Skip to content

Adrian Newman-Tancredi

Neurolixis SAS, Castres, France.

2 papers in the library · 17 citations · publishing 2024-2025

Papers

The 5-HT1A receptor biased agonists, NLX-204 and NLX-101, like ketamine, elicit rapid-acting antidepressant activity in the rat chronic mild stress model via cortical mechanisms.

Journal of psychopharmacology (Oxford, England) July 1, 2024 Mariusz Papp, Piotr Gruca, Ewa Litwa et al. 15 citations

Two compounds that selectively activate serotonin 5-HT1A receptors in a biased manner, NLX-101 and NLX-204, produce rapid antidepressant effects in rats exposed to chronic mild stress, similar to ketamine. When injected directly into the prefrontal cortex, these compounds reversed stress-induced anhedonia, reduced anxiety, and improved working memory deficits. Blocking 5-HT1A receptors in the prefrontal cortex eliminated these benefits, showing that the compounds work specifically through these receptors. The findings suggest that biased agonism at 5-HT1A receptors is a promising strategy for rapid-acting antidepressants that may avoid ketamine's side effects while also addressing cognitive deficits and anxiety.

The antidepressant-like activity of ketamine in the rat chronic mild stress model requires activation of cortical 5-HT 1A receptors.

Behavioural pharmacology June 1, 2025 Ronan Depoortère, Mariusz Papp, Piotr Gruca et al. 2 citations

Ketamine rapidly reverses depression-like symptoms in rats exposed to chronic mild stress, including loss of pleasure and working memory deficits, when given systemically or directly into the prefrontal cortex. Blocking serotonin 5-HT1A receptors in the prefrontal cortex with WAY-100635 prevents these effects, showing that ketamine's rapid antidepressant and pro-cognitive actions require activation of these receptors. The findings suggest that drugs directly targeting prefrontal cortex 5-HT1A receptors could provide rapid antidepressant effects and improve cognitive deficits without ketamine's side effects or need for clinical supervision.