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Dichotomous dopaminergic control of striatal synaptic plasticity. |
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Notes for this articleThis article show that both subpopulations of MSN are able to Hebbian bidirectional plasticity when spike time-dependent plasticity (STDP) protocols are used. Dopamine has rather modulatory function. Upon behaviorally relevant stimulus, enhanced DA release causing stimulation of D1 receptors and unblock the LTP in D1 MSN. A2A and NMDA seems be crucial for LTP, CB1 and mGluR5 for LTD. Three types of interneurons (Cholinergic, NO, ??CB1??) are redundant in the process.
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AbstractAt synapses between cortical pyramidal neurons and principal striatal medium spiny neurons (MSNs), postsynaptic D1 and D2 dopamine (DA) receptors are postulated to be necessary for the induction of long-term potentiation and depression, respectively-forms of plasticity thought to underlie associative learning. Because these receptors are restricted to two distinct MSN populations, this postulate demands that synaptic plasticity be unidirectional in each cell type. Using brain slices from DA receptor transgenic mice, we show that this is not the case. Rather, DA plays complementary roles in these two types of MSN to ensure that synaptic plasticity is bidirectional and Hebbian. In models of Parkinson's disease, this system is thrown out of balance, leading to unidirectional changes in plasticity that could underlie network pathology and symptoms.
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