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Journal of Neuroscience, Vol 11, 1359-1366, Copyright © 1991 by Society for Neuroscience
Glutamate receptor subtypes mediate excitatory synaptic currents of dopamine neurons in midbrain slices
G Mereu, E Costa, DM Armstrong and S Vicini
Fidia-Georgetown Institute for the Neurosciences, Georgetown University, Washington, D.C. 20007.
Although dopamine (DA)-containing neurons participate in a number of
important cerebral functions, the physiology of their synaptic connections
is poorly understood. By using whole-cell patch-clamp recording in thin
slices of rat mesencephalon, we have investigated the biophysical
properties of synaptic events and the nature of neurotransmitter(s) and
receptors involved in the synaptic input to DA neurons in substantia nigra.
The histological and electrophysiological characteristics of these cells
were consistent with those described by recent in vivo and in vitro
studies, thus allowing their unequivocal identification. Under appropriate
experimental conditions, intranigral stimulation produced excitatory
synaptic inputs in DA neurons. By voltage-clamp analysis, most of these
excitatory postsynaptic currents (EPSCs) had a rise time of about 1.0 msec
and a decay phase that could be fit by the sum of two exponential curves so
that a fast and a slow component could be distinguished. The slow component
was enhanced by glycine, by removing Mg2+ from the bath medium, or by
membrane depolarization. Moreover, the slow component was consistently
decreased by selective antagonists of NMDA receptors, whereas an antagonist
for the non-NMDA receptors abolished the fast component slightly affecting
the slow component and reduced peak EPSC amplitude. The results indicate
that both NMDA-sensitive and non-NMDA-sensitive glutamate receptors
contribute to EPSCs of DA neurons. Therefore, it is suggested that these
receptors may play a critical role in the physiology (control of
excitability, pacemaker firing, and dendritic DA release) as well as
pathology (neuronal death in Parkinson's disease, psychosis, and mechanism
of action of drugs of abuse, such as ethanol) related to DA neurons.
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