Publications by authors named "Antonio Waldo Zuardi"

77 Publications

Effects of cannabidiol on symptoms induced by the recall of traumatic events in patients with posttraumatic stress disorder.

Psychopharmacology (Berl) 2022 Jan 14. Epub 2022 Jan 14.

Department of Neuroscience and Behavioral Sciences, Ribeirão Preto School of Medicine, University of São Paulo, São Paulo, Brazil.

Studies with cannabidiol (CBD) suggest that this compound has anxiolytic properties and may mediate the reconsolidation and extinction of aversive memories. The objective of this study was to test whether the administration of CBD 300 mg before the recall of traumatic events attenuated symptoms usually induced by recall in subjects diagnosed with posttraumatic stress disorder (PTSD) and if its potential effects interfere with the reconsolidation of aversive memories. The double-blind trial included 33 participants of both sexes, aged between 18 and 60 years, diagnosed with PTSD according to the SCID-5 and randomly allocated to two groups treated with CBD (n = 17) and placebo (n = 16). In the first experimental section, participants were matched by sex, age, body mass index (BMI), and PTSD symptoms as assessed with the Posttraumatic Stress Disorder Checklist (PCL-5). On the same day, participants prepared the behavior test, recording accounts of their traumas in digital audio for a minute and a half and then imagining the trauma for 30 s. After 7 days, participants received CBD (300 mg) or placebo and performed the behavioral test, listening to the trauma account and imagining themselves in that situation. Before and after the behavioral test, subjective changes in mood and anxiety were recorded (Visual and Analogical Mood Scale - VAMS and STAI-state), along with physiological correlates of anxiety blood pressure (BP), heart rate (HR), and salivary cortisol (SC). Seven days later, participants underwent the same procedures as the previous session, but without the pharmacological intervention, to assess the effect on reconsolidation of traumatic memories. We found that CBD significantly attenuated the increase in the VAMS scale cognitive impairment factor scores, under the CBD's effect, with this effect remaining 1 week after drug administration. No significant differences between the effects of CBD and placebo on anxiety, alertness, and discomfort induced by the recall of the traumatic event during the pharmacological intervention and in the subsequent week, in the absence of it. There were no significant differences between the CBD and placebo groups regarding physiological data (BP, HR, and SC). The attenuation of cognitive impairments during trauma recall under the effect of CBD may have interfered with the reconsolidation of traumatic memories concerning its association with cognitive impairments.
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http://dx.doi.org/10.1007/s00213-021-06043-yDOI Listing
January 2022

Endocannabinoid System Attenuates Oxaliplatin-Induced Peripheral Sensory Neuropathy Through the Activation of CB1 Receptors.

Neurotox Res 2021 Dec 18;39(6):1782-1799. Epub 2021 Nov 18.

Department of Physiology and Pharmacology, Faculty of Medicine, Federal University of Ceará, Fortaleza, CE, Brazil.

Oxaliplatin-induced neurotoxicity is expressed as a dose-limiting peripheral sensory neuropathy (PSN). Cannabinoid substances have been investigated for the analgesic effect. This study aimed to investigate the role of cannabinoid receptors in oxaliplatin-associated PSN. Swiss male mice received nine oxaliplatin injections (2 mg/kg, i.v.). Mechanical and thermal nociceptive tests were performed for 56 days. CB1, CB2, and c-Fos expression were assessed in dorsal root ganglia (DRG), spinal cord (SC), trigeminal ganglia (TG), spinal trigeminal nucleus caudalis (Sp5C), and periaqueductal gray (PAG). Iba-1 expression was assessed in DRG and ATF3 in TG. Cannabidiol (10 mg/kg, p.o.) or a CB1/CB2 non-selective agonist (WIN 55,212-2; 0.5 mg/kg, s.c.) or AM251 (CB1 antagonist) or AM630 (CB2 antagonist) (3 mg/kg, i.p.) were injected before oxaliplatin. Oxaliplatin increased CB1 in DRG, SC, TG, Sp5C, and ventrolateral PAG, with no interference in CB2 expression. Cannabidiol increased CB1 in DRG, reduced mechanical hyperalgesia and c-Fos expression in DRG and SC. Additionally, WIN 55,212-2 increased CB1 in DRG, reduced mechanical hyperalgesia, cold allodynia and c-Fos expression in DRG and SC. CB1 blockage hastened the cold allodynia response, but the CB2 antagonist failed to modulate the oxaliplatin-induced nociceptive behavior. Oxaliplatin also increased Iba-1 in DRG, suggesting immune response modulation which was reduced by cannabidiol and enhanced by AM630. The modulation of the endocannabinoid system, through the CB1 receptor, attenuates the oxaliplatin-associated PNS. The activation of the endocannabinoid system could be considered as a therapeutic target for controlling oxaliplatin-associated neuropathy.
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http://dx.doi.org/10.1007/s12640-021-00442-xDOI Listing
December 2021

Cannabidiol reverses memory impairments and activates components of the Akt/GSK3β pathway in an experimental model of estrogen depletion.

