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  • 1
    Electronic Resource
    Electronic Resource
    Activation of K+ channels by lanthanum contributes to the block of transmitter release in chick and rat sympathetic neurons (1992)
    Springer
    The journal of membrane biology 125 (1992), S. 155-162 
    Details
    ISSN: 1432-1424
    Keywords: ion channels ; Ca2+ transients ; lanthanum ; norepinephrine release ; neuronal cultures
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary We studied the effects of lanthanum (La3+) on the release of 3H-norepinephrine(3H-NE), intracellular Ca2+ concentration, and voltage clamped Ca2+ and K+ currents in cultured sympathetic neurons. La3+ (0.1 to 10 μm) produced concentration-dependent inhibition of depolarization induced Ca2+ influx and 3H-NE release. La3+ was more potent and more efficacious in blocking 3H-NE release than the Ca2+-channel blockers cadmium and verapamil, which never blocked more than 70% of the release. At 3 μm, La3+ produced a complete block of the electrically stimulated rise in intracellular free Ca2+ ([Ca2+] i ) in the cell body and the growth cone. The stimulation-evoked release of 3H-NE was also completely blocked by 3 μm La3+. However, 3 μm La3+ produced only a partial block of voltage clamped Ca2+ current (I Ca). Following La3+ (10 μm) treatment 3H-NE release could be evoked by high K+ stimulation of neurons which were refractory to electrical stimulation. La3+ (1 μm) increased the hyperpolarization activated, 4-aminopyridine (4-AP) sensitive, transient K+ current (I A ) with little effect on the late outward current elicited from depolarized holding potentials. We conclude that the effective block of electrically stimulated 3H-NE release is a result of the unique ability of La3+ to activate a stabilizing, outward K+ current at the same concentration that it blocks inward Ca2+ current.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00233354
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  • 2
    Electronic Resource
    Electronic Resource
    2′-Deoxyadenosine Induces Apoptosis in Rat Chromaffin Cells (1996)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 67 (1996), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: We show here that 2′-deoxyadenosine (2′-dAdo) but not adenosine was toxic to chromaffin cells of 3–4-week-old rat adrenal glands. More than 75% of the cells plated in culture gradually died over a 3-day period in the presence of 100 µM 2′-dAdo plus 3 µM deoxycoformycin (DCF). Morphological observations together with bisbenzimide staining and terminal deoxynucleotidyl transferase-mediated nick end labeling showed membrane blebbing, shrinkage of cell bodies, chromatin condensation, and DNA fragmentation, suggesting apoptosis-like cell death by 2′-dAdo. Lethal effects of 2′-dAdo were potentiated by DCF, a drug that inhibits adenosine deaminase. 2′-dAdo-prompted cell death was not prevented by inhibitors of nucleoside transporter (3 µM dilazep or 1 µM nitrobenzylthioinosine), precursors of pyrimidine nucleotide biosynthesis (300 µM uridine or 100 µM 2′-deoxycytidine), or 5 mM nicotinamide. Cells incubated with 2′-dAdo (100 and 300 µM) showed a three- and ninefold, respectively, increase in content of dATP, a product known to be an inhibitor of ribonucleotide reductase, an enzyme essential for DNA synthesis. Formation of dATP was completely prevented by iodotubercidin (ITu), a drug that inhibits phosphorylation of 2′-dAdo to dATP by nucleoside kinase. It is interesting that nanomolar concentrations of ITu also completely protected chromaffin cells from 2′-dAdo lethality. Our study demonstrates for the first time that mammalian adrenal chromaffin cells undergo apoptotic cell death by a natural nucleoside and suggests that this model could be used to study apoptosis and cell function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1996.67062273.x
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  • 3
    Electronic Resource
    Electronic Resource
    Age-Dependent Sensitivity of Cultured Peripheral Sympathetic Neurons to 1-Methyl-4-Phenylpyridinium: Role of Glutathione (1996)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 67 (1996), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: We demonstrate that 1-methyl-4-phenylpyridinium (MPP+) is toxic to chick peripheral sympathetic neurons maintained in culture in the presence of nerve growth factor (NGF). When MPP+ was added to the culture medium at the time the neurons were plated, cell loss after 3 days in culture was evident at concentrations as low as 3 nM, and near maximal at 1 µM. Toxicity was blocked by brief preincubation with the norepinephrine (NE)-reuptake blocker desipramine (DMI; 10 µM for 30 min). MPP+ blocked the uptake of [3H]NE by sympathetic neurons in a dose-dependent manner with a potency roughly equal to DMI. At concentrations up to 10 µM, MPP+ had no neurotoxic effect on the survival of sensory neurons maintained in the presence of NGF. The sensitivity of sympathetic neurons to the toxic effects of MPP+ diminished gradually with increasing lengths of time in culture. When MPP+ was added to the culture medium 48 h after plating, concentrations up to 100 µM did not cause neuronal death. This increasing resistance of sympathetic neurons to MPP+-induced cell death could not be explained by an increasing capacity for sequestration of MPP+ within synaptic vesicles. The loss of sensitivity with time in culture was, however, accompanied by a threefold increase in the levels of glutathione (GSH). Furthermore, addition of MPP+ (1 µM) to cultures previously maintained for 2 days in the presence of the GSH-synthesis inhibitor l-buthionine-[S,R]-sulfoximine (1 µM) caused the same degree of cell death as when added to freshly plated neurons. These results suggest that the observed toxicity of MPP+ in freshly plated chick sympathetic neurons may involve the formation of free radicals and that GSH plays a role in protecting sympathetic neurons in vivo from the toxicity of MPP+.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1996.67020557.x
