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Endogenous and exogenous dopamine presynaptically inhibits glutamatergic reticulospinal transmission via an action of D 2 ‐receptors on N‐type Ca 2+ channels
Author(s) -
Svensson Erik,
Wikström Martin A.,
Hill Russell H.,
Grillner Sten
Publication year - 2003
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2003.02466.x
Subject(s) - excitatory postsynaptic potential , chemistry , eticlopride , postsynaptic potential , glutamatergic , neuroscience , neurotransmission , dopamine , glutamate receptor , biophysics , inhibitory postsynaptic potential , dopamine receptor d2 , receptor , biology , biochemistry , sch 23390
In this study, the effects of exogenously applied and endogenously released dopamine (DA), a powerful modulator of the lamprey locomotor network, are examined on excitatory glutamatergic synaptic transmission between reticulospinal axons and spinal neurons. Bath application of DA (1–50 µ m ) reduced the amplitude of monosynaptic reticulospinal‐evoked glutamatergic excitatory postsynaptic potentials (EPSPs). The effect of DA was blocked by the D 2 ‐receptor antagonist eticlopride, and mimicked by the selective D 2 ‐receptor agonist 2,10,11 trihydroxy‐ N ‐propyl‐noraporphine hydrobromide (TNPA). Bath application of the DA reuptake blocker bupropion, which increases the extracellular level of dopamine, also reduced the monosynaptic EPSP amplitude. This effect was also blocked by the D 2 ‐receptor antagonist eticlopride. To investigate if the action of DA was exerted at the presynaptic level, the reticulospinal axon action potentials were prolonged by administering K + channel antagonists while blocking l ‐type Ca 2+ channels. A remaining Ca 2+ component, mainly dependent on N and P/Q channels, was depressed by DA. When DA (25–50 µ m ) was applied in the presence of ω‐conotoxin GVIA, a toxin specific for N‐type Ca 2+ channels, it failed to affect the monosynaptic EPSP amplitude. DA did not affect the response to extracellularly ejected d ‐glutamate, the postsynaptic membrane potential, or the electrical component of the EPSPs. DA thus acts at the presynaptic level to modulate reticulospinal transmission.