Dopamine uptake blockers nullify methamphetamine-induced decrease in dopamine uptake and plasma membrane potential in rat striatal synaptosomes
Author(s)
Westphalen, RI
Stadlin, Alfreda
Griffith University Author(s)
Year published
2000
Metadata
Show full item recordAbstract
Rat striatal synaptosomes showed a reduced capacity to generate a membrane potential after being exposed to methamphetamine (METH) for 1 h. As a consequence, the dopamine (DA) synaptosomes were impeded in their electrogenic-dependent reuptake of dopamine. The capacity for METH-exposed nerve terminals to generate a membrane potential may contribute to the ability of METH to destroy dopaminergic neurons. DA uptake inhibitors (DAUIs) were found to counteract the METH-induced decrease in synaptosomal [3H]DA Vmax by stablizing METH-induced reductions in PMP. Because DAUIs showed the same effects as a Na+-channel blocker, DAUIs ...
View more >Rat striatal synaptosomes showed a reduced capacity to generate a membrane potential after being exposed to methamphetamine (METH) for 1 h. As a consequence, the dopamine (DA) synaptosomes were impeded in their electrogenic-dependent reuptake of dopamine. The capacity for METH-exposed nerve terminals to generate a membrane potential may contribute to the ability of METH to destroy dopaminergic neurons. DA uptake inhibitors (DAUIs) were found to counteract the METH-induced decrease in synaptosomal [3H]DA Vmax by stablizing METH-induced reductions in PMP. Because DAUIs showed the same effects as a Na+-channel blocker, DAUIs may prevent METH-induced destruction of dopaminergic neurons by raising plasma membrane potential.
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View more >Rat striatal synaptosomes showed a reduced capacity to generate a membrane potential after being exposed to methamphetamine (METH) for 1 h. As a consequence, the dopamine (DA) synaptosomes were impeded in their electrogenic-dependent reuptake of dopamine. The capacity for METH-exposed nerve terminals to generate a membrane potential may contribute to the ability of METH to destroy dopaminergic neurons. DA uptake inhibitors (DAUIs) were found to counteract the METH-induced decrease in synaptosomal [3H]DA Vmax by stablizing METH-induced reductions in PMP. Because DAUIs showed the same effects as a Na+-channel blocker, DAUIs may prevent METH-induced destruction of dopaminergic neurons by raising plasma membrane potential.
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Journal Title
Annals of the New York Academy of Sciences
Volume
914
Subject
PRE2009-Central Nervous System