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Updated: Jun 8, 2026
09:30
Assessment of Long-term Depression Induction in Adult Cerebellar Slices
Published on: October 16, 2019
Long-term depression at parallel fiber to Golgi cell synapses
Quinten Robberechts1, Mike Wijnants, Michele Giugliano
1Theoretical Neurobiology, Dept. of Biomedical Sciences, Campus Drie Eiken T5.37, Univ. of Antwerp, Universiteitsplein 1, 2610 Antwerpen, Belgium. quinten@tnb.ua.ac.be
Journal of Neurophysiology
|September 24, 2010
Summary
Long-term depression (LTD) was observed at parallel fiber-Golgi cell synapses in the cerebellum. This synaptic plasticity requires group II metabotropic glutamate receptors and protein kinase A activation.
Area of Science:
- Neuroscience
- Cellular Neuroscience
- Synaptic Plasticity
Background:
- Golgi cells (GoCs) are key inhibitory interneurons in the cerebellar granular layer.
- GoC inhibition regulates excitatory input relay to the cerebellar cortex.
- Synaptic transmission at parallel fiber (PF)-GoC synapses involves AMPA, NMDA, and group II metabotropic glutamate receptors.
Purpose of the Study:
- To investigate long-term changes in synaptic efficacy at the PF-GoC synapse.
- To characterize the mechanisms underlying synaptic plasticity at this specific synapse.
Main Methods:
- Whole-cell patch-clamp recordings were performed on GoCs in acute rat cerebellar slices.
- High-frequency burst stimulation was used to induce synaptic plasticity.
- Paired-pulse ratio was analyzed to infer synaptic origin.
Main Results:
- High-frequency burst stimulation induced long-term depression (LTD) at the PF-GoC synapse.
- The observed LTD was postsynaptic, as indicated by unchanged paired-pulse ratios.
- LTD induction was independent of N-methyl-D-aspartate (NMDA) receptor activation.
- PF-GoC LTD specifically requires group II metabotropic glutamate receptors and protein kinase A activation.
Conclusions:
- A novel form of postsynaptic LTD exists at the PF-GoC synapse.
- Group II metabotropic glutamate receptors and protein kinase A are critical for this LTD.
- These findings reveal new insights into cerebellar synaptic plasticity and information processing.
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01:05Long-term Depression
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
01:03Long-term Depression
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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01:25Long-term Potentiation
Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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01:35Long-term Potentiation
Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Golgi matrix proteins are a group of highly dynamic proteins that maintain the stacked structure of Golgi. These proteins adapt to rapid morphological changes of the Golgi during the cell cycle. During cell division, mild proteolysis removes these connections resulting in Golgi unstacking. In The daughter cells, these proteins help reassemble the unstacked Golgi.
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