Abstract :
[en] The activation of N-methyl-D-aspartate receptors (NMDARs) in substantia nigra pars
compacta (SNc) dopamine (DA) cells is central to generate the bursting activity, a
phasic signal linked to DA related behaviors via the change in postsynaptic DA
release. NMDARs are recruited during excitatory synaptic transmission by glutamate
release but the glycine site level of occupancy of these receptors during basal action
potential-dependent activity is not known for SNc DA neurons. We explored NMDARdependent
signals during exogenous applications of co-agonists in midbrain slices
from juvenile rats. We found that both glycine and D-serine strengthened the
NMDAR-dependent component of excitatory postsynaptic currents (EPSCs) in a
concentration-dependent manner. EPSCs were also increased by endogenous
glycine via the blockade of the glycine transport. The glycine site of NMDARs
contributing to synaptic transmission is therefore subsaturated. The behaviorally
relevant burst firing was more sensitive to exogenous D-serine and endogenous
glycine than to exogenous glycine. The mechanisms regulating the availability of the
co-agonists exert consequently a critical influence on the excitability of DA neurons
via NMDARs.
The modulation of the phasic firing in DA neurons by ambient NMDAR co-agonists
may be important for nigral information processing and downstream motor-related
behavior.
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