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Updated: Jan 7, 2026
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Optogenetic Activation of Afferent Pathways in Brain Slices and Modulation of Responses by Volatile Anesthetics
Published on: July 23, 2020
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Cortical Mechanisms Contributing to Ketamine-Induced Dissociation
Kallol Bera1, Loren L Looger1, Alex Proekt2,3
1Department of Neurosciences, Howard Hughes Medical Institute, University of California, San Diego, La Jolla, CA, USA.
Summary
Ketamine, used for anesthesia and depression, alters brain circuits by affecting NMDA receptors and HCN1 channels. This review explores how ketamine impacts consciousness and neuronal function, potentially aiding new therapies.
Area of Science:
- Neuroscience
- Pharmacology
- Anesthesiology
Background:
- Ketamine is an anesthetic inducing dissociative anesthesia.
- Sub-anesthetic ketamine doses show rapid antidepressant effects.
- Ketamine serves as a model for studying consciousness and neuropsychiatric disorders.
Purpose of the Study:
- To review how ketamine alters cortical circuit dynamics to induce dissociation.
- To explore ketamine's intracellular actions and epigenetic effects.
- To advance understanding of ketamine's pharmacology and therapeutic potential.
Main Methods:
- Review of ketamine pharmacology.
- Analysis of cell type-resolved and region-specific in vivo imaging.
- Systems neuroscience approaches to study thalamocortical connectivity.
Main Results:
- Ketamine acts on cortical circuits via NMDA receptor and HCN1 channel antagonism.
- It causes disinhibition of pyramidal neurons and alters thalamocortical connectivity.
- Ketamine may enter intracellular compartments, modulating neuronal excitability and epigenetics.
Conclusions:
- Ketamine's effects on cortical circuits drive dissociation.
- Intracellular ketamine actions influence neuronal signaling and epigenetic states.
- Understanding these mechanisms can inform treatments for depression and consciousness studies.
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