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Danilo de Gregorio

10 papers in the library · 738 citations · publishing 2016-2025

Papers

Hallucinogens in Mental Health: Preclinical and Clinical Studies on LSD, Psilocybin, MDMA, and Ketamine

Journal of Neuroscience November 30, 2020 Danilo de Gregorio, Argel Aguilar‐valles, Katrin H. Preller et al. 258 citations

A renewed interest in hallucinogens for treating psychiatric disorders has emerged. Preclinical and clinical studies have confirmed ketamine's efficacy for depression. Emerging evidence points to psilocybin and LSD's therapeutic properties and their ability to modulate functional brain connectivity. MDMA, an entactogen, has shown usefulness for post-traumatic stress disorder. This review summarizes the pharmacology of hallucinogenic compounds, highlighting differences between psychedelic and nonpsychedelic hallucinogens and entactogens, and describes their behavioral effects in animals and humans. Together, these data substantiate the potential of these compounds for treating mental diseases.

Lysergic acid diethylamide (LSD) promotes social behavior through mTORC1 in the excitatory neurotransmission

Proceedings of the National Academy of Sciences January 25, 2021 Danilo de Gregorio, Jelena Popić, Justine P. Enns et al. 137 citations

Repeated doses of LSD (30 μg/kg daily for 7 days) increase social behavior in male mice without producing antidepressant or anxiety-reducing effects. The prosocial effect requires the integrity of mTORC1 in excitatory glutamatergic neurons of the medial prefrontal cortex (mPFC), as shown by optogenetic inhibition and conditional knockout experiments. LSD potentiates AMPA and 5-HT2A synaptic responses in the mPFC and increases phosphorylation of Akt and mTOR, but does not affect NMDA or 5-HT1A responses. In mice lacking Raptor in GABAergic neurons, LSD still promotes social behavior. The findings suggest that 5-HT2A/AMPA/mTORC1 signaling in mPFC excitatory neurons mediates LSD's prosocial effects, offering a potential target for treating social deficits in autism and social anxiety.

d-Lysergic Acid Diethylamide (LSD) as a Model of Psychosis: Mechanism of Action and Pharmacology

International Journal of Molecular Sciences November 23, 2016 Danilo de Gregorio, Stefano Comai, Luca Posa et al. 125 citations

LSD produces hallucinogenic and psychotic-like effects through a complex mechanism involving multiple neurotransmitter systems. The primary action occurs in the Dorsal Raphe via the serotonergic system, where LSD acts as a partial agonist at 5-HT2A receptors and an agonist at 5-HT1A receptors. At higher doses, it also stimulates dopamine D2 receptors, Trace Amine Associated Receptor 1 (TAAR1), and 5-HT2A in the Ventral Tegmental Area. This pleiotropic mechanism, engaging serotonergic, dopaminergic, and glutamatergic pathways, makes LSD-induced psychosis a useful preclinical model for testing novel antipsychotic drugs, especially those targeting dual serotonergic and dopaminergic systems or TAAR1 receptors. More human studies are needed to clarify these mechanisms.

Repeated lysergic acid diethylamide (LSD) reverses stress-induced anxiety-like behavior, cortical synaptogenesis deficits and serotonergic neurotransmission decline

Neuropsychopharmacology March 17, 2022 Danilo de Gregorio, Antonio Inserra, Justine P. Enns et al. 89 citations

Lysergic acid diethylamide (LSD) is a serotonergic psychedelic being studied for potential anxiety and depression treatments, but its brain mechanisms are unclear. In male mice exposed to chronic restraint stress, acute LSD at doses of 5, 15, 30, and 60 μg/kg did not reduce anxiety or depression in non-stressed mice. However, daily 30 µg/kg LSD for 7 days prevented stress-induced anxiety-like behavior and the stress-induced loss of cortical dendritic spines. Repeated LSD increased the baseline firing rate of serotonin neurons in the dorsal raphe nucleus, which had been lowered by stress, and reduced the neurons' inhibitory response to a 5-HT1A receptor agonist. These effects suggest that repeated LSD prevents stress-induced anxiety by enhancing serotonin transmission and cortical spine density, possibly through desensitization of 5-HT1A receptors.

Evaluating the Potential Use of Serotonergic Psychedelics in Autism Spectrum Disorder

Frontiers in Pharmacology January 27, 2022 Athanasios Markopoulos, Antonio Inserra, Danilo de Gregorio et al. 44 citations

Psychedelic compounds such as LSD, psilocybin, and DMT show empathogenic and prosocial effects, suggesting potential therapeutic benefit for behavioral traits in autism spectrum disorder (ASD), including reduced social behavior and co-occurring anxiety and depression. The review examines dysregulated neurobiological systems in ASD—synaptic function, serotonergic signaling, prefrontal cortex activity, and thalamocortical signaling—that may underlie or limit these effects. Clinical studies from the 1960s and 70s using psychedelics in children with ASD reported positive outcomes like enhanced mood and social behavior, but also adverse effects including increased aggression, dissociation, and psychosis. Further studies are needed to weigh benefits against risks and determine if the 5-HT 2A receptor could be a target for social-behavioral disorders.

