The role of the NMDA synapse in general anesthesia.
H Flohr, U Glade, D Motzko
Toxicology Letters November 23, 1998 DOI: 10.1016/s0378-4274(98)00161-1 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Theoretical or philosophical paper Peer reviewed |
|---|---|
| Key points | Proposes a four-hypothesis theory in which consciousness depends on transient higher-order self-referential representations instantiated by neural cell assemblies, whose formation involves NMDA receptor activation. Argues that modification of NMDA-dependent computational processes is the final common pathway of anesthetic action, so agents directly inactivating the NMDA synapse necessarily have anesthetic properties, while others do so only if they inhibit NMDA-dependent processes. |
Abstract
A theory of anesthesia is presented. It consists of four hypotheses. (1) The occurrence of states of consciousness causally depends on the formation of transient higher-order, self-referential mental representations. The occurrence of such states is identical with the appearance of conscious phenomena. Loss of consciousness will occur, if the brain's representational activity falls below a critical threshold. (2) Higher-order mental representations are instantiated by neural cell assemblies. (3) The formation of such assemblies involves the activation of the NMDA receptor channel complex. The activation state of this receptor determines the rate at which such assemblies are generated. (4) Modification of NMDA-dependent computational processes is the final common pathway of anesthetic action. Agents that directly inactivate the NMDA synapse necessarily have anesthetic properties; agents that do not directly affect the NMDA synapse will exert an anesthetic action, if they inhibit NMDA-dependent processes.
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