PMID- 8937435
OWN - NLM
STAT- MEDLINE
DCOM- 19970102
LR  - 20221207
IS  - 0006-2952 (Print)
IS  - 0006-2952 (Linking)
VI  - 52
IP  - 8
DP  - 1996 Oct 25
TI  - Studies on the mechanism of p-chloroamphetamine neurotoxicity.
PG  - 1271-7
AB  - Studies were conducted to investigate the sensitivity of p-chloroamphetamine 
      (PCA)-induced neurochemical changes to various pharmacological manipulations 
      known to block the neurochemical effects of 3,4-methylenedioxymethamphetamine 
      (MDMA). The monoamine oxidase-B (MAO-B) inhibitor L-deprenyl (2 mg/kg) given 4 hr 
      before a nonneurotoxic dose of PCA (2 mg/kg) was shown not to alter the amount of 
      [3H]paroxetine bound to serotonin (5-HT) uptake sites 7 days after treatment. 
      L-Deprenyl 4 hr before a neurotoxic dose of PCA (10 mg/kg) did not change the 
      acute hyperthermia. Further, neither L-deprenyl nor another selective MAO-B 
      inhibitor, MDL-72,974 (1.25 mg/kg), given 30 min before or daily for 4 days 
      before a single dose of PCA attenuated or potentiated the decrease in the number 
      of [3H]paroxetine binding sites measured 7 days after PCA treatment. The 
      combination of the MAO-A inhibitor clorgyline (2.5 mg/kg) or a nonspecific dose 
      of L-deprenyl (10 mg/kg) with the selective 5-HT releasing agent 
      5,6-methylenedioxy-2-aminoindan did not lead to changes in the levels of 5-HT, 
      5-hydroxyindoleacetic acid or dopamine 7 days after treatment. Finally, the 
      5-HT2A receptor antagonist MDL-11,939 (5 mg/kg) did not protect against the 
      neurotoxicity of PCA. By comparing the present work with previous studies of 
      MDMA, these results can be interpreted to suggest that the mechanism of the 
      neurotoxicity induced by PCA is not identical to that induced by MDMA. The 
      relationship of these results to the neurotoxicity induced by MDMA is also 
      discussed.
FAU - Sprague, J E
AU  - Sprague JE
AD  - Department of Medicinal Chemistry and Molecular Pharmacology, Purdue University, 
      West Lafayette, IN 47907, USA.
FAU - Johnson, M P
AU  - Johnson MP
FAU - Schmidt, C J
AU  - Schmidt CJ
FAU - Nichols, D E
AU  - Nichols DE
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - England
TA  - Biochem Pharmacol
JT  - Biochemical pharmacology
JID - 0101032
RN  - 0 (Indans)
RN  - 0 (Monoamine Oxidase Inhibitors)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Neurotoxins)
RN  - 0 (Serotonin Agents)
RN  - 0 (Serotonin Uptake Inhibitors)
RN  - 0DMJ6G3XBF (5,6-methylenedioxy-2-aminoindane)
RN  - 2K1V7GP655 (Selegiline)
RN  - 333DO1RDJY (Serotonin)
RN  - 41VRH5220H (Paroxetine)
RN  - 54-16-0 (Hydroxyindoleacetic Acid)
RN  - 64-12-0 (p-Chloroamphetamine)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
RN  - LYJ16FZU9Q (Clorgyline)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - Brain/drug effects/metabolism
MH  - Clorgyline/pharmacology
MH  - Dopamine/metabolism
MH  - Fever/chemically induced
MH  - Hydroxyindoleacetic Acid/metabolism
MH  - Indans/pharmacology
MH  - Male
MH  - Monoamine Oxidase Inhibitors/pharmacology
MH  - N-Methyl-3,4-methylenedioxyamphetamine/toxicity
MH  - Neuroprotective Agents/pharmacology
MH  - Neurotoxins/*toxicity
MH  - Paroxetine/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Selegiline/pharmacology
MH  - Serotonin/metabolism
MH  - Serotonin Agents/toxicity
MH  - Selective Serotonin Reuptake Inhibitors/pharmacology
MH  - p-Chloroamphetamine/*toxicity
EDAT- 1996/10/25 00:00
MHDA- 1996/10/25 00:01
CRDT- 1996/10/25 00:00
PHST- 1996/10/25 00:00 [pubmed]
PHST- 1996/10/25 00:01 [medline]
PHST- 1996/10/25 00:00 [entrez]
AID - 0006-2952(96)00482-0 [pii]
AID - 10.1016/0006-2952(96)00482-0 [doi]
PST - ppublish
SO  - Biochem Pharmacol. 1996 Oct 25;52(8):1271-7. doi: 10.1016/0006-2952(96)00482-0.