Functional connectivity between the thalamus and postsubiculum: Analysis of evoked responses elicited by stimulation of the laterodorsal thalamic nucleus in anesthetized rats

The laterodorsal nucleus (LDN) of the thalamus provides a prominent afferent projection to the postsubiculum (dorsal presubiculum). To characterize synaptic transmission in this pathway, we placed stimulating electrodes in the LDN and recorded fEPSPs elicited in the postsubiculum of urethane‐anesthetized rats. LDN stimulation elicited a source‐sink dipole between the deep and superficial layers of the postsubiculum, respectively, consistent with anatomical evidence for the termination of thalamic afferents in the superficial layers of the structure, and the existence of deep layer neurons with apical dendrites extending into these layers. Postsubicular fEPSPs were typically 0.5–1.0 mV in amplitude, with a peak latency of approximately 6 ms. Consistent with anatomical observations, the short onset latency of fEPSPs elicited by LDN stimulation, and their ability to follow a 60‐Hz train of stimulation, indicate that the projection is monosynaptic. Paired‐pulse stimulation revealed pronounced paired‐pulse depression that was maximal at 100 ms, suggesting that initial release probabilities are high at LDN‐postsubiculum synapses, in common with many neocortical pathways. A conventional tetanus protocol that yields LTP in hippocampal pathways had no effect on postsubicular fEPSPs, but long‐term depression could be induced by 60‐Hz stimulation. Drug infusion studies revealed that synaptic transmission in the LDN‐postsubiculum projection is predominantly AMPA‐receptor mediated. Rats were implanted with indwelling infusion cannulae targeting the postsubiculum, and, after a recovery period, were anaesthetized withurethane, and implanted with stimulating and recording electrodes. Infusion of CNQX almost completely abolished postsubicular fEPSPs, whereas D‐AP5 had little effect. However, 60‐Hz LTD was blocked by D‐AP5 infusion, revealing that this form of synaptic plasticity is NMDA‐receptor dependent. © 2013 Wiley Periodicals, Inc.