Abstract
The phasic release of dopamine in the hippocampal formation has been shown to facilitate the encoding of novel information. There is evidence that the subiculum operates as a detector and distributor of sensory information, which incorporates the novelty and relevance of signals received from CA1. The subiculum acts as the final hippocampal relay station for outgoing information. Subicular pyramidal cells have been classified as regular- and burst-spiking neurons. The goal of the present study was to study the effect of dopamine D1/D5 receptor activation on synaptic transmission and plasticity in the subicular regular-spiking neurons of 4–6 week old Wistar rats. We demonstrate that prior activation of D1/D5 receptors reduces the threshold for the induction of long-term potentiation (LTP) in subicular regular-spiking neurons. Our results indicate that D1/D5 receptor activation facilitates a postsynaptic form of LTP in subicular regular-spiking cells that is NMDA receptor-dependent, relies on postsynaptic Ca2+ signaling, and requires the activation of protein kinase A. The enhanced propensity of subicular regular-spiking cells to express postsynaptic LTP after activation of D1/D5 receptors provides an intriguing mechanism for the encoding of hippocampal output information.
Highlights
Cornu ammonis (CA) 1 pyramidal cells receive direct sensory information from the cortex, as well as sequential phase-precession information from the dentate gyrus (DG)–CA3 network
The present study reveals that D1/D5 receptor activation facilitates a postsynaptic form of long-term potentiation (LTP) in subicular regular-spiking cells that is NMDA receptor-mediated and Ca2+-dependent, and which requires the activation of protein kinase A (PKA)
We conclude that in both CA1 and subicular pyramidal cells, synaptic plasticity can be facilitated by D1/D5 receptor activation, implying that both regions may be involved in dopaminedependent encoding of novel information
Summary
Cornu ammonis (CA) 1 pyramidal cells receive direct sensory information from the cortex, as well as sequential phase-precession information from the dentate gyrus (DG)–CA3 network. CA1 pyramidal cells may, detect mismatches between the information coding of predictions from the DG–CA3 network that is relayed through the Schaffer collaterals and actual sensory input from the cortex. This detection of discrepancies implies that it is possible to estimate predictions for new information [1,2]. There is strong evidence that the subiculum acts as the final major hippocampal relay station within the hippocampus – ventral tegmental area (VTA) loop for the unidirectional outgoing information, that seems to control the input of novel sensory information into long-term memory [8]. Timelocked release of dopamine in the hippocampal formation likely allows for the encoding of novel information [1,9,10,11]
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