How we recall (or don't): the hippocampal memory machine and anesthetic amnesia

Abstract

Purpose: The hippocampal formation occupies a central position for the processing of sensory input into learned, remembered, and consciously retrievable information. The mechanisms by which anesthetic drugs interfere with these processes are now emerging. We review the current understanding of the role of the hippocampal formation in the generation of memory traces and how anesthetics might interfere with its function.

Clinical features: Intraoperative amnesia is a desired endpoint of general anesthesia from the perspective of both the patient and the practitioner. "Intraoperative awareness with recall" can result when learning and memory do occur. In addition, anesthetics are capable of inducing a state of "conscious amnesia" that can provide insight into the workings of the brain and might be useful clinically.

Conclusions: Anesthesiologists routinely induce the most fascinating pharmacologic effects in existence, the reversible interference of anesthetics with higher cognitive functions. Understanding how the drugs in our custody exert their effects should be our contribution to mankind's universal knowledge base.

Fig. 1

Schematic representation of the hippocampal tri-synaptic excitatory circuit based on the classic drawing by Santiago Ramon y Cajal. The entorhinal cortex (EC) projects to the hippocampal CA1 area monosynaptically by way of the perforant path and via synapses in the dentate gyrus (DG) and the CA3. All excitatory synapses in this circuit can undergo plastic changes, but the molecular mechanisms differ. The drawing does not capture the intricate inhibitory circuitry that controls excitatory synaptic transmission. (The drawing is downloaded from the public domain by way of the Wikipedia. Originally the drawing was published in `Histologie du Systeme Nerveux de l'Homme et des Vertebres')

Fig. 2

Schematic overview over the different memory systems. The long-term, declarative, and episodic memory axis is thought to be critically dependent on intact function of the hippocampus/the medial temporal lobe

Fig. 3

A model for θ-γ-nesting as a means to maintaining items in the working memory buffer. Seven memories (A–G) are multiplexed. Memory A, represented by a certain spatial pattern of cell firing, i.e., a cell assembly (oval insert), is active in the first γ-subcycle of a θ-oscillation, followed by memory B in the next γ-cycle, etc. After a dead time (d), the seven memories repeat in the subsequent θ-cycle. Reproduced with permission from reference