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  • 4
    Electronic Resource
    Electronic Resource
    The Mechanism of Inhibition of 3H-Norepinephrine Release by Norepinephrine in Cultured Sympathetic Neurons (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 604 (1990), 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.1749-6632.1990.tb31993.x
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  • 5
    Electronic Resource
    Electronic Resource
    Protein Kinase C of Sympathetic Neuronal Membrane Is Activated by Phorbol Ester-Correlation Between Transmitter Release, 45Ca2+ Uptake, and the Enzyme Activity (1988)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 51 (1988), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effects of phorbol esters [phorbol 12,13-dibutyrate (PDB), 12-O-tetradecanoylphorbol 13-acetate (TPA), and phorbol 13-acetate] were investigated on the release of [3H]norepinephrine, 45Ca2+ accumulation, and protein kinase C activity in cultured sympathetic neurons of the chick embryo. Sympathetic neurons derived from 10-day-old chick embryo were cultured in serum-free medium supplemented with insulin, transferrin, and nerve growth factor. After 3 days, neurons were loaded with [3H]-norepinephrine and the release of [3H]norepinephrine was determined before and after electrical stimulation. Stimulation at 1 Hz for 15 s increased the release of [3H]-norepinephrine over the nonstimulation period. Stimulation-evoked release gradually declined with time during subsequent stimulation periods. Incubation of neurons in Ca2+-free Krebs solution containing 1 mM EGTA completely blocked stimulation-evoked release of [3H]-norepinephrine. Stimulation-evoked release of [3H]-norepinephrine was markedly facilitated by 3 and 10 nM PDB or TPA. The spontaneous release was also enhanced by PDB and TPA. The net accumulation of 45Ca2+ during stimulation of sympathetic neurons was increased by two-to fourfold in the presence of PDB or TPA. PDB at 1–100 nM produced a concentration-dependent increase in the activation of protein kinase C. PDB at 30 nM increased the activity of protein kinase C of the paniculate fraction from 0.09 to 0.58 pmol/min/mg protein. There was no significant change in protein kinase C activity of the cytosolic fraction (0.14 pmol/min/mg versus 0.13 pmol/min/mg protein). The ratio of the paniculate to cytosolic protein kinase C increased from a control value of 0.62 to 4.39 after treatment with 30 nM PDB. TPA (10 and 30 nM) also increased protein kinase C activity of the paniculate fraction by six- to eightfold. Phorbol 13-acetate had no effect on protein kinase C activity, [3H]norepinephrine release, and 45Ca2+ accumulation. These results provide direct evidence that activation of protein kinase C enhances Ca2+ accumulation, which in turn leads to the facilitation of transmitter release in sympathetic neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1988.tb01834.x
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  • 6
    Electronic Resource
    Electronic Resource
    Excess K+ and Phorbol Ester Activate Protein Kinase C and Support the Survival of Chick Sympathetic Neurons in Culture (1988)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 51 (1988), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effects of phorbol esters were investigated on the survival of chick sympathetic neurons in a serum-free culture medium. The protein kinase C activator phorbol 12,13-dibutyrate (PDB) supported about 40% of the plated sympathetic neurons. This number was comparable to that supported by nerve growth factor (NGF). A combination of phorbol ester and NGF did not significantly increase the number of surviving neurons. Phorbol ester-supported sympathetic neurons possessed desipramine-sensitive [3H]-norepinephrine uptake mechanism, and therefore were noradrenergic in character. Two days after the start of cultures, if NGF was replaced by phorbol ester, or phorbol ester was replaced by NGF, the number of surviving sympathetic neurons was essentially the same in both groups, and the uptake of [3H]norepinephrine was also comparable when examined 2 days after the switchover. Interchangeability between phorbol ester and NGF in the survival of sympathetic neurons suggests that both agents act on the same subpopulation of neurons of the chick sympathetic ganglia. The protein kinase C activity of cytosol and particulate fractions of NGF-supported neurons was 0.14 and 0.09 pmol/min/mg protein, respectively. In phorbol estersupported neurons the activity in the