ArticleTranslational psychiatry2026
Impact of subanesthetic ketamine delivered via AmyloLipid nanovesicle (ALN)-based intranasal system on biobehavioral responses in an animal model of PTSD.
Article in Translational psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Acute pretrauma ethanol exacerbates PTSD-like phenotype in rats and is reversed by early intranasal ketamine.Scientific reports · 2026Article
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5 authors.
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Abstract
Ketamine holds promise for the treatment of post-traumatic stress disorder (PTSD), but challenges remain in delivery and sustained effects. This controlled study evaluates a novel intranasal formulation, employing AmyloLipid nanovesicles (ALN) to enhance ketamine's therapeutic efficacy in a predator-scent stress (PSS) rat model of PTSD. A total of 130 rats underwent PSS or sham-PSS exposure, followed by intranasal administration of ketamine-ALN (4.8, 2.4, 1.2 and 0.6 mg/kg), unloaded-ALN, saline, or standard ketamine three times weekly for two weeks, starting seven days post-trauma. Behavioral assessments, including the elevated plus maze, acoustic startle response, and contextual freezing tests, were complemented by immunohistochemical and Golgi-Cox analyses of hippocampal and paraventricular nucleus (PVN) tissues. Low-dose ketamine-ALN (0.6 mg/kg) significantly reduced anxiety-like behaviors, hyperarousal, and the prevalence of PTSD-like responses (extreme behavior responses) by 45% compared to unloaded-ALN controls. Unlike standard ketamine, ALN-mediated delivery bypassed the blood-brain barrier, enhancing bioavailability and sustaining therapeutic benefit. Mechanistically, ketamine-ALN normalized the expression of hyperpolarization-activated cyclic nucleotide-gated (HCN1) channels-which were upregulated in the CA1 stratum lacunosum-moleculare (SLM) post-PSS-thereby stabilizing neuronal excitability. This normalization of HCN1, critical for regulating neuronal excitability and membrane potential, was accompanied by increased levels of brain-derived neurotrophic factor (BDNF) and neuropeptide Y (NPY), enhancing neuroplasticity and dendritic complexity. These findings demonstrate that ALN-based intranasal delivery of ketamine is more effective than standard administration, particularly at low doses. The results suggest that low-dose ketamine-ALN modulates a hippocampal circuit involving HCN1, BDNF, and NPY to foster adaptive stress responses. Collectively, ketamine-ALN represents a promising targeted therapy for PTSD, with HCN1 channels as a key mediator of stress-induced neuronal dysfunction and ketamine's therapeutic action, thus advancing the prospects for precision treatment of stress-related disorders.
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