CA1 — Function, Location & Quiz

CA1 is a major output stage of the hippocampal circuit, receiving CA3 information through Schaffer collaterals before passing processed signals toward subiculum and entorhinal cortex. It is the field most closely associated with the original experimental description of long-term potentiation.

Its vulnerability to oxygen deprivation gives the tiny subfield large clinical importance. Selective CA1 injury after ischemia can produce profound anterograde memory difficulty even when the entire medial temporal lobe has not been destroyed.

Test this anatomy in the Brain Regions Quiz or open the interactive 3D brain model.

Location and anatomical map

Hippocampal subregion receiving Schaffer collaterals, site of NMDA-dependent LTP.

Atlas category: subcortical.

Functions

  • Output stage of hippocampal trisynaptic circuit
  • Receives Schaffer collaterals from CA3
  • Site where LTP (Long-Term Potentiation) was first described

Pathways and connections

  • CA3 → CA1 (Schaffer collaterals — where LTP was discovered)
  • CA1 → Subiculum → Entorhinal cortex (hippocampal output pathway)

Clinical relevance

  • CA1 is especially vulnerable to ischemia/hypoxia — often damaged first in cardiac arrest
  • Selective CA1 damage → anterograde amnesia

Key facts

  • Bliss & Lomo (1973): discovered LTP at Schaffer collateral → CA1 synapse
  • Tonegawa knockout mice: lacking NMDA receptors in CA1 = no LTP = impaired spatial learning
  • Tonegawa experiment proved the causal link between LTP and memory

Exam tip

CA1 = where LTP was discovered (Bliss & Lomo) and where Tonegawa proved the LTP-memory link with NMDA knockouts.

Common questions

What does hippocampal CA1 do?

CA1 integrates input from CA3 and acts as a major hippocampal output stage, sending information toward subiculum and entorhinal cortex.

Which pathway connects CA3 to CA1?

Schaffer collateral axons project from CA3 to CA1. These synapses are the classic site at which long-term potentiation was first described.

Why is CA1 clinically vulnerable?

CA1 neurons are especially sensitive to ischemia and hypoxia, so they may be injured early after cardiac arrest and produce anterograde memory impairment.