Abstract
The mechanisms regulating expression of the dopamine transporter are poorly understood. We tested the hypothesis that neuronal activity is one of the non-genetic determinants of dopamine transporter abundance. Sustained changes in neuronal activity caused by tetrodotoxin and 4-aminopyridine altered the dopamine uptake and abundance of dopamine transporter and its mRNA in rat mesencephalic cultures. The altered neuronal activity caused by these two drugs is accompanied by changes in intracellular calcium concentrations and Ca 2+/calmodulin-dependent protein (CaM) kinase II activity in dopamine neurons. Chronic treatment with an L-type calcium channel blocker (nifedipine) or CaM kinase inhibitor (KN93) decreased dopamine transporter-mediated uptake and occluded the effects of tetrodotoxin and 4-aminopyridine. These data suggest that neuronal activity can regulate dopamine transporter function and abundance via calcium/CaM kinase II signaling.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 2017-2027 |
| Number of pages | 11 |
| Journal | European Journal of Neuroscience |
| Volume | 28 |
| Issue number | 10 |
| DOIs | |
| State | Published - Nov 1 2008 |
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Keywords
- Action potential
- Calcium
- Mesencephalic
- Monoamine
- Rat
- Uptake
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Activity-dependent regulation of the dopamine transporter is mediated by Ca2+/calmodulin-dependent protein kinase signaling. / Padmanabhan, Shalini; Lambert, Nevin A; Prasad, Balakrishna M.
In: European Journal of Neuroscience, Vol. 28, No. 10, 01.11.2008, p. 2017-2027.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Activity-dependent regulation of the dopamine transporter is mediated by Ca2+/calmodulin-dependent protein kinase signaling
AU - Padmanabhan, Shalini
AU - Lambert, Nevin A
AU - Prasad, Balakrishna M.
PY - 2008/11/1
Y1 - 2008/11/1
N2 - The mechanisms regulating expression of the dopamine transporter are poorly understood. We tested the hypothesis that neuronal activity is one of the non-genetic determinants of dopamine transporter abundance. Sustained changes in neuronal activity caused by tetrodotoxin and 4-aminopyridine altered the dopamine uptake and abundance of dopamine transporter and its mRNA in rat mesencephalic cultures. The altered neuronal activity caused by these two drugs is accompanied by changes in intracellular calcium concentrations and Ca 2+/calmodulin-dependent protein (CaM) kinase II activity in dopamine neurons. Chronic treatment with an L-type calcium channel blocker (nifedipine) or CaM kinase inhibitor (KN93) decreased dopamine transporter-mediated uptake and occluded the effects of tetrodotoxin and 4-aminopyridine. These data suggest that neuronal activity can regulate dopamine transporter function and abundance via calcium/CaM kinase II signaling.
AB - The mechanisms regulating expression of the dopamine transporter are poorly understood. We tested the hypothesis that neuronal activity is one of the non-genetic determinants of dopamine transporter abundance. Sustained changes in neuronal activity caused by tetrodotoxin and 4-aminopyridine altered the dopamine uptake and abundance of dopamine transporter and its mRNA in rat mesencephalic cultures. The altered neuronal activity caused by these two drugs is accompanied by changes in intracellular calcium concentrations and Ca 2+/calmodulin-dependent protein (CaM) kinase II activity in dopamine neurons. Chronic treatment with an L-type calcium channel blocker (nifedipine) or CaM kinase inhibitor (KN93) decreased dopamine transporter-mediated uptake and occluded the effects of tetrodotoxin and 4-aminopyridine. These data suggest that neuronal activity can regulate dopamine transporter function and abundance via calcium/CaM kinase II signaling.
KW - Action potential
KW - Calcium
KW - Mesencephalic
KW - Monoamine
KW - Rat
KW - Uptake
UR - http://www.scopus.com/inward/record.url?scp=55949104934&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=55949104934&partnerID=8YFLogxK
U2 - 10.1111/j.1460-9568.2008.06496.x
DO - 10.1111/j.1460-9568.2008.06496.x
M3 - Article
VL - 28
SP - 2017
EP - 2027
JO - European Journal of Neuroscience
JF - European Journal of Neuroscience
SN - 0953-816X
IS - 10
ER -