Behav Brain Res 2022 Jan 24;417:113555. Epub 2021 Aug 24.

National Institute of Science and Technology for Translational Medicine (INCT-TM), Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq), Brasília, Brazil; Department of Physiology, Institute for Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, Brazil. Electronic address:

Clinical and preclinical evidence has indicated that estrogen depletion leads to memory impairments and increases the susceptibility to neural damage. Here, we have sought to investigate the effects of Cannabidiol (CBD) a non-psychotomimetic compound from Cannabis sativa, on memory deficits induced by estrogen depletion in rats, and its underlying mechanisms. Adult rats were subjected to bilateral ovariectomy, an established estrogen depletion model in rodents, or sham surgery and allowed to recover for three weeks. After that, they received daily injections of CBD (10 mg/kg) for fourteen days. Rats were tested in the inhibitory avoidance task, a type of emotionally-motivated memory. After behavioral testing they were euthanized, and their hippocampi were isolated for analysis of components of the Akt/GSK3β survival pathway and the antiapoptotic protein Bcl2. Results revealed that ovariectomy impaired avoidance memory, and CBD was able to completely reverse estrogen depletion-induced memory impairment. Ovariectomy also reduced Akt/GSK3β pathway's activation by decreasing the phosphorylation levels of Akt and GSK3β and Bcl2 levels, which were ameliorated by CBD. The present results indicate that CBD leads to a functional recovery accompanied by the Akt/GSK3β survival pathway's activation, supporting its potential as a treatment for estrogen decline-induced deterioration of neural functioning and maintenance.
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http://dx.doi.org/10.1016/j.bbr.2021.113555DOI Listing
January 2022

Risk and Protective Factors for the Mental Health of Brazilian Healthcare Workers in the Frontline of COVID-19 Pandemic.

Front Psychiatry 2021 28;12:662742. Epub 2021 Jul 28.

Medical School of Ribeirão Preto, São Paulo University, São Paulo, Brazil.

The objective was to compare the mental health indicators of health workers providing care to individuals with COVID-19 in Brazil, considering sociodemographic and occupational variables and the risk perception of contamination by the Sars-CoV-2 of workers from different professions, identifying risk and protective factors. A sample of 916 health workers was assessed: physicians, nursing workers, and workers from other professions (psychologists, physical therapists, nutritionists, speech therapists, occupational therapists, dentists, pharmacists, and social workers). REDCAP software was used to collect data online, using standardized instruments to assess anxiety, depression, posttraumatic stress, and insomnia, and one questionnaire addressed risk and protective variables. Statistical techniques for comparing groups were used along with logistic regression analysis. The results revealed that all the groups presented indicators of significant mental health problems (>36%), especially the nursing group. A larger percentage of participants, regardless of the profession, presented a high rate of insomnia disorders, while posttraumatic stress was the least expressive. Occupational variables stand out as risk factors for mental health, with specificities among the different groups. A protective factor for all the groups was having positive professional prospects. The protective factors for the physicians group included support provided by co-workers, being older and a man, while being satisfied with physical protective measures implemented by the employing institution was a protective factor for the groups composed of nursing workers and other professionals. These findings are relevant for devising mental health care strategies.
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http://dx.doi.org/10.3389/fpsyt.2021.662742DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8355424PMC
July 2021

Is Cannabidiol During Neurodevelopment a Promising Therapy for Schizophrenia and Autism Spectrum Disorders?

Front Pharmacol 2020 4;11:635763. Epub 2021 Feb 4.

Molecular and Behavioral Neuroscience Laboratory, Departamento de Farmacologia, Universidade Federal de São Paulo, São Paulo, Brazil.

Schizophrenia and autism spectrum disorders (ASD) are psychiatric neurodevelopmental disorders that cause high levels of functional disabilities. Also, the currently available therapies for these disorders are limited. Therefore, the search for treatments that could be beneficial for the altered course of the neurodevelopment associated with these disorders is paramount. Preclinical and clinical evidence points to cannabidiol (CBD) as a promising strategy. In this review, we discuss clinical and preclinical studies on schizophrenia and ASD investigating the behavioral, molecular, and functional effects of chronic treatment with CBD (and with cannabidivarin for ASD) during neurodevelopment. In summary, the results point to CBD's beneficial potential for the progression of these disorders supporting further investigations to strengthen its use.
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http://dx.doi.org/10.3389/fphar.2020.635763DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7890086PMC
February 2021

Oral Cannabidiol Does Not Convert to Δ-THC or Δ-THC in Humans: A Pharmacokinetic Study in Healthy Subjects.

