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Actions of 5-hydroxytryptamine on neurons of neonatal rat rostral ventrolateral medulla in vitro.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Actions of 5-hydroxytryptamine on neurons of neonatal rat rostral ventrolateral medulla in vitro./
作者:
Hwang, Ling-Ling.
出版者:
Ann Arbor : ProQuest Dissertations & Theses, : 1997,
面頁冊數:
202 p.
附註:
Source: Dissertations Abstracts International, Volume: 59-10, Section: B.
Contained By:
Dissertations Abstracts International59-10B.
標題:
Neurology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9812198
ISBN:
9780591629637
Actions of 5-hydroxytryptamine on neurons of neonatal rat rostral ventrolateral medulla in vitro.
Hwang, Ling-Ling.
Actions of 5-hydroxytryptamine on neurons of neonatal rat rostral ventrolateral medulla in vitro.
- Ann Arbor : ProQuest Dissertations & Theses, 1997 - 202 p.
Source: Dissertations Abstracts International, Volume: 59-10, Section: B.
Thesis (Ph.D.)--Medical College of Ohio, 1997.
This item must not be sold to any third party vendors.
Whole-cell patch recordings were made from rostral ventrolateral medulla (RVLM) neurons of brainstem slices from neonatal rats. 5-Hydroxytryptamine elicited three types of responses: hyperpolarization (outward current, I$\\sb{\\rm o}),$ depolarization (inward current, I$\\sb{\\rm i}),$ and biphasic response (a compound of hyperpolarization and depolarization). 5-Hydroxytryptamine hyperpolarizations were mimicked by 8-OH-DPAT, attenuated by pindobind-5-HT$\\sb{\\rm 1A}$ and spiperone, and not affected by ketanserin. $\\alpha$-Methyl-5-HT mimicked, ketanserin attenuated, and Pindobind-5-HT$\\sb{\\rm 1A}$ did not affect 5-HT depolarizations. 5-Hydroxytryptamine hyperpolarizations were often accompanied by an input resistance decrease, the reversal potential was $-$92 mV and shifted to $-$69 mV in high (K$\\sp{+}\\rbrack\\sb{\\rm o}.$ The steady-state I-V relation of I$\\sb{\\rm o}$ showed an inward rectification, which was suppressed by barium (0.1 mM). 5-Hydroxytryptamine depolarizations were associated with a decrease or no apparent change of input resistance. Two types of steady-state I-V relations for I$\\sb{\\rm i}$ were observed. Type I I$\\sb{\\rm i}$ was associated with a membrane conductance decrease, while type II I$\\sb{\\rm i}$ was independent of membrane potentials. Types I and II I$\\sb{\\rm i}$ were greatly reduced by lowering extracellular sodium and their steady-state I-V curves became linear, declined with hyperpolarization, and reversed polarity at negative to E$\\sb{\\rm K}.$ The use of substituted cesium-containing pipettes did not change the percentage of neurons showing I$\\sb{\\rm i},$ but reduced the amplitude of I$\\sb{\\rm i}.$ Extracellular cesium did not affect the I$\\sb{\\rm i}.$ Pretreatment of slices with pertussis toxin reduced 5-HT hyperpolarizations, but not depolarizations. Inclusion of GDP-ss-S in the patch solution reduced both 5-HT hyperpolarizations and depolarizations. The result suggested that 5-HT hyperpolarizes RVLM neurons via activation of 5-HT$\\sb{\\rm 1A}$ receptors, which increases an inwardly rectifying potassium conductance through a pertussis toxin-sensitive G-protein. 5-Hydroxytryptamine depolarizes RVLM neurons through 5-HT$\\sb2$ receptor activation leading to a combination of potassium conductance decrease and cation conductance increase via a pertussis toxin-insensitive G-protein. 5-Hydroxytryptamine suppressed fast EPSCs and IPSCs in RVLM. 5-Hydroxytryptamine effects were independent of changes in membrane conductance. Glutamate, GABA- and glycine-induced currents were not reduced by 5-HT. 5-Carboxamidotryptamine, sumatriptan, TFMPP, and 8-OH-DPAT mimicked, and pindolol partially antagonized the synaptic depressant effects of 5-HT; pindobind-5-HT$\\sb{\\rm 1A}$ and ketanserin had no effects. The synaptic depressant effect of 5-HT may involve a presynaptic mechanism via the activation of 5-HT$\\sb{\\rm 1B}$/5-HT$\\sb{\\rm 1D}$ receptors.
