AI Article Synopsis
- Amphetamine (AMPH) leads to the degeneration of dopamine terminals in the central nervous system, but the exact mechanisms are still unclear.
- Researchers found that AMPH reduces the levels of GAP-43, a protein important for neuron growth, in the striatum of rats and in PC12 cells, which are models for dopaminergic neurons.
- The study indicates that AMPH causes neuron damage by inhibiting the PKCβ1/GAP-43 pathway, suggesting that activation of PKC can counteract this damage and promote neuron health.
Article Abstract
Amphetamine (AMPH) causes the degeneration of dopamine terminals in the central nervous system. The mechanisms for this damage are unclear. We found AMPH reduced level of GAP-43 in the striatum of rats that receives rich dopaminergic terminals. Using PC12 cells as dopaminergic neuronal models, we further found that AMPH inhibited GAP-43 and GAP-43 phosphorylation in PC12 cells. The reduced GAP-43 was correlated with neurite injury of PC12 cells. The PKCβ1, an upstream molecule of GAP-43, was also inhibited by AMPH. Phorbol 12-myristate 13-acetate (PMA) as a specific activator of PKC increased levels of PKCβ1 and GAP-43, and efficiently prevented neurite degeneration of PC12 cells induced by AMPH. On the other side, enzastuarin, an inhibitor of PKC, decreased levels of PKCβ1 and GAP-43, and caused neurite injury of PC12 cells. Together, our results suggest that AMPH induces neurite injury in PC12 cells through inhibiting PKCβ1/GAP-43 pathway.
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| http://dx.doi.org/10.1016/j.neuro.2022.09.004 | DOI Listing |
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