paniculate fraction increased by about fivefold. Removal of the phorbol ester after 2 days resulted in restoration of the enzyme activity in 〈1 h, and readdition of the phorbol ester again increased the activity by fivefold. When NGF was added to these neurons (1 μg for 15 min), there was no change in the enzyme activity. Phorbol 13-acetate was ineffective in supporting sympathetic neurons in culture, as well as in enhancing protein kinase C activity. We also compared the protein kinase C activity of sympathetic neurons supported in culture by NGF and excess potassium (35 mM K+). Neurons supported in culture by 35 mM K+ for 2 days had almost eightfold more protein kinase C activity in their particulate fraction than in cytosol fraction. If NGF-supported neurons were acutely treated with excess K+, the protein kinase C activity was increased in the particulate fraction by about sevenfold in a concentration- and time-dependent manner. Excess K+ plus phorbol ester did not produce an additive effect on protein kinase C activity. PDB and excess K+ had no effect on cyclic AMP content of sympathetic neurons. In summary, the present data suggest that the neurotrophic action of PDB and excess K+ is probably mediated through protein kinase C.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1988.tb01835.x
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  • 7
    Electronic Resource
    Electronic Resource
    Forskolin Mediates the Survival of Nerve Growth Factor-Dependent Sympathetic Neurons of Chick Embryo by a Cyclic AMP-Independent Mechanism (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 54 (1990), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Forskolin has become an invaluable tool for exploring the involvement of cyclic AMP in a variety of cellular functions. The diterpine directly activates the catalytic subunit of adenylate cyclase, causing a marked increase in cyclic AMP content. Because of this well-characterized action, practically all the observed effects of forskolin are commonly attributed to cyclic AMP-dependent processes. We show here that forskolin exerts a neurotrophic action that is almost identical to that of nerve growth factor (NGF) and phorbol 12,13–dibutyrate (PDB) but independent of cyclic AMP. Sympathetic neurons of the chick embryo supported in culture for 2 days by NGF, forskolin plus 3-isobutyl-l-methylxanthine (IBMX), or PDB had almost identical levels of cyclic AMP (between 9 and 12 pmol/mg protein). Neurons supported in culture for 2 days by NGF or PDB when challenged with forskolin plus IBMX showed almost a 15-fold increase in cyclic AMP, but those supported by forskolin plus IBMX and then exposed to the same combination of drugs did not show an increase in cyclic AMP, exhibiting a marked downregulation. Exposure of neurons to forskolin for 2 h was ineffective in supporting long-term survival, suggesting that an initial increase in cyclic AMP formation is not sufficient but the continued presence of the drug is essential for survival. Effects of forskolin on the survival of these neurons could be observed even in the presence of dideoxyadenosine, an inhibitor of adenylate cyclase. Neurons supported by PDB for 2 days in culture when exposed to NGF for the first time did not show any increase in cyclic AMP, providing clear evidence that NGF does not affect this second messenger in its target cells. Similarly, neurons supported by NGF for 2 days when exposed to PDB did not show an increase in cyclic AMP. All these results rule out the involvement of cyclic AMP not only in the neurotrophic action of forskolin but also in that of NGF and PDB, and suggest that forskolin supports neuronal survival by some, as yet, unknown mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1990.tb01960.x
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  • 8
    Electronic Resource
    Electronic Resource
    Ca2+ Mobilized by Caffeine from the Inositol 1,4,5-Trisphosphate-Insensitive Pool of Ca2+ in Somatic Regions of Sympathetic Neurons Does Not Evoke [3H]Norepinephrine Release (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 55 (1990), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effects of electrical stimulation, muscarinic and serotonergic agonists, and caffeine on [3H]inositol 1,4,5-trisphosphate ([3H]Ins(1,4,5)P3) content, intracellular free Ca2+ concentration ([Ca2+]i), and release of [3H]norepinephrine ([3H]NE) were studied in cultured sympathetic neurons. Neuronal cell body [Ca2+]i was unaffected by muscarinic or serotonergic receptor stimulation, which significantly increased [3H]Ins(1,4,5)P3 content. Stimulation at 2 Hz and caffeine had no effect on [3H]Ins(1,4,5)P3, but caused greater than two-fold increase in [Ca2+]i. Only 2-Hz stimulation released [3H]NE. Caffeine had no effect on the release. When [Ca2+]i was measured in growth cones, only electrical stimulation produced an increase in [Ca2+]i. The other agents had no effect on Ca2+ at the terminal regions of the neurons. We conclude that Ins(1,4,5)P3-insensitive, but caffeine-sensitive Ca2+ stores in sympathetic neurons are located only in the cell body and are not coupled to [3H]NE release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1990.tb04972.x
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  • 9
    Electronic Resource
    Electronic Resource
