Abstract
The feedforward dentate gyrus-CA3 microcircuit in the hippocampus is thought to activate ensembles of CA3 pyramidal cells and interneurons to encode and retrieve episodic memories. The creation of these CA3 ensembles depends on neuromodulatory input and synaptic plasticity within this microcircuit. Here we review the mechanisms by which the neuromodulators aceylcholine, noradrenaline, dopamine, and serotonin reconfigure this microcircuit and thereby infer the net effect of these modulators on the processes of episodic memory encoding and retrieval.
Highlights
The hippocampus has been strongly implicated in encoding and retrieval of memories since the early work of Scoville and Milner several decades ago (Scoville and Milner, 1957; Squire, 1992), but the mechanisms through which this is achieved remain largely elusive
An important and often ignored component of memory encoding and retrieval is the neuromodulatory influence of acetylcholine (ACh), dopamine (DA), noradrenaline (NA), and serotonin (5-HT)
Many researchers have proposed that recurrent synapses amongst CA3 pyramidal cells endow the CA3 network with autoassociative and heteroassociative properties (Marr, 1971; Treves and Rolls, 1994; Lisman, 1999; Bush et al, 2010; Savin et al, 2014; Guzman et al, 2016) such that ensembles of strongly associated CA3 pyramidal cells can be reactivated when only a subset of their constituent CA3 pyramidal cells have been activated by external sources
Summary
The hippocampus has been strongly implicated in encoding and retrieval of memories since the early work of Scoville and Milner several decades ago (Scoville and Milner, 1957; Squire, 1992), but the mechanisms through which this is achieved remain largely elusive. Encoding and retrieval engage distinct processes as demonstrated by evidence that contralateral lesions to dentate gyrus and CA3 impaired encoding, but not retrieval in a spatial maze learning task relative to ipsilateral lesioned and unlesioned animals (Jerman et al, 2006) whilst damage to direct entorhinal-CA3 inputs impairs retrieval but not encoding (Lee and Kesner, 2004). These and other data support a long held hypothesis of a double dissociation in encoding and retrieval pathways to CA3 (Treves and Rolls, 1994). CIRCUIT MECHANISMS FOR MEMORY ENCODING AND RETRIEVAL IN THE CA3 REGION OF THE HIPPOCAMPUS
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