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NMDA-receptor-independent long-term potentiation
D Johnston1, S Williams, D Jaffe
1Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030.
Annual Review of Physiology
|January 1, 1992
Summary
Many forms of long-term potentiation (LTP) do not require NMDA receptors. Voltage-gated calcium channels, particularly L-type channels, are implicated in NMDA-receptor-independent LTP induction in the hippocampus.
Area of Science:
- Neuroscience
- Synaptic Plasticity
- Calcium Signaling
Background:
- N-methyl-D-aspartate receptor (NMDA-R)-dependent long-term potentiation (LTP) is well-studied in the hippocampus.
- However, numerous forms of LTP are independent of NMDA receptors.
- NMDA-R-independent LTP has been observed in invertebrates and multiple hippocampal pathways.
Purpose of the Study:
- To explore the diverse mechanisms underlying NMDA-R-independent LTP.
- To investigate the role of calcium (Ca2+) in NMDA-R-independent LTP.
- To examine the involvement of voltage-gated Ca2+ channels in hippocampal LTP.
Main Methods:
- Review of existing literature on NMDA-R-independent LTP.
- Analysis of studies investigating Ca2+ involvement in LTP.
- Examination of evidence for voltage-gated Ca2+ channel activation in LTP induction.
Main Results:
- NMDA-R-independent LTP mechanisms are diverse, but often involve Ca2+.
- Voltage-gated Ca2+ channels, specifically L-type channels, are proposed triggers for LTP at hippocampal CA3 mossy fiber (MF) and CA1 Schaffer collateral (SC) synapses.
- Beta-adrenoreceptor and muscarinic agonists modulate MF LTP and Ca2+ channels, suggesting L-type channel criticality.
Conclusions:
- Voltage-gated Ca2+ channels, particularly L-type channels, are likely crucial for NMDA-R-independent LTP induction in the hippocampus.
- Further research is needed to confirm the role of these channels.
- Investigating voltage-gated Ca2+ channels in LTP in other brain regions like the cortex and amygdala is warranted.