Somatodendritic release of glutamate regulates synaptic inhibition in cerebellar Purkinje cells via autocrine mGluR1 activation.

@article{Duguid2007SomatodendriticRO,
  title={Somatodendritic release of glutamate regulates synaptic inhibition in cerebellar Purkinje cells via autocrine mGluR1 activation.},
  author={Ian Duguid and Yuriy Pankratov and Guy William John Moss and Trevor G Smart},
  journal={The Journal of neuroscience : the official journal of the Society for Neuroscience},
  year={2007},
  volume={27 46},
  pages={12464-74}
}
In the cerebellum, the process of retrograde signaling via presynaptic receptors is important for the induction of short- and long-term changes in inhibitory synaptic transmission at interneuron-Purkinje cell (PC) synapses. Endocannabinoids, by activating presynaptic CB1 receptors, mediate a short-term decrease in inhibitory synaptic efficacy, whereas glutamate, acting on presynaptic NMDA receptors, induces a longer-latency sustained increase in GABA release. We now demonstrate that either low… CONTINUE READING

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We now demonstrate that either low - frequency climbing fiber stimulation or direct somatic depolarization of Purkinje cells results in SNARE - dependent vesicular release of glutamate from the soma and dendrites of PCs .
We now demonstrate that either low - frequency climbing fiber stimulation or direct somatic depolarization of Purkinje cells results in SNARE - dependent vesicular release of glutamate from the soma and dendrites of PCs .
We now demonstrate that either low - frequency climbing fiber stimulation or direct somatic depolarization of Purkinje cells results in SNARE - dependent vesicular release of glutamate from the soma and dendrites of PCs .
Endocannabinoids , by activating presynaptic CB1 receptors , mediate a short - term decrease in inhibitory synaptic efficacy , whereas glutamate , acting on presynaptic NMDA receptors , induces a longer - latency sustained increase in GABA release .
Endocannabinoids , by activating presynaptic CB1 receptors , mediate a short - term decrease in inhibitory synaptic efficacy , whereas glutamate , acting on presynaptic NMDA receptors , induces a longer - latency sustained increase in GABA release .
In the cerebellum , the process of retrograde signaling via presynaptic receptors is important for the induction of short- and long - term changes in inhibitory synaptic transmission at interneuron - Purkinje cell ( PC ) synapses .
In the cerebellum , the process of retrograde signaling via presynaptic receptors is important for the induction of short- and long - term changes in inhibitory synaptic transmission at interneuron - Purkinje cell ( PC ) synapses .
In the cerebellum , the process of retrograde signaling via presynaptic receptors is important for the induction of short- and long - term changes in inhibitory synaptic transmission at interneuron - Purkinje cell ( PC ) synapses .
In the cerebellum , the process of retrograde signaling via presynaptic receptors is important for the induction of short- and long - term changes in inhibitory synaptic transmission at interneuron - Purkinje cell ( PC ) synapses .
The activity of excitatory amino acid transporters regulated the spatial spread of glutamate and thus the extent of PC mGluR1 activation .
We now demonstrate that either low - frequency climbing fiber stimulation or direct somatic depolarization of Purkinje cells results in SNARE - dependent vesicular release of glutamate from the soma and dendrites of PCs .
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