Cannabis Cannabinoid Res 2020 Mar 27;5(1):89-98. Epub 2020 Feb 27.

Prati Donaduzzi & Cia Ltda, Toledo, Brazil.

Recent studies have suggested that cannabidiol (CBD) could interconvert into Delta-8- and Delta-9- tetrahydrocannabinol. Thus, we tested the plasma samples of 120 healthy human subjects (60 male and 60 female), 60 in fasting and the other 60 under normal feeding conditions after acute administration of an oral solution containing CBD 300 mg. To do this, we developed a bioanalytical method to determine CBD and the presence of THC in plasma samples by Ultra-High Performance Liquid Chromatography Coupled to Tandem Mass Spectrometry. The results showed that THC was not detected in plasma after the administration of CBD, and those study participants did not present psychotomimetic effects. The findings presented here are consistent with previous evidence suggesting that the oral administration of CBD in a corn oil formulation is a safe route for the administration of the active substance without bioconversion to THC in humans.
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http://dx.doi.org/10.1089/can.2019.0024DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7173681PMC
March 2020

Cannabinoids for the treatment of mental disorders.

Lancet Psychiatry 2020 02;7(2):125-126

Department of Neuroscience and Behavior, School of Medicine of Ribeirão Preto, University of São Paulo, Hospital das Clinicas Ribeirão Preto, São Paulo 14025600, Brazil; National Institute of Science and Technology for Translational Medicine, Brazilian National Council for Scientific and Technological Development, Brasília, Brazil.

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http://dx.doi.org/10.1016/S2215-0366(19)30516-4DOI Listing
February 2020

Pharmacological interventions during the process of reconsolidation of aversive memories: A systematic review.

Neurobiol Stress 2019 Nov 21;11:100194. Epub 2019 Aug 21.

Department of Neuroscience and Behavioral Science, Medical School of Ribeirão Preto, São Paulo, Brazil, University of São Paulo, Avenue Tenente Catão Roxo, 2650. Ribeirão Preto, São Paulo, 14051-140, Brazil.

Reconsolidation is the return of a memory to a transient state of lability, following memory consolidation, that can occur when memories are evoked. During the process of reconsolidation, memories may be modified by different means, including the administration of drugs, during a period called the "reconsolidation window". This process has been widely studied in animals, but human studies are limited and include several methodological pitfalls. Our objective was to conducte a systematic review of the literature that utilizes pharmacological interventions during the process of reconsolidation of aversive memories in humans, with a critical analysis of the methodologies used. Searches were made in the electronic databases PubMed, Scopus, Web of Science and SciELO using the following search terms: (memory) AND (consolidation OR reconsolidation) AND (pharmacological manipulation OR pharmacological intervention). We found 294 references and ten (3.4%) were included in the review, based on preestablished eligibility criteria. All studies were randomized, double-blind clinical trials. The most commonly studied drug was propranolol. Two studies used a protocol involving autobiographical aversive memories, while in the remaining aversive memories were produced in the laboratory. The timing of pharmacological interventions is a controversial issue in the field, as drug activity must occur within the reconsolidation window. The small number of studies and some methodological difficulties of this type of research highlights the need for studies that individually evaluate some of the issues discussed, particularly the timing of pharmacological interventions and the duration of reconsolidation windows.
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http://dx.doi.org/10.1016/j.ynstr.2019.100194DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6889468PMC
November 2019

Changes in Cortisol Awakening Response Before and After Development of Posttraumatic Stress Disorder, Which Cannot be Avoided with Use of Cannabidiol: A Case Report.

Perm J 2019 27;23. Epub 2019 Sep 27.

Department of Neuroscience and Behavior, Ribeirão Preto Medical School, University of São Paulo, Brazil.

Introduction: Previous studies have shown attenuated cortisol awakening response in patients with posttraumatic stress disorder (PTSD).

Case Presentation: A 15-year-old girl, a survivor of acute sexual violence, received a 7-day oral treatment with cannabidiol. She was followed-up from the first 24 hours after the event for 6 months, for assessment of the effects of this treatment on the reconsolidation of memories related to the traumatic event.

