ReviewNeuron2025
Synaptic priming: A framework for pharmacotherapy in depression.
Review in Neuron, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Ketamine preserves perineuronal nets in chronic stressed mice brain through the inhibition of microglia activation.IBRO neuroscience reports · 2026Article
- Enhancing plasticity to treat depression and other central nervous system diseases using event-driven pharmacology.Journal of psychopharmacology (Oxford, England) · 2026Review
- Intermittent Ketamine and Neuromodulation Treatment Evoke Synergistic Antidepressant-Relevant Action.Biological psychiatry · 2026Article
- A Time-Sensitive Plasticity Distinguishes the Rapid and Sustained Synaptic Actions of Ketamine from Its (2The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Disrupted synapses: prefrontal cortex-reward circuit dysfunction in stress-induced depression-like behaviors.Frontiers in cellular neuroscience · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Recent antidepressant drug development focuses on a next generation of drugs to rapidly relieve symptoms. Yet, how ketamine, the prototype rapid-acting antidepressant, maintains symptom relief days after drug elimination, and how repeated doses sustain longer-lasting therapeutic effects, remains unclear. Derived from elements of metaplasticity (synaptic priming), this review discusses a framework in which rapid-acting antidepressants prime synapses such that subsequent doses evoke stronger plasticity. Within this framework, we describe how the indirect relationship between ketamine's pharmacokinetics and sustained antidepressant pharmacodynamics reveals a dosing model (primer pharmacology) that can be harnessed to fine-tune therapeutic outcomes. This review also explores how plasticity machinery engaged by antidepressant pharmacotherapies overlaps with priming induced by contextual conditions relevant to depression (e.g., stress and psychotherapy), suggesting innovative opportunities for treatment strategies with emerging primers (e.g., psychedelics such as psilocybin). The integration of synaptic priming with primer pharmacology reveals a model to guide clinical and translational work in psychiatry.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.