Abstract
In the molecular layer of the cerebellar cortex, Purkinje cells and interneurons receive a common excitatory input from parallel fibers. The AMPA/kainate receptor-mediated parallel fiber excitatory postsynaptic current (EPSC) recorded in Purkinje cells decays much more slowly than that recorded in interneurons. We show that this slowness of decay does not result from dendritic filtering and that it is unlikely to reflect the deactivation kinetics of the postsynaptic receptors. Agents blocking glutamate uptake prolong the EPSC in Purkinje cells. We conclude that the slow EPSC decay results from the continued presence of transmitter glutamate. This may be due to retarded transmitter diffusion around spines or to cross-talk between neighboring active synapses.
MeSH terms
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Animals
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Aspartic Acid / pharmacology
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Cerebellar Cortex / drug effects
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Cerebellar Cortex / physiology
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Dendrites / physiology
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Electric Stimulation
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Evoked Potentials / drug effects
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Evoked Potentials / physiology
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Glutamates / metabolism*
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Glutamates / pharmacology*
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Glutamic Acid
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In Vitro Techniques
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Interneurons / drug effects
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Interneurons / physiology
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Male
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Mathematics
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Models, Neurological
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Nerve Fibers / physiology
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Purkinje Cells / drug effects
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Purkinje Cells / physiology*
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Rats
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Rats, Wistar
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Receptors, AMPA / physiology
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Receptors, Glutamate / drug effects
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Receptors, Glutamate / physiology*
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Receptors, Kainic Acid / physiology
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Synapses / physiology*
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Synaptic Transmission / drug effects
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Synaptic Transmission / physiology*
Substances
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Glutamates
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Receptors, AMPA
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Receptors, Glutamate
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Receptors, Kainic Acid
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Aspartic Acid
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Glutamic Acid