PMID- 16326431
OWN - NLM
STAT- MEDLINE
DCOM- 20060106
LR  - 20181203
IS  - 1528-7394 (Print)
IS  - 0098-4108 (Linking)
VI  - 68
IP  - 23-24
DP  - 2005 Dec 10
TI  - Increases in [(3)H]-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid 
      (AMPA) receptor binding and mRNA expression of AMPA-sensitive glutamate receptor 
      A (GluR-A) subunits in rats withdrawn from butorphanol.
PG  - 2163-74
AB  - An autoradiographic study of 
      [(3)H]-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid(AMPA) receptor 
      binding and an assessment of in situ hybridization of AMPA-sensitive glutamate 
      receptor A (GluR-A) subunits in the rat brain were performed 7 h after withdrawal 
      from butorphanol infusion. Animals were rendered dependent by 
      intracerebroventricular (icv) infusion of butorphanol (26 nmol/microl/h) via 
      osmotic minipumps for 3 d. Brain sections for binding of [(3)H]AMPA were 
      incubated with 15 nM [(3)H]AMPA. The probes for in situ hybridization were 
      labeled at its 3 cent end using terminal deoxynucleotidyl transferase and 
      [(35)S]dATP. The highest degree of [(3)H]AMPA binding was shown in the 
      hippocampus. The extent of [(3)H]AMPA binding was increased significantly in each 
      of the brain areas examined, cortex, septum, caudate putamen, and hippocampus of 
      rats, following withdrawal from butorphanol. The highest level of mRNA for GluR-A 
      receptor for flop and flip subunits, was found in the dentate gyrus and in the 
      CA3 region of the hippocampus. The amounts of mRNA for the flop form of GluR-A 
      receptor were significantly increased in the cortex, caudate putamen, thalamus, 
      and dentate gyrus of hippocampus of rat brain. The amounts of mRNA for the flip 
      form of GluR-A receptor were markedly elevated in the cortex, thalamus, caudate 
      putamen, and hippocampus. These findings suggest that increases in expression of 
      mRNA for the GluR-A receptor and in the binding of AMPA to its receptor may play 
      an important role during withdrawal from butorphanol dependence.
FAU - Lee, Seok-Yong
AU  - Lee SY
AD  - Department of Pharmacology, College of Pharmacy, Sungkyunkwan University, Suwon, 
      Republic of Korea.
FAU - Jang, Choon-Gon
AU  - Jang CG
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Toxicol Environ Health A
JT  - Journal of toxicology and environmental health. Part A
JID - 100960995
RN  - 0 (Analgesics, Opioid)
RN  - 0 (Narcotic Antagonists)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, AMPA)
RN  - 10028-17-8 (Tritium)
RN  - QV897JC36D (Butorphanol)
RN  - TFZ3H25BS1 (glutamate receptor ionotropic, AMPA 1)
SB  - IM
MH  - Analgesics, Opioid
MH  - Animals
MH  - Autoradiography
MH  - Brain/*metabolism
MH  - *Butorphanol/administration & dosage
MH  - Gene Expression Regulation
MH  - In Situ Hybridization
MH  - Injections, Intraventricular
MH  - Male
MH  - *Narcotic Antagonists
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, AMPA/genetics/*metabolism
MH  - Substance Withdrawal Syndrome/*metabolism
MH  - Tritium
EDAT- 2005/12/06 09:00
MHDA- 2006/01/07 09:00
CRDT- 2005/12/06 09:00
PHST- 2005/12/06 09:00 [pubmed]
PHST- 2006/01/07 09:00 [medline]
PHST- 2005/12/06 09:00 [entrez]
AID - K33565L7668R106Q [pii]
AID - 10.1080/15287390500177263 [doi]
PST - ppublish
SO  - J Toxicol Environ Health A. 2005 Dec 10;68(23-24):2163-74. doi: 
      10.1080/15287390500177263.