A lack of neural plasticity in the hippocampus has been implicated in the development of depression. Ketamine is able to restore hippocampal plasticity in a rat model of depression, potentially illustrating a mechanism for the drug's anti-depressant effects

ResultsSignificanceThis study's findings support the theory that ketamine may reverse the stress-induced loss of connectivity in key neural circuits by engaging synaptic plasticity processes to “reset the system”.Although ketamine’s ability to restore hippocampal- dependent function by modulating synaptic plasticity is a plausible mechanism for some of its therapeutic effects related to functions mediated by the dorsal hippocampus, it is highly unlikely that such localized effects can account for ketamine’s wide range of antidepressant effects.

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