東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

Nicotine and methylphenidate on adol...

George Mason University.

FindBook

Google Book

Amazon

博客來

Nicotine and methylphenidate on adolescent brain development and addiction liability: Dose investigation.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Nicotine and methylphenidate on adolescent brain development and addiction liability: Dose investigation./
作者:	Wheeler, Tracey L.
面頁冊數:	100 p.
附註:	Adviser: Robert F. Smith.
Contained By:	Dissertation Abstracts International69-08B.
標題:	Biology, Neuroscience. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3327222
ISBN:	9780549797128

Nicotine and methylphenidate on adolescent brain development and addiction liability: Dose investigation.
Wheeler, Tracey L.

Nicotine and methylphenidate on adolescent brain development and addiction liability: Dose investigation. - 100 p.

Adviser: Robert F. Smith.

Thesis (Ph.D.)--George Mason University, 2009.

The present study investigated the combined effects of chronic adolescent nicotine and methylphenidate on behavioral tolerance to these drugs in adulthood and how they relate to glutamate and dopamine receptor mRNA expression in the medial prefrontal cortex and striatum. Adolescent rats [P28] received low dose nicotine (2 mg/kg per day) through subcutaneously implanted osmotic pumps. Subsequently [P35] low dose methylphenidate (1.5 mg/kg) was administered orally (twice daily 5 days per week) and both drugs continued until the end of adolescence [P56]. Following a one-month drug free period all animals were challenged with either a stimulant (nicotine, 0.5 mg/kg) or saline in the open field. Twenty-four hours following testing animals were sacrificed and mRNAs of the dopamine [D1, D2, D3, D3nf splice variant] and glutamate N-methyl-D-aspartic acid [NR2a and NR2b subunits] receptors were examined. Animals with combined exposure displayed stronger tolerance to the stimulant challenge compared to single drug exposure or control groups indicating that combined consumption has an additive effect. This additive relationship persisted in mRNA expression of various dopamine and glutamate receptor indices. Many of these neurochemical changes were only revealed following the single adult stimulant exposure. Adolescent stimulant exposure resulted in long-term changes in mRNAs of the NR2b subunit as well as D1, D2 and D3nf expression in many brain regions we investigated. These changes are possibly related to addiction liability but unrelated to behavioral tolerance. To our knowledge this is the first study that has shown long-term behavioral and neurochemical changes stemming from very low chronic exposure of these two commonly co-consumed stimulants during adolescence.

ISBN: 9780549797128Subjects--Topical Terms:

1017680
Biology, Neuroscience.

Nicotine and methylphenidate on adolescent brain development and addiction liability: Dose investigation.
LDR:02740nmm 2200301 a 45 001 867320
005 20100804
008 100804s2009 ||||||||||||||||| ||eng d
020 $a 9780549797128
035 $a (UMI)AAI3327222
035 $a AAI3327222
040 $a UMI $c UMI
100 1 $a Wheeler, Tracey L. $3 1036044
245 1 0 $a Nicotine and methylphenidate on adolescent brain development and addiction liability: Dose investigation.
300 $a 100 p.
500 $a Adviser: Robert F. Smith.
500 $a Source: Dissertation Abstracts International, Volume: 69-08, Section: B, page: 5096.
502 $a Thesis (Ph.D.)--George Mason University, 2009.
520 $a The present study investigated the combined effects of chronic adolescent nicotine and methylphenidate on behavioral tolerance to these drugs in adulthood and how they relate to glutamate and dopamine receptor mRNA expression in the medial prefrontal cortex and striatum. Adolescent rats [P28] received low dose nicotine (2 mg/kg per day) through subcutaneously implanted osmotic pumps. Subsequently [P35] low dose methylphenidate (1.5 mg/kg) was administered orally (twice daily 5 days per week) and both drugs continued until the end of adolescence [P56]. Following a one-month drug free period all animals were challenged with either a stimulant (nicotine, 0.5 mg/kg) or saline in the open field. Twenty-four hours following testing animals were sacrificed and mRNAs of the dopamine [D1, D2, D3, D3nf splice variant] and glutamate N-methyl-D-aspartic acid [NR2a and NR2b subunits] receptors were examined. Animals with combined exposure displayed stronger tolerance to the stimulant challenge compared to single drug exposure or control groups indicating that combined consumption has an additive effect. This additive relationship persisted in mRNA expression of various dopamine and glutamate receptor indices. Many of these neurochemical changes were only revealed following the single adult stimulant exposure. Adolescent stimulant exposure resulted in long-term changes in mRNAs of the NR2b subunit as well as D1, D2 and D3nf expression in many brain regions we investigated. These changes are possibly related to addiction liability but unrelated to behavioral tolerance. To our knowledge this is the first study that has shown long-term behavioral and neurochemical changes stemming from very low chronic exposure of these two commonly co-consumed stimulants during adolescence.
590 $a School code: 0883.
650 4 $a Biology, Neuroscience. $3 1017680
650 4 $a Health Sciences, Mental Health. $3 1017693
650 4 $a Health Sciences, Toxicology. $3 1017752
650 4 $a Psychology, Physiological. $3 1017869
690 $a 0317
690 $a 0347
690 $a 0383
690 $a 0989
710 2 $a George Mason University. $3 1019450
773 0 $t Dissertation Abstracts International $g 69-08B.
790 $a 0883
790 1 0 $a Smith, Robert F., $e advisor
791 $a Ph.D.
792 $a 2009
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3327222