early Afterdepolarizations Generated by Cs+ in Canine and Guinea Pig Purkinje Fibers (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 6 (1995), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Ca2+-Loading and EAD. introduction: Our previous observations indicate that the Na2+:Ca2+ exchange current (INa:Ca) plays an important role in early afterdepolarizations occurring at more negative Vm (L-EAD). The purpose of these studies was to examine the role of Ca2+-loading, which stimulates INa:Ca, in generation of L-EAD. Methods and Results: Purkinje strands and preparations of ventricular myocardium from dogs and guinea pigs were superfused with oxygenated physiologic buffer solutions at 37°C, To induce EADs, [K+]0 was reduced to 2.0 to 3.0 mM and [Cs+]0, (3.6 to 4.0 mM) was added at slow rates of ≤ 0.3 Hz. Isometric contraction in canine Purkinje strands and guinea pig papillary muscles doubled in 1-hour exposure to Cs+ and low [K+]0 at slow rates, and the uptake of 45Ca2+ was approximately doubled after 30 minutes. Forty-three percent of Purkinje fibers developed L-EAD after a latent period of 17 to 123 minutes of exposure. Ouabain (0.2 μM) suppressed LEAD within 10 minutes reversibly. Ca2+-loading (low [Na+]0 or high [Ca2+]0 for 5 to 10 minutes before exposure to Cs+, low [K+]0, and slow rates resulted in rapid development of L-EAD in all preparations during subsequent exposure. In Ca2+-loaded preparations, delayed afterdepolarizations (DADs) as well as L-EADs developed. Conclusion: Reduction of K+ currents with Cs+, low [K+]0, and slow rates induced L-EAD in a fraction of Purkinje fibers after a latent period during which Ca2+-loading of the sarcoplasmic reticulum occurred, while fibers preloaded with Ca2+ developed L-EAD rapidly and uniformly. These findings indicate that Ca2+-loading is a critical condition for the development of L-EAD. Early suppression of L-EAD by ouabain suggests a dependence of L-EAD on low [Na+]1. These findings implicate INa:Ca in the generation of L-EAD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.1995.tb00356.x
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  • 6
    Electronic Resource
    Electronic Resource
    Role of Na+:Ca2+ Exchange Current in Cs+-Induced Early Afterdepolarizations in Purkinje Fibers (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 5 (1994), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Na+:Ca2+ Exchanger and EADs. Introduction: The ionic mechanisms for early afterdepolarizations (EADs) have not been fully clarified. It has been suggested that L-type Ca2+ current (IcaL) is the primary current generating EADs that occur near the plateau level (E-EADs) of the membrane potential (Vm) when IcaL is enhanced. The purpose of these studies was to determine accurately the range of Vm at which EADs occur in Purkinje fibers with K+ currents blocked by Cs+ and to investigate the importance of Na+:Ca2+ exchange current (INa:ca) as opposed to lCaL and other currents in the generation of EADs occurring later during repolarization (L-EADs). Methods and Results: Shortened Purkinje strands from dogs and guinea pigs were superfused with physiologic solution containing Cs+ (3.6 mM) and a low [K+]o (3.0 or 2.0 mM) to induce EADs. The Vm of origin of EADs and their evolution were measured with the aid of phase plane plots of the rate of repolarization against Vm. L-EADs occurred over a wide range of Vm (−35 to −90 mV), generally more negative in guinea pig than in dog. Elevation of [Ca2+]o, from 1.8 to 3.6 mM suppressed L-EADs within a few cycles, and they returned with continued exposure. After repeated exposures to high [Ca:2+]0, L-EADs migrated toward less negative Vm when |Ca2+]0, was reestablished to 1.8 mM in the presence of Cs+. Reduction of [Na+]0 from 147.5 to 112.5 mM by substitution with Li+ or sucrose also rapidly depressed L-EADs. Conclusions: The observation of Cs+-induced L-EADs over a wide range of Vm indicates that there is not a single inward gated current as a common ionic mechanism for L-EADs but does not exclude an important role for INa:Ca, which can operate over a wide range of Vm. The rapid suppression of L-EADs with elevated [Ca2+]o, and reduced [Na+]o, and the migration of EADs to more positive Vm after exposures to high |Ca2+]o, are compatible with INc:Ca as the major charge carrier for L-EADs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.1994.tb01133.x
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  • 7
    Electronic Resource
    Electronic Resource
    Adrenergic Induction of Delayed Afterdepolarizations in Ventricular Myocardial Cells: β Induction and α Modulation (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 2 (1991), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Adrenergic Afterdepolarizations in Ventricular Cells. Introduction: The purpose of these studies was to expose canine multicellular ventricular endocardial preparations and disaggregated myocytes to adrenergic agonists and antagonists, and to investigate the generation of delayed afterdepolarizations and triggered action potentials. Methods and Results: We used multicellular preparations and disaggregated myocytes from canine ventricles. The threshold concentration for induction of delayed afterdepolarizations in isolated myocytes for norepinephrine was between 1 × 10−8 M and 5 × 10−5 M, with 50% of the cells showing delayed afterdepolarizations at 4.3 × 10−8 M. Higher concentrations of epinephrine are required with 50% of the cells responding to 8.3 × 10−8 M. The threshold concentrations for