Object-in-place associative recognition memory depends on glutamate receptor neurotransmission within two defined hippocampal-cortical circuits: A critical role for AMPA and NMDA receptors in the hippocampus, perirhinal and prefrontal cortices.

Object-in-place associative recognition memory depends on an inter-
10 action between the hippocampus (HPC), perirhinal (PRH), and medial
prefrontal (mPFC) cortices, yet the contribution of glutamate receptor
neurotransmission to these interactions is unknown. NMDA
receptors (NMDAR) in the HPC were critical for encoding of objectin-
place memory but not for single-item object recognition. Next, a
15 disconnection procedure was used to examine the importance of
“concurrent” glutamate neurotransmission in the HPC-mPFC and
HPC-PRH. Contralateral unilateral infusions of NBQX (AMPAR antagonist),
into the HPC-mPFC, or HPC-PRH, either before acquisition or
test, impaired object-in-place performance. Thus, both circuits are
20 necessary for encoding and retrieval. Crossed unilateral AP5 (NMDAR
antagonist) infusions into the HPC-mPFC or HPC-PRH impaired encoding,
but not retrieval. Specifically crossed HPC-mPFC infusions
impaired both short-term (5 min) and longer term (1 h) memory while
HPC-PRH infusions impaired longer term memory only. This delay-
25 dependent effect of AP5 in the HPC-PRH on object-in-place memory,
accords with its effects in the PRH, on single item object recognition
memory, thereby suggesting that a single PRH synaptic plasticity
mechanism underpins different recognition memory processes. Further,
blocking excitatory neurotransmission in any pair of structures
30 within the networks impaired “both” encoding and retrieval, thus
object-in-place memory clearly requires network interdependency
across multiple structures.