Modulation of DNA methylation and protein expression in the prefrontal cortex by repeated administration of D-lysergic acid diethylamide (LSD): Impact on neurotropic, neurotrophic, and neuroplasticity signaling

Progress in Neuro-Psychopharmacology and Biological Psychiatry June 28, 2022 Antonio Inserra, Antonella Campanale, David Cheishvili et al. 39 citations

Repeated administration of lysergic acid diethylamide (LSD) to mice over seven days altered DNA methylation at 635 sites and changed the expression of 178 proteins in the prefrontal cortex. The affected genes and proteins are involved in nervous system development, axon guidance, synaptic plasticity, and cell viability. Four specific genes—Coro7, Pef1, Rps24, and Abhd6—showed both increased methylation and increased transcription. These results suggest that LSD modifies epigenetic and protein-expression pathways related to neuroplasticity, which may underlie its therapeutic effects in mental disorders.

Effects of Chronic Exposure to Low-Dose delta-9-Tetrahydrocannabinol in Adolescence and Adulthood on Serotonin/Norepinephrine Neurotransmission and Emotional Behavior

The International Journal of Neuropsychopharmacology July 23, 2020 Danilo de Gregorio, Joshua Dean Conway, Martha-Lopez Canul et al. 39 citations

Chronic exposure to a low dose of THC (1 mg/kg) during adolescence in rats leads to depressive-like behaviors (increased immobility in the forced swim test and anhedonia in the sucrose preference test) and anxiety-like behavior (fewer open-arm entries in the elevated plus maze). Adult exposure also produces anxiety but not depressive-like behaviors. Both adolescent and adult THC exposure reduce the activity of serotonin neurons in the dorsal raphe, while noradrenergic neurons in the locus coeruleus remain unaffected. These findings suggest that the serotonin system is vulnerable to chronic low-dose THC, and that adolescents are particularly susceptible to THC-induced depressive effects.

Lysergic acid diethylamide (LSD) promotes social behaviour through 5-HT 2A and ampa in the medial prefrontal cortex (MPFC)

European Psychiatry April 1, 2021 Athanasios Markopoulos, Antonio Inserra, Danilo de Gregorio et al. 5 citations

Repeated low doses of lysergic acid diethylamide (LSD) increase social behavior in male mice. This pro-social effect is mediated by the medial prefrontal cortex (mPFC), specifically through the 5-HT2A and AMPA receptors. Blocking either receptor in the mPFC prevented LSD's behavioral effects. LSD also potentiated the excitatory responses of mPFC neurons to agonists of these receptors. The findings suggest a mechanism by which LSD promotes sociability, relevant to understanding its potential therapeutic use for conditions involving social dysfunction, such as autism spectrum disorder and social anxiety disorder.

Differential effects of psilocybin and lisuride on serotonin and dopamine neuronal activity and behavior

Progress in Neuro-Psychopharmacology and Biological Psychiatry October 1, 2025 Brandon Richardson, Antonio Inserra, Michael Pileggi et al. 2 citations

Psilocybin and lisuride both activate 5-HT2A receptors, but only psilocybin triggers the head twitch response (HTR) in mice, a proxy for hallucinogenic activity. In adult male C57BL/6N mice, psilocybin (0.3–3 mg/kg) inhibited serotonin neuron firing in the dorsal raphe nucleus via 5-HT2A receptors, while lisuride (0.1–0.5 mg/kg) did not. Both drugs reduced dopamine neuron firing in the substantia nigra, but lisuride's effect was more sensitive to 5-HT2A antagonism. Psilocybin elicited HTR; lisuride did not. Only high-dose lisuride reduced immobility in the forced swim test. Both drugs reduced locomotion in open field and elevated plus maze tests. Principal component analysis separated the drug effects, indicating distinct neurobiological pathways: psilocybin produces psychedelic-like, serotonin-dominant effects, while lisuride displays dopamine-linked improvements in coping behavior.

363. DIFFERENTIAL EFFECTS OF PSILOCYBIN AND LISURIDE ON SEROTONIN AND DOPAMINE NEURONAL ACTIVITY AND BEHAVIOR

The International Journal of Neuropsychopharmacology August 1, 2025 B. D. Richardson, Marco Pileggi, Thomas Prudhomme et al.

Psilocybin and lisuride both bind to 5-HT2A receptors, but only psilocybin produces hallucinogenic effects. In adult male mice, both drugs inhibited serotonin neuron activity in the dorsal raphe nucleus and dopamine neuron firing in the substantia nigra. A 5-HT2A antagonist blocked psilocybin's serotonin inhibition but not lisuride's, suggesting different mechanisms. Only lisuride showed an antidepressant-like effect at the highest doses. Psilocybin, but not lisuride, elicited head-twitch responses, and lisuride blocked those induced by psilocybin. Both drugs reduced locomotion. The findings indicate lisuride has antidepressant and sedative effects without hallucinogenic action, likely due to its distinct effects on serotonin and dopamine neurons.