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  • 1
    Electronic Resource
    Electronic Resource
    Dual phases of functional change in norepinephrine transporter in cultured bovine adrenal medullary cells by long-term treatment with clozapine (2001)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 77 (2001), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effects of long-term treatment with clozapine, a prototype of atypical antipsychotic drugs, on the functional activity, synthesis and mRNA of norepinephrine (NE) transporter were examined in bovine adrenal medullary cells in culture. Treatment of cells with clozapine at 0.1–3.0 µm concentrations produced dual phases of changes in [3H]NE uptake, i.e. the first phase showed a decrease in [3H]NE uptake at 2–48 h, and the following phase showed an increase in uptake at 72–168 h. Treatment with clozapine for 6 h decreased Vmax to 40% of the control without changing the Km value for [3H]NE uptake. However, treatment with clozapine for 96 h increased Vmax by 56% over the control without a change in Km. Scatchard plot analysis of [3H]desipramine (DMI) binding to membranes isolated from cells treated with clozapine for 6 h revealed a decrease in Bmax without any change in Kd; in contrast, treatment with clozapine for 96 h caused an increase in Bmax without any change in Kd. Both actinomycin D and cycloheximide, which are inhibitors of protein synthesis, suppressed the clozapine (96 h)-induced increase in [3H]NE uptake. Treatment of cells with clozapine for 12–96 h increased the level of NE transporter mRNA in a concentration-dependent manner (0.3–3.0 µm). These findings suggest that treatment of cells with clozapine results in the down-regulation and subsequent up-regulation of NE transporter. The latter change may be caused by the synthesis of new proteins of NE transporter via an increase in its mRNA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2001.00316.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Inhibition by carbamazepine of various ion channels-mediated catecholamine secretion in cultured bovine adrenal medullary cells (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 297-303 
    Details
    ISSN: 1432-1912
    Keywords: Key words: Adrenal medullary cells ; Carbamazepine ; Nicotinic acetylcholine receptor-associated ion channel ; Voltage-dependent Na+ channel ; Voltage-dependent Ca2+ channel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The effects of carbamazepine (CBZ) on 22Na+ influx, 45Ca2+ influx, catecholamine secretion and cyclic GMP production were examined in cultured bovine adrenal medullary cells. 1) CBZ (40–120 μmol/l) inhibited 22Na+ influx evoked by carbachol in a concentration-dependent manner. CBZ inhibited carbachol-evoked 45Ca2+ influx and catecholamine secretion at concentrations similar to those which suppressed 22Na+ influx. 2) CBZ (4–120 μmol/l) inhibited veratridine-induced 22Na+ influx, 45Ca2+ influx and catecholamine secretion. 3) CBZ (12 or 40–120 μmol/l) suppressed 56 mmol/l K+-evoked 45Ca2+ influx and catecholamine secretion, respectively. 4) Combination of CBZ with nitrendipine or ω-agatoxin-IVA produced further inhibition of 56 mmol/l K+- evoked 45Ca2+ influx and catecholamine secretion, compared to the effect of CBZ alone, whereas CBZ plus ω-conotoxin-GVIA did not produce any further inhibition. 5) CBZ (40 μmol/l) attenuated the production of cyclic GMP caused by muscarine. These results suggest that CBZ at therapeutic concentrations (16–48 μmol/l: 4–12 μg/ml) inhibits catecholamine secretion by interfering with nicotinic acetylcholine receptor-associated ion channels, voltage-dependent Na+ channels and N-type voltage-dependent Ca2+ channels, and may have an antimuscarinic effect in adrenal medullary cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168560
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Inhibition by carbamazepine of various ion channels-mediated catecholamine secretion in cultured bovine adrenal medullary cells (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 297-303 
    Details
    ISSN: 1432-1912
    Keywords: Adrenal medullary cells ; Carbamazepine ; Nicotinic acetylcholine receptor-associated ion channel ; Voltage-dependent Na+ channel ; Voltage-dependent Ca2+ channel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of carbamazepine (CBZ) on 22Na+ influx, 45Ca2+ influx, catecholamine secretion and cyclic GMP production were examined in cultured bovine adrenal medullary cells. 1 CBZ (40–120 μmol/l) inhibited 22Na+ influx evoked by carbachol in a concentration-dependent manner. CBZ inhibited carbachol-evoked 45Ca2+ influx and catecholamine secretion at concentrations similar to those which suppressed 22Na+ influx. 2 CBZ (4–120 μmol/l) inhibited veratridine-induced 22Na+ influx, 45Ca2+ influx and catecholamine secretion. 3 CBZ (12 or 40–120 μmol/l) suppressed 56 mmol/1 K+-evoked 45Ca2+ influx and catecholamine secretion, respectively. 4 Combination of CBZ with nitrendipine or ω-agatoxin-IVA produced further inhibition of 56 mmol/l K+ - evoked 45Ca2+ influx and catecholamine secretion, compared to the effect of CBZ alone, whereas CBZ plus ω-conotoxin-GVIA did not produce any further inhibition. 5 CBZ (40 μmol/1) attenuated the production of cyclic GMP caused by muscarine. These results suggest that CBZ at therapeutic concentrations (16–48 μmol/l: 4–12 μg/ml) inhibits catecholamine secretion by interfering with nicotinic acetylcholine receptor-associated ion channels, voltage-dependent Na+ channels and N-type voltage-dependent Ca2+ channels, and may have an antimuscarinic effect in adrenal medullary cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168560
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    An active metabolite of carbamazepine, carbamazepine-10,11-epoxide, inhibits ion channel-mediated catecholamine secretion in cultured bovine adrenal medullary cells (1998)
    Springer
    Psychopharmacology 135 (1998), S. 368-373 
    Details
    ISSN: 1432-2072
    Keywords: Key words Carbamazepine-10 ; 11-epoxide ; Carbamazepine-10 ; 11-diol ; Catecholamine secretion ; Nicotinic acetylcholine receptor-associated ion channel ; Voltage-dependent Na+ channel ; N-type voltage-dependent Ca2+ channel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We have recently reported inhibitory effects of carbamazepine (CBZ) on ion channel-mediated secretion of catecholamines in bovine adrenal medullary cells. Here, we report the effects of carbamazepine-10,11-epoxide (CBZ-E), an active metabolite of CBZ, and carbamazepine-10,11-diol (CBZ-D), a non-active metabolite, on 22Na+ influx, 45Ca2+ influx and catecholamine secretion in cultured adrenal medullary cells. CBZ-E, but not CBZ-D inhibited 22Na+ influx, 45Ca2+ influx and catecholamine secretion induced by carbachol or veratridine with a half-maximal inhibitory concentration (IC50) of 0.26 or 0.68 μg/ml, respectively. CBZ-E also inhibited high K+-evoked 45Ca2+ influx and catecholamine secretion (IC50 = 0.3 μg/ml), but CBZ-D did not. These findings suggest that CBZ-E, but not CBZ-D, attenuates catecholamine secretion by inhibiting nicotinic acetylcholine receptor-associated ion channels, voltage-dependent Na+ channels and voltage-dependent Ca2+ channels in the cells. This inhibition of CBZ-E as well as CBZ may be related to the clinical effects in neuropsychiatric disorders.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002130050524
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    Paper (German National Licenses)
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