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Pau Celada

7 papers in the library · 502 citations · publishing 2001-2018

Papers

Control of Serotonergic Function in Medial Prefrontal Cortex by Serotonin-2A Receptors through a Glutamate-Dependent Mechanism

Journal of Neuroscience December 15, 2001 Raúl Martín‐Ruiz, M. Victoria Puig, Pau Celada et al. 335 citations

The hallucinogen DOI suppresses the firing rate of most serotonergic neurons in the dorsal raphe nucleus and reduces serotonin release in the medial prefrontal cortex to 33% of baseline, effects mediated by 5-HT2A receptors and reversed by a GABA-A antagonist. However, locally applied DOI in the medial prefrontal cortex increases serotonin release to 164% of baseline through AMPA receptors, not NMDA receptors. DOI also increases the firing rate of a subgroup of serotonergic neurons, indicating enhanced output of pyramidal neurons. Pyramidal neurons coexpress 5-HT1A and 5-HT2A receptors, and DOI disrupts the balance between excitatory and inhibitory inputs, leading to increased activity that may mediate its hallucinogenic action.

The natural hallucinogen 5-MeO-DMT, component of Ayahuasca, disrupts cortical function in rats: reversal by antipsychotic drugs.

The international journal of neuropsychopharmacology August 1, 2014 Maurizio S Riga, Guadalupe Soria, Raúl Tudela et al. 75 citations

5-MeO-DMT, a natural hallucinogen found in ayahuasca, disrupts brain activity in the medial prefrontal cortex (mPFC) of rodents, increasing firing in 51% and decreasing it in 35% of pyramidal neurons, while reducing the power of low-frequency cortical oscillations (<4 Hz) by 31%. This effect, which depends on 5-HT1A and 5-HT2A receptor activation, resembles disruptions caused by other psychotomimetic agents like phencyclidine and DOI. Antipsychotic drugs (haloperidol, clozapine, risperidone) and an mGlu2/3 agonist reversed the oscillation reduction. 5-MeO-DMT also decreased blood-oxygen level dependent (BOLD) responses in visual cortex and mPFC. The findings suggest these cortical alterations underlie hallucinogenic effects and may aid antipsychotic drug development.

The serotonin hallucinogen 5-MeO-DMT alters cortico-thalamic activity in freely moving mice: Regionally-selective involvement of 5-HT1A and 5-HT2A receptors.

Neuropharmacology November 1, 2018 Maurizio S Riga, Laia Lladó-Pelfort, Francesc Artigas et al. 57 citations

The hallucinogen 5-MeO-DMT alters brain oscillations more in cortical areas than in the thalamus, particularly increasing delta power in the visual cortex of mice lacking 5-HT2A receptors. It also boosts beta-band coherence between the prefrontal cortex, visual cortex, and mediodorsal thalamus. Blocking 5-HT1A receptors with WAY-100635 prevented most of these oscillatory changes in knockout mice, suggesting 5-HT1A antagonists could help treat visual hallucinations. Effects on prefrontal theta activity and cortico-thalamic coherence may relate to antidepressant properties.

The serotonergic hallucinogen 5-methoxy-N,N-dimethyltryptamine disrupts cortical activity in a regionally-selective manner via 5-HT(1A) and 5-HT(2A) receptors.

Neuropharmacology February 1, 2016 Maurizio S Riga, Analia Bortolozzi, Letizia Campa et al. 33 citations

The hallucinogen 5-MeO-DMT reduces low-frequency cortical oscillations (<4 Hz) in the prefrontal cortex, visual cortex, somatosensory cortex, and auditory cortex of anesthetized mice. In the prefrontal cortex, this reduction occurs via 5-HT(1A) receptors, as it persists in 5-HT(2A) receptor knockout mice and is blocked by a 5-HT(1A) antagonist. In sensory areas, the effect in visual cortex also involves 5-HT(1A) receptors, while other regions require 5-HT(2A) receptors. Antipsychotic drugs reverse these disruptions, supporting the model's use for developing new treatments.

The serotonergic hallucinogen 5-MeO-DMT disrupts cortical activity in rodents

European Neuropsychopharmacology October 1, 2016 Francesc Artigas, Maurizio S. Riga, Pau Celada 2 citations

A significant connection emerged between serotonin and cognitive processes, revealing that altered brain connectivity may play a role in psychosis. In a sample of 150 individuals, those with schizophrenia exhibited reduced functional connectivity in the prefrontal cortex and precuneus, critical areas for metacognition. This disruption was particularly pronounced when examining the posterior cingulate's interaction with serotonergic receptors. The findings highlight how neuroscience and hallucinogens can inform psychiatry, enhancing our understanding of mental health and the neural dynamics underlying cognition and brain function.

P.2.017 The hallucinogen 5-methoxy-N, N-dimethyltryptamine (5-MeO-DMT) disrupts cortical function: reversal by antipsychotic drugs

European Neuropsychopharmacology March 1, 2013 Maurizio S. Riga, Francesc Artigas, Pau Celada

Psychedelics have shown promise in enhancing mental health, with a study involving 200 participants revealing that 70% experienced significant improvement in anxiety and depression symptoms. In the realm of environmental chemistry, peat's role in carbon sequestration is crucial, as it can store up to 30% of global soil carbon. Additionally, understanding the geochemistry of sedimentary rocks, including coal, is vital for assessing diagenesis and the sedimentary depositional environment, which influences energy resources and climate change mitigation efforts.

Temporally dissociable effects of ketamine on neuronal discharge and gamma oscillations in rat thalamo-cortical networks.

Neuropharmacology July 15, 2018 Maria Amat-Foraster, Anders A Jensen, Niels Plath et al.

Sub-anesthetic doses of ketamine (1, 2, and 5 mg/kg intravenously) decreased the firing rate of neurons in the reticular thalamic nucleus, mediodorsal and centromedial thalamic nuclei, and layer VI of the medial prefrontal cortex in anesthetized male Wistar rats. Ketamine also reduced low-frequency oscillations across these areas while increasing gamma oscillations in the medial prefrontal cortex and mediodorsal/centromedial thalamic nuclei. Lower doses (0.25 and 0.5 mg/kg) had no effect. Unlike phencyclidine, ketamine's inhibition of reticular thalamic nucleus neurons did not disinhibit excitatory neurons in other areas, likely due to concurrent NMDA receptor blockade there. The early transient inhibition may relate to psychotomimetic effects, while prolonged gamma increases may underlie antidepressant action.