Cerebellar Purkinje neurons (PNs) receive two main excitatory inputs, from climbing fibers and parallel fibers, and inhibitory inputs, from GABAergic interneurons. The synapses formed by parallel fibers and by inhibitory interneurons on PNs are able to undergo long-lasting changes in efficacy. Thus, the excitatory parallel fiber-PN synapse undergoes long-term depression when it is activated in conjunction with climbing fibers. Synaptic inhibition can be potentiated by climbing fiber activity by a mechanism named rebound potentiation, resulting in a more powerful inhibitory effect of GABAergic interneurons. The induction of both long-term depression and rebound potentiation requires a transient elevation of the cytoplasmic calcium concentration ([Ca2+]i). The [Ca2+]i-transient is caused by Ca2+ entry through voltage-gated Ca2+ channels and, possibly, by release of Ca2+ from IP3- and ryanodine-sensitive stores. Direct Ca2+ entry through synaptic AMPA receptor channels seems not to contribute significantly to the Ca2+ signal mediating the induction of both long-term depression and rebound potentiation.
Calcium requirement of long-term depression and rebound potentiation in cerebellar Purkinje neurons.
TEMPIA, Filippo;
1994-01-01
Abstract
Cerebellar Purkinje neurons (PNs) receive two main excitatory inputs, from climbing fibers and parallel fibers, and inhibitory inputs, from GABAergic interneurons. The synapses formed by parallel fibers and by inhibitory interneurons on PNs are able to undergo long-lasting changes in efficacy. Thus, the excitatory parallel fiber-PN synapse undergoes long-term depression when it is activated in conjunction with climbing fibers. Synaptic inhibition can be potentiated by climbing fiber activity by a mechanism named rebound potentiation, resulting in a more powerful inhibitory effect of GABAergic interneurons. The induction of both long-term depression and rebound potentiation requires a transient elevation of the cytoplasmic calcium concentration ([Ca2+]i). The [Ca2+]i-transient is caused by Ca2+ entry through voltage-gated Ca2+ channels and, possibly, by release of Ca2+ from IP3- and ryanodine-sensitive stores. Direct Ca2+ entry through synaptic AMPA receptor channels seems not to contribute significantly to the Ca2+ signal mediating the induction of both long-term depression and rebound potentiation.
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