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Marta De Felice

3 papers in the library · 1 citation · publishing 2021-2025

Papers

The antioxidant N-acetylcysteine prevents cortical neuropathological phenotypes caused by adolescent Δ-9-tetrahydrocannabinol exposure in male rats.

Translational psychiatry October 6, 2025 Hanna J Szkudlarek, Rajkamalpreet Singh Mann, Krystyna Wieczerzak et al. 1 citation

Adolescent exposure to THC, the main psychoactive component of cannabis, increases the risk of later neuropsychiatric symptoms, and the medial prefrontal cortex is a key brain region involved. The antioxidant N-acetylcysteine (NAC) prevented cognitive, synaptic, neuronal, and neurochemical deficits caused by chronic adolescent THC exposure in a rodent model. This suggests that THC-induced oxidative stress contributes to neuropsychiatric risk and identifies NAC as a potential preventive treatment.

Adolescent female rats are resistant to the affective and cognitive impacts of Δ9-tetrahydrocannabinol exposure despite long-lasting molecular and neuronal disturbances in the hippocampal-hypothalamic network.

Psychopharmacology November 1, 2025 Marta De Felice, Hanna J Szkudlarek, Matthew J Jones et al.

Adolescent female rats exposed to THC gained weight slower than controls during treatment. In adulthood, they showed no behavioral abnormalities in tests of locomotion, sensorimotor gating, memory, or anxiety. However, long-lasting molecular adaptations occurred: altered expression of estrogen receptor-α and fatty acid amid hydrolase in the hypothalamus and hippocampus, along with enduring changes in hippocampal oscillatory patterns. These sex-specific adaptations may protect females against the long-term behavioral abnormalities consistently seen in male cohorts.

THC and CBD produce divergent effects on perception and panic behaviours via distinct cortical molecular pathways.

Progress in neuro-psychopharmacology & biological psychiatry January 10, 2021 Hanna J Szkudlarek, Mar Rodríguez-ruiz, Roger Hudson et al.

In rats, THC infused directly into the medial prefrontal cortex (PFC) caused strong panic-like responses, while CBD did not affect panic but blocked the formation of associative fear memories and impaired latent inhibition and oddity discrimination. CBD counteracted THC-induced panic and prevented THC-driven phosphorylation of ERK1/2. CBD's effects on perception and latent inhibition depended on 5-HT1A receptor transmission and were accompanied by reduced phosphorylation of p70S6K, independently of THC. The findings suggest dissociable molecular mechanisms: THC promotes panic via ERK1/2 phosphorylation, while CBD impairs perceptive functions via 5-HT1A receptors and reduced p70S6K phosphorylation.