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Mechanisms of induction of neuroadap...

Park, Yang Hae.

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Mechanisms of induction of neuroadaptations following repeated, intermittent amphetamine.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Mechanisms of induction of neuroadaptations following repeated, intermittent amphetamine./
Author:	Park, Yang Hae.
Description:	144 p.
Notes:	Source: Dissertation Abstracts International, Volume: 65-02, Section: B, page: 0675.
Contained By:	Dissertation Abstracts International65-02B.
Subject:	Health Sciences, Pharmacology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3122019
ISBN:	9780496693702

Mechanisms of induction of neuroadaptations following repeated, intermittent amphetamine.
Park, Yang Hae.

Mechanisms of induction of neuroadaptations following repeated, intermittent amphetamine. - 144 p.

Source: Dissertation Abstracts International, Volume: 65-02, Section: B, page: 0675.

Thesis (Ph.D.)--University of Michigan, 2004.

Repeated, intermittent treatment with amphetamine (AMPH) induces neuroadaptations in animals. Due to the complexity of the brain, it is advantageous to investigate these neuroadaptations is best done in a simpler cellular system. Here, we chose rat pheochromocytoma. (PC12) cells to study. PC12 cells were treated with 1muM AMPH for 5 min a day, for 5 days. After ten drug-free days, we found neurite outgrowth and enhanced AMPH-stimulated dopamine release. These neuroadaptations develop over time and require repeated, intermittent AMPH treatment and the presence of a catecholamine transporter. The roles of protein kinases in the induction of AMPH-mediated neuroadaptation were determined using inhibitors of protein kinase C (PKC), mitogen activated protein (MAP) kinase and protein kinase A (PKA). PKC inhibitors and a MAP kinase inhibitor blocked both neuroadaptations but a selective PKA inhibitor, 100muM cAMP-8-Br-Rp isomer, blocked only the development of enhanced AMPH-mediated dopamine release. Acute treatment with AMPH activated PKC and MAP kinase, but not PKA. This result differentiates the mechanisms by which AMPH induces neurite outgrowth and enhanced dopamine release. Therefore, repeated intermittent AMPH treatment can induce neuroadaptations in PC12 cells by the activation of PKC and MAP kinase.

ISBN: 9780496693702Subjects--Topical Terms:

1017717
Health Sciences, Pharmacology.

Mechanisms of induction of neuroadaptations following repeated, intermittent amphetamine.
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020 $a 9780496693702
035 $a (UnM)AAI3122019
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100 1 $a Park, Yang Hae. $3 1914941
245 1 0 $a Mechanisms of induction of neuroadaptations following repeated, intermittent amphetamine.
300 $a 144 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-02, Section: B, page: 0675.
500 $a Chairs: Margaret E. Gnegy; Kevin K. Wang.
502 $a Thesis (Ph.D.)--University of Michigan, 2004.
520 $a Repeated, intermittent treatment with amphetamine (AMPH) induces neuroadaptations in animals. Due to the complexity of the brain, it is advantageous to investigate these neuroadaptations is best done in a simpler cellular system. Here, we chose rat pheochromocytoma. (PC12) cells to study. PC12 cells were treated with 1muM AMPH for 5 min a day, for 5 days. After ten drug-free days, we found neurite outgrowth and enhanced AMPH-stimulated dopamine release. These neuroadaptations develop over time and require repeated, intermittent AMPH treatment and the presence of a catecholamine transporter. The roles of protein kinases in the induction of AMPH-mediated neuroadaptation were determined using inhibitors of protein kinase C (PKC), mitogen activated protein (MAP) kinase and protein kinase A (PKA). PKC inhibitors and a MAP kinase inhibitor blocked both neuroadaptations but a selective PKA inhibitor, 100muM cAMP-8-Br-Rp isomer, blocked only the development of enhanced AMPH-mediated dopamine release. Acute treatment with AMPH activated PKC and MAP kinase, but not PKA. This result differentiates the mechanisms by which AMPH induces neurite outgrowth and enhanced dopamine release. Therefore, repeated intermittent AMPH treatment can induce neuroadaptations in PC12 cells by the activation of PKC and MAP kinase.
520 $a The AMPH-induced neurotrophic effect suggests that AMPH could be used for the treatment of neurodegenerative diseases such as Parkinson's disease. In a rat model of Parkinson's disease, simultaneous grafting of fetal ventral mesencephalon (VM) tissue into the striatum and substantia nigra improve behavioral movement and reduces drug-induced turning. Therefore, in this study, we determined whether AMPH can potentiate the effect of grafting in rat with 6-OHDA lesion. The rats with 6-OHDA lesion were treated with AMPH (1.75 mg/kg, i.p.) every 3 days for one month after fetal VM graft surgery. AMPH treatment significantly reduced apomorphine- but not AMPH-induced turning in rats containing the fetal VM graft. Repeated AMPH also increased the level of growth associated protein-43, a marker for neurite outgrowth, in the dorsal and ventral striatum. This is the first study demonstrating that AMPH treatment may potentiate the effects of a fetal VM graft in a rodent model of Parkinson's disease.
590 $a School code: 0127.
650 4 $a Health Sciences, Pharmacology. $3 1017717
690 $a 0419
710 2 0 $a University of Michigan. $3 777416
773 0 $t Dissertation Abstracts International $g 65-02B.
790 1 0 $a Gnegy, Margaret E., $e advisor
790 1 0 $a Wang, Kevin K., $e advisor
790 $a 0127
791 $a Ph.D.
792 $a 2004
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3122019