    Survival of Chick Embryonic Sensory Neurons in Culture Is Supported by Phorbol Esters (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 54 (1990), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Sensory neurons of the chick embryo are supported in culture by several neurotrophic factors, including the phorbol esters. Because phorbol esters are known to activate one of the second messengers, namely, protein kinase C, it was of interest to see if the neurotrophic action of phorbol 12,13-dibutyrate (PDB) was related to the activation of protein kinase C in sensory neurons. Sensory neurons were obtained from dorsal root ganglia of 10-day-old chick embryos and maintained in a serum-free medium for several days to quantify survival and analyze protein kinase C activity. PDB (30 nM) supported the survival of ± 50% of the total number of neurons plated. This value was comparable to that supported by nerve growth factor (NGF; 40 ng/ml). If PDB and NGF were added together, there was no additive effect on the survival. The protein kinase C activity of the particulate and cytosolic fractions of sensory neurons supported by NGF for 3 days was 1.26 ± 0.1 and 2.9 ± 0.32 pmol/min/mg of protein, respectively. In contrast, neurons supported by PDB showed an ± 500% increase in enzyme activity in their particulate fraction. The enzyme activity of the cytosolic fraction was decreased by ± 40%. If NGF-supported neurons were treated with PDB (30 nM) for 15 min, protein kinase C activity increased 〉 400% in the particulate fraction, whereas an ± 50% decrease was observed in the cytosolic fraction. The protein kinase C value, expressed as a ratio of the activities in the particulate to cytosol fractions, showed large increases after phorbol treatment. The ratio was 0.43 in NGF-supported neurons and increased to 3.57 in PDB-supported neurons. NGF-supported neurons treated with PDB for 15 min had a ratio of 4.1. Phorbol-13-acetate did not support the survival, nor did it increase protein kinase C activities in NGF-supported neurons. Because sensory neurons contain substantial amounts of choline acetyltransferase (ChAT) activity, we compared ChAT activity in NGF- and PDB-supported sensory neurons. Values were 21.93 ± 3.7 and 22.09 ± 4.6 pmol of acetylcholine formed/min/mg of protein, respectively. These results suggest that neurotrophic action of PDB on chick sensory neurons is probably mediated through protein kinase C. The present data also suggest that NGF and PDB act on the same subpopulation of sensory neurons of the dorsal root ganglia of the chick to support their survival in culture.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1990.tb01917.x
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  • 10
    Electronic Resource
    Electronic Resource
    Restoration of Catecholamine Content of Previously Depleted Adrenal Medulla In Vitro: Importance of Synthesis in Maintaining the Catecholamine Stores (1988)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 51 (1988), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The functional integrity of adrenal chromaffin storage vesicles was studied in the perfused rat adrenal gland subjected to intense exocytosis. Continuous perfusion with 55 mM K+-Krebs solution produced a large and uninterrupted secretion of catecholamines. Total amounts secreted within 45 min were 4.66 μg and represented almost 30% of the total tissue catecholamine content. If perfusion with excess K+ was extended to 90 min, the secretion increased further to 5.76 μg. Despite such a large secretory response, the catecholamine content of the K+-stimulated adrenal medulla was comparable to that of unstimulated control, suggesting an enhanced resynthesis to maintain the normal levels. Pretreatment of rats with α-methyl-p-tyrosine, and including this agent in the perfusion medium during stimulation with K+, caused a marked reduction in catecholamine content. The degree of depletion depended on the extent of stimulation with K+ (45% in 45 min and 60% in 90 min). Although depleted catecholamine stores did not show spontaneous recovery in 2 h, inclusion of tyrosine, l-3,4-dihydroxyphenylalanine or dopamine (but not epinephrine or norepinephrine) completely restored the catecholamine content of previously depleted adrenal me dulla. Repletion achieved by tyrosine was time dependent (evident in 30 min and maximum in 2 h) and blocked by α-methyl-p-tyrosine but not by calcium deprivation. The ratio of epinephrine to norepinephrine remained constant during various stages of the experiment, suggesting both types of vesicles were equally affected by different treatments. The secretory response (10 Hz for 30 s) was unaffected even though tissue catecholamine stores were significantly depleted (50%). In summary, we have demonstrated that catecholamine content of the isolated perfused adrenal gland can be reduced by stimulation of exocytotic secretion in the presence of tyrosine hydroxylase inhibitor. Since the depleted stores can be fully refilled by synthesis of catecholamines from its precursors, it is suggested that chromaffin vesicles may be reutilized for the purpose of synthesis, storage, and secretion of adrenal medullary hormones.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1988.tb01817.x
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