ISBN: 9780591629637Subjects--Topical Terms:
588698
Neurology.
Subjects--Index Terms:
cardiovascular
Actions of 5-hydroxytryptamine on neurons of neonatal rat rostral ventrolateral medulla in vitro.
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Whole-cell patch recordings were made from rostral ventrolateral medulla (RVLM) neurons of brainstem slices from neonatal rats. 5-Hydroxytryptamine elicited three types of responses: hyperpolarization (outward current, I$\\sb{\\rm o}),$ depolarization (inward current, I$\\sb{\\rm i}),$ and biphasic response (a compound of hyperpolarization and depolarization). 5-Hydroxytryptamine hyperpolarizations were mimicked by 8-OH-DPAT, attenuated by pindobind-5-HT$\\sb{\\rm 1A}$ and spiperone, and not affected by ketanserin. $\\alpha$-Methyl-5-HT mimicked, ketanserin attenuated, and Pindobind-5-HT$\\sb{\\rm 1A}$ did not affect 5-HT depolarizations. 5-Hydroxytryptamine hyperpolarizations were often accompanied by an input resistance decrease, the reversal potential was $-$92 mV and shifted to $-$69 mV in high (K$\\sp{+}\\rbrack\\sb{\\rm o}.$ The steady-state I-V relation of I$\\sb{\\rm o}$ showed an inward rectification, which was suppressed by barium (0.1 mM). 5-Hydroxytryptamine depolarizations were associated with a decrease or no apparent change of input resistance. Two types of steady-state I-V relations for I$\\sb{\\rm i}$ were observed. Type I I$\\sb{\\rm i}$ was associated with a membrane conductance decrease, while type II I$\\sb{\\rm i}$ was independent of membrane potentials. Types I and II I$\\sb{\\rm i}$ were greatly reduced by lowering extracellular sodium and their steady-state I-V curves became linear, declined with hyperpolarization, and reversed polarity at negative to E$\\sb{\\rm K}.$ The use of substituted cesium-containing pipettes did not change the percentage of neurons showing I$\\sb{\\rm i},$ but reduced the amplitude of I$\\sb{\\rm i}.$ Extracellular cesium did not affect the I$\\sb{\\rm i}.$ Pretreatment of slices with pertussis toxin reduced 5-HT hyperpolarizations, but not depolarizations. Inclusion of GDP-ss-S in the patch solution reduced both 5-HT hyperpolarizations and depolarizations. The result suggested that 5-HT hyperpolarizes RVLM neurons via activation of 5-HT$\\sb{\\rm 1A}$ receptors, which increases an inwardly rectifying potassium conductance through a pertussis toxin-sensitive G-protein. 5-Hydroxytryptamine depolarizes RVLM neurons through 5-HT$\\sb2$ receptor activation leading to a combination of potassium conductance decrease and cation conductance increase via a pertussis toxin-insensitive G-protein. 5-Hydroxytryptamine suppressed fast EPSCs and IPSCs in RVLM. 5-Hydroxytryptamine effects were independent of changes in membrane conductance. Glutamate, GABA- and glycine-induced currents were not reduced by 5-HT. 5-Carboxamidotryptamine, sumatriptan, TFMPP, and 8-OH-DPAT mimicked, and pindolol partially antagonized the synaptic depressant effects of 5-HT; pindobind-5-HT$\\sb{\\rm 1A}$ and ketanserin had no effects. The synaptic depressant effect of 5-HT may involve a presynaptic mechanism via the activation of 5-HT$\\sb{\\rm 1B}$/5-HT$\\sb{\\rm 1D}$ receptors.
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