induction of delayed afterdepolarizations in myocardial cells of multicellular preparations were an order of magnitude higher. Delayed afterdepolarizations could not be induced in Purkinje fibers with concentrations up to 10−4 M with norepinephrine. Adrenergic delayed afterdepolarizations were inhibited promptly by reduction of pO2 in superfusate that was equilibrated with N2 (95%) in place of O2. The amplitudes of adrenergic delayed afterdepolarizations and the propensity to triggered action potentials were inversely related to cycle length down to the shortest cycle length tested (330 msec). Adrenergic delayed afterdepolarizations were induced by isoproterenol but not by α-adrenergic agonists (methoxamine or phenylephrine). They were inhibited by a β antagonist (propranolol) but not by α antagonists (prazosin or yohimbine). Delayed afterdepolarizations induced by isoproterenol were inhibited by α agonists (methoxamine or phenylephrine). The α-adrenergic inhibitory effects on β-adrenergic delayed afterdepolarizations could be reversed by prazosin, but not by yohimbine. Conclusions: We conclude the natural catecholamines norepinephrine and epinephrine generate delayed afterdepolarizations in myocardial cells, but not in Purkinje cells, by activating β receptors, but activation of α1 receptors inhibits adrenergic delayed afterdepolarizations. Individual myocytes exhibit widely varying sensitivities for induction of adrenergic delayed afterdepolarizations, but some cells respond to concentrations similar to those that may exist in vivo. Therefore, sympathetic activation in vivo may generate delayed afterdepolarizations, triggered action potentials, and arrhythmias.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.1991.tb01350.x
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  • 8
    Electronic Resource
    Electronic Resource
    Canine Ventricular Myocyte β2-Adrenoceptors Are Not Functionally Coupled to L-Type Calcium Current (1999)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 10 (1999), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Selective Stimulation of β AR Subtypes and ICaL. Introduction: To establish the functional coupling of beta adrenoceptor (βAR) subtypes β1, AR and β2AR to L-type calcium current (ICaL)we investigated the nonselective agonist isoproterenol (ISO) and the relatively selective β1AR antagonists zinterol (ZIN) and salbutamol (SAL) on ICaL in isolated canine ventricular myocytes in the presence and absence of CGP 20712A (CGP) and atenolol (AT), selective β1AR antagonists, and ICI 118,551 (ICI) a selective β2AR antagonist. Methods and Results: Peak ICaL determined using “patch type” microelectrodes and whole cell voltage clamp. ISO (0.5 μM) increased ICaL, maximally 3.5 ± 0.67 fold. ZIN (10.0 μM) and SAL (10.0 μM) increased ICaL maximally 1.5 ± 0.2 fold (n = 5) and 1.4 ± 0.1 fold (n = 5) respectively. These effects were fully inhibited by CGP (0.3 μM) and AT (1.0 μM), which are inhibitors of β1AR, but not by ICI (0.1 μM), which is a β2AR inhibitor. ZIN at relatively lower concentrations (≤0.1 μM) did not increase ICaL. CGP (0.3 μM) but not AT and ICI inhibited ICaL in the absence of βAR agonists. CGP inhibition of ICaL, was absent in the presence of forskolin (1.0 μM), which increases cAMP levels and ICaL by directly stimulating the adenylate cyclase. These data indicate that none of the antagonists affect ICaL through an action downstream βAR. Conclusion: β-Adrenergic agonists increase ICaL via β1AR but not β2AR in canine ventricular myocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.1999.tb00302.x
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  • 9
    facet.materialart.
    Unknown
    Woodcuts (1966)
    Madison, N.J., etc. : Periodicals Archive Online (PAO)
    The Literary Review. 9:3 (1966:Spring) 352 
    Details
    ISSN: 0024-4589
    Topics: Linguistics and Literary Studies
    Notes: Hungary Number
    URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pao:&rft_dat=xri:pao:article:5170-1966-009-03-000034
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  • 10
    Electronic Resource
    Electronic Resource
    The subcellular location of potassium flux pathways in frog skeletal muscle (1981)
    Springer
    Pflügers Archiv 390 (1981), S. 250-255 
    Details
    ISSN: 1432-2013
    Keywords: K-, Rb-uptake ; Ouabain ; Physostigmine ; Glycerol treatment ; Surface membrane ; Transverse tubules ; Frog muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The influence of ouabain and physostigmine on42K and86Rb uptake in isolated frog sartorii with normal [Na] i (12–14 mmol·kg−1 wet weight) and low [Na] i (6 mmol·kg−1 wet weight) was compared. Both in normal-sodium and in low-sodium muscles application of 10−3 M physostigmine reduces potassium influx by about 70%. About one fourth of potassium-uptake in normal-sodium muscles is inhibited by ouabain (10−4M) and only a very slight fraction of potassium uptake is ouabain-sensitive in low-sodium muscle. The effects of ouabain and physostigmine on42K influx are additive. The greater parts of the Rb-fluxes are through the ouabainsensitive pathway. Glycerol treatment has no effect on ouabain-sensitive channels although it inhibits markedly the K-flux through the physostigmine-sensitive pathway. The results suggest that the Na−K-ATPase is located in the surface membrane while most of the physostigmine-sensitive K-exchange is within the tubules.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00658270
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