PMID- 17084036
OWN - NLM
STAT- MEDLINE
DCOM- 20070315
LR  - 20210218
IS  - 0306-4522 (Print)
IS  - 0306-4522 (Linking)
VI  - 144
IP  - 1
DP  - 2007 Jan 5
TI  - The effect of amphetamine analogs on cleaved microtubule-associated protein-tau 
      formation in the rat brain.
PG  - 223-31
AB  - The present study quantified the cleaved form of the microtubule-associated 
      protein tau (cleaved MAP-tau, C-tau), a previously demonstrated marker of CNS 
      toxicity, following the administration of monoamine-depleting regimens of the 
      psychostimulant drugs amphetamine (AMPH), methamphetamine (METH), 
      +/-3,4-methylenedioxymethamphetamine (MDMA), or para-methoxyamphetamine (PMA) in 
      an attempt to further characterize psychostimulant-induced toxicity. A dopamine 
      (DA)-depleting regimen of AMPH produced an increase in C-tau immunoreactivity in 
      the striatum, while a DA- and serotonin (5-HT)-depleting regimen of METH produced 
      an increase in the number of C-tau immunoreactive cells in the striatum and 
      CA2/CA3 and dentate gyrus regions of the hippocampus. MDMA and PMA, two 
      psychostimulant drugs that produce selective 5-HT depletion in the striatum, had 
      no effect on C-tau immunoreactivity in the striatum or hippocampus. Furthermore, 
      5,7-dihydroxytryptamine (5,7-DHT), an established 5-HT selective neurotoxin, did 
      not produce an increase in C-tau immunoreactivity. Dual fluorescent 
      immunocytochemistry with antibodies to glial fibrillary acidic protein (GFAP) and 
      C-tau indicated that C-tau immunoreactivity was present in astrocytes, not 
      neurons, suggesting that increased C-tau may be an alternative indicator of 
      reactive gliosis. The present results are consistent with previous findings that 
      the DA-depleting psychostimulants AMPH and METH produce reactive gliosis whereas 
      the 5-HT-depleting drugs MDMA and PMA, as well as the known 5-HT selective 
      neurotoxin 5,7-DHT, do not produce an appreciable glial response.
FAU - Straiko, M M W
AU  - Straiko MM
AD  - Neuroscience Graduate Program, University of Cincinnati, Cincinnati, OH 45267, 
      USA.
FAU - Coolen, L M
AU  - Coolen LM
FAU - Zemlan, F P
AU  - Zemlan FP
FAU - Gudelsky, G A
AU  - Gudelsky GA
LA  - eng
GR  - R01 DA007427/DA/NIDA NIH HHS/United States
GR  - DA 07427/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20061102
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Amphetamines)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Microtubule-Associated Proteins)
RN  - 0 (Serotonin Agents)
RN  - 0 (tau Proteins)
RN  - 31363-74-3 (5,7-Dihydroxytryptamine)
RN  - 333DO1RDJY (Serotonin)
RN  - 44RAL3456C (Methamphetamine)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
RN  - OVB8F8P39Q (4-methoxyamphetamine)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - 5,7-Dihydroxytryptamine/pharmacology
MH  - Amphetamines/*pharmacology
MH  - Animals
MH  - Brain Chemistry/*drug effects
MH  - Data Interpretation, Statistical
MH  - Dopamine/metabolism
MH  - Glial Fibrillary Acidic Protein/biosynthesis/metabolism
MH  - Immunohistochemistry
MH  - Male
MH  - Methamphetamine/pharmacology
MH  - Microtubule-Associated Proteins/*biosynthesis
MH  - N-Methyl-3,4-methylenedioxyamphetamine/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Serotonin/metabolism
MH  - Serotonin Agents/pharmacology
MH  - tau Proteins/*biosynthesis
PMC - PMC1817812
MID - NIHMS14879
EDAT- 2006/11/07 09:00
MHDA- 2007/03/16 09:00
PMCR- 2008/01/31
CRDT- 2006/11/07 09:00
PHST- 2006/03/30 00:00 [received]
PHST- 2006/08/26 00:00 [revised]
PHST- 2006/08/29 00:00 [accepted]
PHST- 2006/11/07 09:00 [pubmed]
PHST- 2007/03/16 09:00 [medline]
PHST- 2006/11/07 09:00 [entrez]
PHST- 2008/01/31 00:00 [pmc-release]
AID - S0306-4522(06)01177-8 [pii]
AID - 10.1016/j.neuroscience.2006.08.073 [doi]
PST - ppublish
SO  - Neuroscience. 2007 Jan 5;144(1):223-31. doi: 10.1016/j.neuroscience.2006.08.073. 
      Epub 2006 Nov 2.