Functional hyperdopaminergia in dopamine transporter knock-out mice.
Dopamine is an important regulator of many central nervous system functions. Hyperfunction of the dopaminergic system is believed to be related to several pathological conditions. Genetic deletion of the dopamine transporter gene in mice results in a persistent extracellular hyperdopaminergic tone, that is functionally revealed as hyperactivity. The lack of a reuptake mechanism produces a marked increase in functional extracellular dopamine which results in profound plasticity of pre- and postsynaptic parameters of dopamine homeostasis. The mice lacking the dopamine transporter gene may represent an appropriate model to elucidate the molecular adaptive changes accompanying pathological states associated with hyperdopaminergic function.
Gainetdinov
R R
RR
Howard Hughes Medical Institute Laboratories, Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Jones
S R
SR
Caron
M G
MG
D000818:Animals; D002352:Carrier Proteins / Q000235:genetics*; D003342:Corpus Striatum / Q000378:metabolism; D004298:Dopamine / Q000032:analysis / Q000235:genetics* / Q000378:metabolism; D005110:Extracellular Space / Q000737:chemistry; D017353:Gene Deletion; D005818:Genetic Engineering; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D017551:Microdialysis; D009473:Neuronal Plasticity / Q000502:physiology; D009474:Neurons / Q000737:chemistry; D017981:Receptors, Neurotransmitter / Q000737:chemistry; D013997:Time Factors
D002352:Carrier Proteins; D017981:Receptors, Neurotransmitter; D004298:Dopamine