PMID- 11754489
OWN - NLM
STAT- MEDLINE
DCOM- 20020201
LR  - 20181130
IS  - 0887-4476 (Print)
IS  - 0887-4476 (Linking)
VI  - 43
IP  - 2
DP  - 2002 Feb
TI  - Striatal dopamine output is compromised within +/- BDNF mice.
PG  - 112-7
AB  - We reported previously that mice lacking one brain-derived neurotrophic factor 
      (BDNF) allele demonstrate elevated striatal dopamine (DA) concentrations but 
      impaired behavioral responses involving the nigrostriatal dopaminergic (NSDA) 
      system. To test the hypothesis that these elevated striatal DA concentrations are 
      associated with perturbed NSDA functioning, we compared striatal DA output 
      between heterozygous mutant (+/-) and wild-type littermate control (+/+) BDNF 
      mice under conditions of an intact NSDA system, as well as following 
      methamphetamine (MA)-induced neurotoxicity. Basal DA output from superfused CS 
      tissue fragments did not differ between +/+ and +/- BDNF mice. Potassium (K+) 
      stimulated DA outputs from intact striatal fragments of +/+ mice were 
      significantly greater than that of +/- BDNF mice. Following MA treatment, K+ 
      stimulated DA output of +/+ mice was statistically equivalent to +/- BDNF mice. 
      Striatal DA concentrations of +/- BDNF mice were elevated, albeit not 
      significantly, in both intact and MA-treated mice relative to +/+ mice. Following 
      MA treatment, striatal DA concentrations were significantly decreased for both 
      genotypes; however, the degree of DA depletion was significantly greater in +/+ 
      mice. Analyzed collectively, these data show the differential effects exerted by 
      a BDNF mutation upon striatal DA concentrations and output. Notably, lower 
      striatal DA concentrations of +/+ vs. +/- BDNF mice can be contrasted with the 
      significantly greater K+ stimulated DA output from the former. This difference 
      was abolished following MA treatment. These results suggest that processes 
      involved with the dynamics of DA release within the NSDA system may be 
      compromised in +/- BDNF mutant mice.
CI  - Copyright 2001 Wiley-Liss, Inc.
FAU - Dluzen, Dean E
AU  - Dluzen DE
AD  - Department of Anatomy, Northeastern Ohio University College of Medicine 
      (NEOUCOM), Rootstown, Ohio 44272-0095, USA. ded@neoucom.edu
FAU - Anderson, Linda I
AU  - Anderson LI
FAU - McDermott, Janet L
AU  - McDermott JL
FAU - Kucera, Jan
AU  - Kucera J
FAU - Walro, Jon M
AU  - Walro JM
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Synapse
JT  - Synapse (New York, N.Y.)
JID - 8806914
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 44RAL3456C (Methamphetamine)
RN  - RWP5GA015D (Potassium)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*deficiency/genetics
MH  - Dopamine/*metabolism
MH  - Drug Interactions/physiology
MH  - Extracellular Space/drug effects/metabolism
MH  - Female
MH  - Genotype
MH  - Male
MH  - Methamphetamine/pharmacology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Knockout
MH  - Neostriatum/drug effects/*metabolism/physiopathology
MH  - Neural Pathways/drug effects/*metabolism/physiopathology
MH  - Neurons/drug effects/*metabolism
MH  - Parkinsonian Disorders/genetics/*metabolism/physiopathology
MH  - Perfusion/methods
MH  - Potassium/metabolism/pharmacology
MH  - Substantia Nigra/drug effects/*metabolism/physiopathology
EDAT- 2002/01/05 10:00
MHDA- 2002/02/02 10:01
CRDT- 2002/01/05 10:00
PHST- 2002/01/05 10:00 [pubmed]
PHST- 2002/02/02 10:01 [medline]
PHST- 2002/01/05 10:00 [entrez]
AID - 10.1002/syn.10027 [pii]
AID - 10.1002/syn.10027 [doi]
PST - ppublish
SO  - Synapse. 2002 Feb;43(2):112-7. doi: 10.1002/syn.10027.