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Gamma hydroxybutyrate (GHB): Mechani...

Lyng, Eric E.

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Gamma hydroxybutyrate (GHB): Mechanisms of central nervous system toxicity.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Gamma hydroxybutyrate (GHB): Mechanisms of central nervous system toxicity./
Author:	Lyng, Eric E.
Description:	206 p.
Notes:	Source: Dissertation Abstracts International, Volume: 67-03, Section: B, page: 1222.
Contained By:	Dissertation Abstracts International67-03B.
Subject:	Biology, General. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3213445
ISBN:	9780542628207

Gamma hydroxybutyrate (GHB): Mechanisms of central nervous system toxicity.
Lyng, Eric E.

Gamma hydroxybutyrate (GHB): Mechanisms of central nervous system toxicity. - 206 p.

Source: Dissertation Abstracts International, Volume: 67-03, Section: B, page: 1222.

Thesis (Ph.D.)--Baylor University, 2006.

Gamma Hydroxybutyrate (GHB) is an endogenous metabolite of gamma-aminobutyric acid (GABA) and a putative neurotransmitter found in mammalian brain. The illicit use of GHB is a growing health care concern in the U.S. Low doses have euphoric and stimulatory effects while high doses act as a CNS depressant and can cause respiratory failure. In addition to fatalities and drug facilitated rape, in 2004 over 7000 GHB overdoses were reported in the U.S. Gamma Butyrolactone (GBL) and 1,4-Butanediol (1,4-BD), precursors of GHB, can cause similar effects after being converted to GHB in the body. While GHB is a Schedule I compound, recently it was given a Schedule III classification as a drug for treatment of cataplexy associated with narcolepsy. Individuals affected by the inherited disorder succinic semialdehyde dehydrogenase (SSADH) deficiency have significant elevation of GABA and GHB in body tissues, and a range of neurological complications. Currently there is no treatment option for a GHB overdose situation or for SSADH patients.

ISBN: 9780542628207Subjects--Topical Terms:

1018625
Biology, General.

Gamma hydroxybutyrate (GHB): Mechanisms of central nervous system toxicity.
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100 1 $a Lyng, Eric E. $3 1920600
245 1 0 $a Gamma hydroxybutyrate (GHB): Mechanisms of central nervous system toxicity.
300 $a 206 p.
500 $a Source: Dissertation Abstracts International, Volume: 67-03, Section: B, page: 1222.
500 $a Adviser: Teodoro G. Bottiglieri.
502 $a Thesis (Ph.D.)--Baylor University, 2006.
520 $a Gamma Hydroxybutyrate (GHB) is an endogenous metabolite of gamma-aminobutyric acid (GABA) and a putative neurotransmitter found in mammalian brain. The illicit use of GHB is a growing health care concern in the U.S. Low doses have euphoric and stimulatory effects while high doses act as a CNS depressant and can cause respiratory failure. In addition to fatalities and drug facilitated rape, in 2004 over 7000 GHB overdoses were reported in the U.S. Gamma Butyrolactone (GBL) and 1,4-Butanediol (1,4-BD), precursors of GHB, can cause similar effects after being converted to GHB in the body. While GHB is a Schedule I compound, recently it was given a Schedule III classification as a drug for treatment of cataplexy associated with narcolepsy. Individuals affected by the inherited disorder succinic semialdehyde dehydrogenase (SSADH) deficiency have significant elevation of GABA and GHB in body tissues, and a range of neurological complications. Currently there is no treatment option for a GHB overdose situation or for SSADH patients.
520 $a GHB has been shown to inhibit striatal dopamine release leading to sedation and loss of locomotor activity in rodents. However, GHB's mechanism of action is poorly understood. This dissertation investigated acute and chronic effects of GBL, a precursor to GHB, on locomotor function and monoamine neurotransmitter metabolism in mice. Dose response studies were performed to characterize the effects of GBL. Compounds aimed at increasing central dopaminergic activity or antagonism of GABAergic activity were tested for their ability to antagonize the locomotor effects induced by GBL. In total, eight different compounds were studied of which pergolide and nomifensine were successful at antagonizing the loss of locomotor activity when administered either prior to or after GBL. Chronic administration of GBL over the course of 14 days was evaluated in mice using a rotarod system. These studies did not reveal any long term detrimental effect of GBL on locomotor function.
520 $a This dissertation is the first report showing the ability of pergolide and nomifensine to antagonize the loss of locomotor activity induced by GBL. These studies provide insight into treatment options for GHB toxicity or overdose as well as for patients with SSADH deficiency.
590 $a School code: 0014.
650 4 $a Biology, General. $3 1018625
650 4 $a Health Sciences, Toxicology. $3 1017752
650 4 $a Health Sciences, Pharmacology. $3 1017717
650 4 $a Biology, Animal Physiology. $3 1017835
650 4 $a Chemistry, Biochemistry. $3 1017722
690 $a 0306
690 $a 0383
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690 $a 0487
710 2 0 $a Baylor University. $3 771397
773 0 $t Dissertation Abstracts International $g 67-03B.
790 1 0 $a Bottiglieri, Teodoro G., $e advisor
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791 $a Ph.D.
792 $a 2006
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3213445