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Area postrema: A potential CNS targ...

Jun, Jenny Mary.

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Area postrema: A potential CNS target for PYY effects on feeding.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Area postrema: A potential CNS target for PYY effects on feeding./
Author:	Jun, Jenny Mary.
Description:	69 p.
Notes:	Source: Masters Abstracts International, Volume: 45-05, page: 2336.
Contained By:	Masters Abstracts International45-05.
Subject:	Biology, Animal Physiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=MR26480
ISBN:	9780494264805

Area postrema: A potential CNS target for PYY effects on feeding.
Jun, Jenny Mary.

Area postrema: A potential CNS target for PYY effects on feeding. - 69 p.

Source: Masters Abstracts International, Volume: 45-05, page: 2336.

Thesis (M.Sc.)--Queen's University (Canada), 2007.

The regulation of energy homeostasis depends on the coordination of signals impacting feeding behaviour and energy balance. Peptide YY (PYY), a satiety signal released postprandially from the distal gut in proportion to caloric intake and meal composition, acts on the neuropeptide Y (NPY) family of receptors. The area postrema (AP) is a sensory circumventricular organ sensitive to circulating factors, which has been shown to exert significant control over autonomic and neuroendocrine functions including vascular tone, fluid balance, and food intake. Previous data demonstrating the presence of Y1, Y 2 and Y5 receptors suggest roles for PYY in the control of energy intake through actions at the AP. In this study, we examined the effects of bath administration of PYY on dissociated rat AP neurons at concentrations ranging from 100 pM to 1 muM. Changes in membrane potential were monitored and analyzed using current-clamp techniques. Clear hyperpolarizing and depolarizing effects were observed depending on the concentration administered. Mean depolarizations of 9.8 +/- 1.0 mV and 4.3 +/- 0.4 mV were observed in response to 100 pM and 10 nM concentrations of PYY1-36, respectively. In contrast, high 1 muM concentrations of PYY3-36 resulted in hyperpolarization of AP neurons, with a mean value of -3.1 +/- 0.1 mV. These responses were pharmacologically determined as mediated by the activation of specific NPY receptor subtypes using specific Y1 and Y2 receptor antagonists. Specifically, PYY1-36 acts at its high affinity Y 1 receptor to cause depolarization and PYY3-36 acts at its preferential Y2 receptor to cause hyperpolarization of AP neurons. Cells were also tested for changes in current following peptide administration under voltage-clamp conditions. Our preliminary slow voltage ramp data suggest that PYY1-36 (10 nM) enhanced an outward voltage-activated current, as demonstrated in 5/8 cells tested. These results demonstrate the effects of PYY in controlling the excitability of AP neurons, suggesting a potential mechanisms through which this circulating peptide may influences the CNS without having to cross the blood brain barrier.

ISBN: 9780494264805Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Area postrema: A potential CNS target for PYY effects on feeding.
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035 $a (UMI)AAIMR26480
035 $a AAIMR26480
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100 1 $a Jun, Jenny Mary. $3 1267768
245 1 0 $a Area postrema: A potential CNS target for PYY effects on feeding.
300 $a 69 p.
500 $a Source: Masters Abstracts International, Volume: 45-05, page: 2336.
502 $a Thesis (M.Sc.)--Queen's University (Canada), 2007.
520 $a The regulation of energy homeostasis depends on the coordination of signals impacting feeding behaviour and energy balance. Peptide YY (PYY), a satiety signal released postprandially from the distal gut in proportion to caloric intake and meal composition, acts on the neuropeptide Y (NPY) family of receptors. The area postrema (AP) is a sensory circumventricular organ sensitive to circulating factors, which has been shown to exert significant control over autonomic and neuroendocrine functions including vascular tone, fluid balance, and food intake. Previous data demonstrating the presence of Y1, Y 2 and Y5 receptors suggest roles for PYY in the control of energy intake through actions at the AP. In this study, we examined the effects of bath administration of PYY on dissociated rat AP neurons at concentrations ranging from 100 pM to 1 muM. Changes in membrane potential were monitored and analyzed using current-clamp techniques. Clear hyperpolarizing and depolarizing effects were observed depending on the concentration administered. Mean depolarizations of 9.8 +/- 1.0 mV and 4.3 +/- 0.4 mV were observed in response to 100 pM and 10 nM concentrations of PYY1-36, respectively. In contrast, high 1 muM concentrations of PYY3-36 resulted in hyperpolarization of AP neurons, with a mean value of -3.1 +/- 0.1 mV. These responses were pharmacologically determined as mediated by the activation of specific NPY receptor subtypes using specific Y1 and Y2 receptor antagonists. Specifically, PYY1-36 acts at its high affinity Y 1 receptor to cause depolarization and PYY3-36 acts at its preferential Y2 receptor to cause hyperpolarization of AP neurons. Cells were also tested for changes in current following peptide administration under voltage-clamp conditions. Our preliminary slow voltage ramp data suggest that PYY1-36 (10 nM) enhanced an outward voltage-activated current, as demonstrated in 5/8 cells tested. These results demonstrate the effects of PYY in controlling the excitability of AP neurons, suggesting a potential mechanisms through which this circulating peptide may influences the CNS without having to cross the blood brain barrier.
590 $a School code: 0283.
650 4 $a Biology, Animal Physiology. $3 1017835
690 $a 0433
710 2 $a Queen's University (Canada). $3 1017786
773 0 $t Masters Abstracts International $g 45-05.
790 $a 0283
791 $a M.Sc.
792 $a 2007
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