The study investigates the role of dopamine (DA) in striatal synaptic plasticity, particularly in medium spiny neurons (MSNs) that express either D1 or D2 DA receptors. It challenges the previous notion that DA is essential for the induction of synaptic plasticity and suggests that DA plays a complementary role in ensuring bidirectional and Hebbian plasticity. Using brain slices from DA receptor transgenic mice, the researchers found that DA signaling in D2 MSNs promotes long-term potentiation (LTP), while in D1 MSNs, it promotes long-term depression (LTD). However, the induction of these plasticity forms is not unidirectional but rather depends on the type of DA receptor present. The study also examines the impact of Parkinson's disease (PD) models on this balance, showing that DA depletion leads to a disruption of bidirectional plasticity, which could contribute to network pathology and symptoms in PD. The findings highlight the importance of DA in regulating striatal network function and suggest that the imbalance in DA signaling may underlie the functional deficits observed in PD.The study investigates the role of dopamine (DA) in striatal synaptic plasticity, particularly in medium spiny neurons (MSNs) that express either D1 or D2 DA receptors. It challenges the previous notion that DA is essential for the induction of synaptic plasticity and suggests that DA plays a complementary role in ensuring bidirectional and Hebbian plasticity. Using brain slices from DA receptor transgenic mice, the researchers found that DA signaling in D2 MSNs promotes long-term potentiation (LTP), while in D1 MSNs, it promotes long-term depression (LTD). However, the induction of these plasticity forms is not unidirectional but rather depends on the type of DA receptor present. The study also examines the impact of Parkinson's disease (PD) models on this balance, showing that DA depletion leads to a disruption of bidirectional plasticity, which could contribute to network pathology and symptoms in PD. The findings highlight the importance of DA in regulating striatal network function and suggest that the imbalance in DA signaling may underlie the functional deficits observed in PD.