Regulation of synaptic plasticity in hippocampal area CA2
KE Carstens, SM Dudek - Current opinion in neurobiology, 2019 - Elsevier
Current opinion in neurobiology, 2019•Elsevier
Highlights•Pyramidal neurons in hippocampal area CA2 are molecularly distinct from
neighboring CA1 and CA3 pyramidal cells.•Schaffer collateral synapses onto CA2 pyramidal
neurons are normally resistant to the induction of synaptic plasticity.•Plasticity can be
enabled or induced in CA2 by neuromodulators and by the deletion of negative regulators of
plasticity.•The developmental profile of several CA2-enriched molecules is highly suggestive
of a critical window of plasticity.Synaptic plasticity in the hippocampus is thought to play a …
neighboring CA1 and CA3 pyramidal cells.•Schaffer collateral synapses onto CA2 pyramidal
neurons are normally resistant to the induction of synaptic plasticity.•Plasticity can be
enabled or induced in CA2 by neuromodulators and by the deletion of negative regulators of
plasticity.•The developmental profile of several CA2-enriched molecules is highly suggestive
of a critical window of plasticity.Synaptic plasticity in the hippocampus is thought to play a …
Highlights
- Pyramidal neurons in hippocampal area CA2 are molecularly distinct from neighboring CA1 and CA3 pyramidal cells.
- Schaffer collateral synapses onto CA2 pyramidal neurons are normally resistant to the induction of synaptic plasticity.
- Plasticity can be enabled or induced in CA2 by neuromodulators and by the deletion of negative regulators of plasticity.
- The developmental profile of several CA2-enriched molecules is highly suggestive of a critical window of plasticity.
Synaptic plasticity in the hippocampus is thought to play a vital role in both the refinement of neuronal circuits during development and in learning in the mature brain. Synapses in hippocampal area CA1 are known for a robust capacity for long-term potentiation (LTP), whereas synapses in the stratum radiatum of hippocampal area CA2 are particularly resistant to such changes. Although we have yet to fully understand the mechanisms behind this resistance to plasticity, a number of genes and extracellular matrix components highly expressed in CA2 appear to function as molecular brakes on plasticity and develop postnatally in the rodent brain. Curiously, the developmental profile of several CA2-enriched molecules is suggestive of a still undefined critical window of plasticity in the hippocampus.
Elsevier
