PMID- 23283760
OWN - NLM
STAT- MEDLINE
DCOM- 20140303
LR  - 20211021
IS  - 1476-3524 (Electronic)
IS  - 1029-8428 (Linking)
VI  - 24
IP  - 2
DP  - 2013 Aug
TI  - Involvement of the alpha(1D)-adrenergic receptor in methamphetamine-induced 
      hyperthermia and neurotoxicity in rats.
PG  - 130-8
LID - 10.1007/s12640-012-9369-9 [doi]
AB  - Methamphetamine (METH) is a psychostimulant that damages nigrostriatal 
      dopaminergic terminals, primarily by enhancing dopamine and glutamate release. 
      alpha(1)-adrenergic receptor (AR) subtype involved in METH-induced neurotoxicity in 
      rats was investigated using selective alpha(1)-AR antagonists. METH neurotoxicity was 
      evaluated by (1) measuring body temperature; (2) determining tyrosine hydroxylase 
      (TH) immunoreactivity levels; (3) examining levels of dopamine and its 
      metabolites; and (4) assessing glial fibrillary acidic protein (GFAP) and 
      microglial immunoreactivity in the striatum. METH caused a decrease in dopamine 
      and TH levels and induced hyperthermia which is an exacerbating factor of METH 
      neurotoxicity. Concurrently, METH increased GFAP expression and the number of 
      activated microglia. Pretreatment with prazosin, a nonselective alpha(1)-AR antagonist, 
      completely abolished METH-induced decrease in both dopamine and TH and caused a 
      partial reduction in hyperthermia. Prazosin also prevented METH-induced increase 
      in both GFAP expression and the number of activated microglia. In vivo 
      microdialysis analysis revealed that prazosin, however, does not alter the 
      METH-induced dopamine release in the striatum. The neuroprotective effects of 
      prazosin could be mimicked by a selective alpha(1D) antagonist, BMY 7378, but not by 
      selective alpha(1A) or alpha(1B) antagonists. These results suggest that the alpha(1D)-AR is 
      involved in METH-induced hyperthermia and neurotoxicity in rats.
FAU - Kikuchi-Utsumi, Kazue
AU  - Kikuchi-Utsumi K
AD  - Department of Pharmacology, Teikyo University School of Medicine, 2-11-1 Kaga, 
      Itabashi Ward, Tokyo 173-8605, Japan.
FAU - Ishizaka, Mami
AU  - Ishizaka M
FAU - Matsumura, Nobuko
AU  - Matsumura N
FAU - Watabe, Masahiko
AU  - Watabe M
FAU - Aoyama, Koji
AU  - Aoyama K
FAU - Sasakawa, Nobuyuki
AU  - Sasakawa N
FAU - Nakaki, Toshio
AU  - Nakaki T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130103
PL  - United States
TA  - Neurotox Res
JT  - Neurotoxicity research
JID - 100929017
RN  - 0 (Adrenergic alpha-Antagonists)
RN  - 0 (Receptors, Adrenergic, alpha-1)
RN  - 44RAL3456C (Methamphetamine)
SB  - IM
MH  - Adrenergic alpha-Antagonists/*pharmacology
MH  - Animals
MH  - Corpus Striatum/*drug effects/*pathology
MH  - *Hyperthermia, Induced/methods
MH  - Male
MH  - Methamphetamine/*toxicity
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, Adrenergic, alpha-1/*physiology
EDAT- 2013/01/04 06:00
MHDA- 2014/03/04 06:00
CRDT- 2013/01/04 06:00
PHST- 2011/12/27 00:00 [received]
PHST- 2012/12/12 00:00 [accepted]
PHST- 2012/12/11 00:00 [revised]
PHST- 2013/01/04 06:00 [entrez]
PHST- 2013/01/04 06:00 [pubmed]
PHST- 2014/03/04 06:00 [medline]
AID - 10.1007/s12640-012-9369-9 [doi]
PST - ppublish
SO  - Neurotox Res. 2013 Aug;24(2):130-8. doi: 10.1007/s12640-012-9369-9. Epub 2013 Jan 
      3.