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Related Concept Videos

Neuroplasticity01:01

Neuroplasticity

Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.
Long-term Potentiation01:25

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
LTP can occur when presynaptic neurons...
Long-term Potentiation01:35

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.

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Ketamine and Evolving Neuroplasticity.

Angel Prabakar1

  • 1Stony Brook University, Stony Brook, USA. angel.prabakar@stonybrook.edu.

Clinical Drug Investigation
|June 13, 2026
PubMed
Summary
This summary is machine-generated.

Ketamine rapidly treats depression by targeting NMDA receptors, promoting neuroplasticity. This review details the time-dependent molecular and behavioral effects of ketamine, linking preclinical findings to clinical recovery in mood disorders.

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Area of Science:

  • Neuroscience
  • Psychiatry
  • Pharmacology

Background:

  • Ketamine offers rapid antidepressant effects for treatment-resistant depression, acting via N-methyl-D-aspartate (NMDA) receptor antagonism.
  • Unlike traditional antidepressants, ketamine triggers glutamatergic signaling, promoting synaptic plasticity and neurogenesis.
  • The precise temporal dynamics of ketamine-induced neuroplasticity and its behavioral impact require further definition.

Purpose of the Study:

  • To synthesize preclinical and clinical evidence on the time-dependent effects of ketamine.
  • To delineate the molecular, cellular, and behavioral changes associated with ketamine treatment.
  • To connect mechanistic insights with observed clinical outcomes and antidepressant response timing.

Main Methods:

  • Review of preclinical studies examining molecular and synaptic changes (e.g., BDNF, mTOR, AMPA receptors).
  • Analysis of clinical studies correlating biological processes with mood, cognition, and functional outcomes.
  • Emphasis on the temporal progression of ketamine's effects from hours to days.

Main Results:

  • Preclinical data reveal rapid molecular and synaptic remodeling driven by ketamine.
  • Clinical data show correlations between neuroplastic changes and improvements in mood and cognition.
  • Ketamine's effects unfold over hours to days, linking biological mechanisms to clinical recovery.

Conclusions:

  • Ketamine's antidepressant action is best understood through a plasticity-centered model.
  • Understanding the temporal trajectory of neuroplasticity is crucial for optimizing ketamine therapy.
  • This review highlights research gaps and proposes a roadmap for future fast-acting antidepressants.