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Pierre Blier

University of Ottawa, Ottawa, ON, Canada.

4 papers in the library · 524 citations · publishing 1987-2025

Papers

Modification of 5‐HT neuron properties by sustained administration of the 5‐HT1A agonist gepirone: Electrophysiological studies in the rat brain

Synapse January 1, 1987 Pierre Blier, Claude de Montigny 428 citations

Rats given the 5-HT1A agonist gepirone for 14 days initially showed reduced firing of serotonin neurons in the dorsal raphe, which gradually returned to normal. After 14 days, the response of these neurons to intravenous LSD was markedly reduced, while responses to 8-OH-DPAT and gepirone were unchanged. Direct application of serotonin, LSD, 8-OH-DPAT, and gepirone to the neurons showed reduced responsiveness, but not to GABA. Postsynaptic hippocampal neurons remained normally responsive to serotonin and related drugs. The findings suggest that desensitization of somatodendritic 5-HT autoreceptors, combined with normal postsynaptic receptor activation, leads to increased tonic activation of postsynaptic 5-HT1A receptors, consistent with the delayed clinical anxiolytic and antidepressant effects of gepirone.

International pooled patient-level meta-analysis of ketamine infusion for depression: In search of clinical moderators

Molecular Psychiatry September 7, 2022 Rebecca B Price, Nicholas Kissel, Andrew Baumeister et al. 80 citations

Ketamine given intravenously rapidly reduces depressive symptoms, with effects lasting at least a week. In an analysis of 17 randomized controlled trials with 809 participants, the benefit over placebo was larger for patients who had already failed two or more prior antidepressant trials. However, no patient-level clinical or demographic characteristics—such as age, sex, or diagnosis—could predict who would respond best, limiting the ability to personalize ketamine prescriptions. The findings confirm ketamine's broad effectiveness for depression but show that precision medicine approaches cannot yet guide treatment decisions.

Enhancing action of LSD on neuronal responsiveness to serotonin in a brain structure involved in obsessive–compulsive disorder

The International Journal of Neuropsychopharmacology March 1, 2003 Tarek Zghoul, Pierre Blier 13 citations

LSD enhances the inhibitory effect of serotonin on neurons in the orbitofrontal cortex, a brain region linked to obsessive-compulsive disorder (OCD), while reducing serotonin's inhibitory effect in the hippocampus, a region linked to depression. In rats under anesthesia, LSD applied directly to neurons decreased their firing rate and boosted serotonin's inhibitory action in the orbitofrontal cortex, but weakened it in the hippocampus. After four daily injections of LSD, the same pattern persisted 24 hours after the last dose, suggesting a lasting change in serotonin responsiveness. This enhancement in the orbitofrontal cortex may explain why some hallucinogens have anti-OCD effects that outlast their psychotomimetic action.

Acute subanesthetic ketamine-induced effects on the mismatch negativity and their relationship to early and sustained treatment response in major depressive disorder.

Journal of psychopharmacology (Oxford, England) February 26, 2025 Sara de la Salle, Jennifer L Phillips, Pierre Blier et al. 3 citations

A sub-anesthetic dose of ketamine, an NMDAR antagonist, produces rapid antidepressant effects in treatment-resistant major depressive disorder. In 24 patients, ketamine reduced frontal mismatch negativity (MMN) amplitude, theta event-related oscillations, and source-localized frontal generator activity immediately and 2 hours after infusion, compared to midazolam. Larger reductions in MMN measures, particularly left frontal amplitude and theta oscillations, correlated with and predicted greater early and sustained symptom improvement on the Montgomery-Åsberg Depression Rating Scale. Baseline phase-locking factor also predicted sustained response. The findings suggest that acute NMDAR blockade reduces frontal MMN, and that MMN indices may serve as non-invasive biomarkers for predicting antidepressant response to glutamatergic agents.