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Long-term depression is induced in Ca2+/calmodulin kinase-inhibited visual cortex neurons
M Funauchi1, T Tsumoto, A Nishigori
1Department of Neurophysiology, Biomedical Research Center, Osaka University Medical School, Japan.
Neuroreport
|February 1, 1992
Summary
Calcium-Calmodulin-dependent protein kinase II (CaMKII) inhibition in rat visual cortex neurons induced long-term depression (LTD) instead of long-term potentiation (LTP). This suggests postsynaptic CaMKII is crucial for LTP/LTD induction.
Area of Science:
- Neuroscience
- Cellular Neuroscience
- Synaptic Plasticity
Background:
- Long-term potentiation (LTP) and long-term depression (LTD) are key mechanisms for synaptic plasticity in the brain.
- Calcium-Calmodulin-dependent protein kinase II (CaMKII) is implicated in learning and memory processes.
Purpose of the Study:
- To investigate the specific role of CaMKII in the induction of LTP in the visual cortex.
- To determine if CaMKII activity is essential for establishing input-specific synaptic plasticity.
Main Methods:
- Inhibition of CaMKII using KN-62 in layer 2/3 neurons of young rat visual cortex slices.
- Tetanic stimulation applied to induce plasticity.
- Measurement of excitatory postsynaptic potentials (EPSPs) to assess synaptic strength changes.
Main Results:
- CaMKII inhibition resulted in long-term depression (LTD) instead of LTP following tetanic stimulation in 9 out of 14 cells.
- The induced LTD was input-specific, affecting only the stimulated pathway.
- Neurons with intact CaMKII function exhibited LTP under similar stimulation conditions.
Conclusions:
- Postsynaptic CaMKII activity is critical for the induction of long-term potentiation (LTP) in the visual cortex.
- CaMKII plays a differential role in mediating LTP and LTD, highlighting its complex involvement in synaptic plasticity.
Related Concept Videos
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.
Calcium Ion Concentration Mechanism
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Calcium Ion Concentration Mechanism
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01:16Calmodulin-dependent Signaling
Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...