Discussion: Cannabidiol treatment did not prevent the onset of PTSD. Cortisol awakening responses after the onset of the disorder were attenuated compared with those observed in the same individual before the onset of PTSD, in line with previous evidence from studies comparing groups with and without PTSD.
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http://dx.doi.org/10.7812/TPP/18.300DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6836527PMC
July 2020

Modulation of the Endocannabinoid and Oxytocinergic Systems as a Potential Treatment Approach for Social Anxiety Disorder.

CNS Drugs 2019 10;33(10):1031-1038

Department of Neurosciences and Behavior, Ribeirão Preto Medical School, University of São Paulo, Av. Bandeirantes, Ribeirão Preto, São Paulo, 3900, Brazil.

Social anxiety disorder (SAD), or social phobia, is one of the most common types of anxiety disorder, with a lifetime prevalence that can reach 15%. Pharmacological treatments for SAD have moderate efficacy and are associated with significant adverse reactions. Therefore, recent studies have focused on searching for new treatments for this disorder. Preclinical studies and preliminary evidence in humans suggest that the phytocannabinoid cannabidiol and the neuropeptide oxytocin have anxiolytic effects. In the present text, we review this evidence and its implications for pharmacological treatment. We conclude that although current available studies show promising results regarding both the safety and efficacy of cannabidiol and oxytocin for the treatment of SAD, most studies were performed using single or few doses of these compounds, with small sample sizes. Therefore, future studies should explore the anxiolytic potential of these compounds using long-term, placebo-controlled designs with larger samples to elucidate the possible use of these compounds in the treatment of SAD.
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http://dx.doi.org/10.1007/s40263-019-00669-5DOI Listing
October 2019

Role of the endocannabinoid and endovanilloid systems in an animal model of schizophrenia-related emotional processing/cognitive deficit.

Neuropharmacology 2019 09 16;155:44-53. Epub 2019 May 16.

Department of Pharmacology, Federal University of São Paulo (Universidade Federal de São Paulo - UNIFESP/EPM), São Paulo, Brazil; National Institute for Translational Medicine (INCT-TM, CNPq), Ribeirão Preto, Brazil. Electronic address:

Studies suggest that the endocannabinoid and endovanilloid systems are implicated in the pathophysiology of schizophrenia. The Spontaneously Hypertensive Rats (SHR) strain displays impaired contextual fear conditioning (CFC) attenuated by antipsychotic drugs and worsened by pro-psychotic manipulations. Therefore, SHR strain is used to study emotional processing/associative learning impairments associated with schizophrenia and effects of potential antipsychotic drugs. Here, we evaluated the expression of CB and TRPV1 receptors in some brain regions related to the pathophysiology of schizophrenia. We also assessed the effects of drugs that act on the endocannabinoid/endovanilloid systems on the CFC task in SHRs and control animals (Wistar rats - WRs). The following drugs were used: AM404 (anandamide uptake/metabolism inhibitor), WIN55-212,2 (non-selective CB agonist), capsaicin (TRPV1 agonist), and capsazepine (TRPV1 antagonist). SHRs displayed increased CB expression in prelimbic cortex and cingulate cortex area 1 and in CA3 region of the dorsal hippocampus. Conversely, SHRs exhibited decreases in TRPV1 expression in prelimbic and CA1 region of dorsal hippocampus and increases in the basolateral amygdala. AM404, WIN 55,212-2 and capsaicin attenuated SHRs CFC deficit, although WIN 55,212-2 worsened SHRs CFC deficit in higher doses. WRs and SHRs CFC were modulated by distinct doses, suggesting that these strains display different responsiveness to cannabinoid and vanilloid drugs. Treatment with capsazepine did not modify CFC in either strains. The effects of AM404 on SHRs CFC deficit was not blocked by pretreatment with rimonabant (CB antagonist) or capsazepine. These results reinforce the involvement of the endocannabinoid/endovanilloid systems in the SHRs CFC deficit and point to these systems as targets to treat the emotional processing/cognitive symptoms of schizophrenia.
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http://dx.doi.org/10.1016/j.neuropharm.2019.05.015DOI Listing
September 2019

Cannabidiol attenuates mechanical allodynia in streptozotocin-induced diabetic rats via serotonergic system activation through 5-HT1A receptors.

Brain Res 2019 07 18;1715:156-164. Epub 2019 Mar 18.

Department of Pharmacology, Biological Science Sector, Federal University of Paraná, Curitiba, Paraná, Brazil; Institute of Neurosciences and Behavior (INeC) and Laboratory of Neuropsychopharmacology of Faculty of Philosophy, Sciences and Letters of University of São Paulo, Ribeirão Preto, São Paulo, Brazil. Electronic address:

Most diabetic patients describe moderate to severe pain symptoms whose pharmacological treatment is palliative and poorly effective. Cannabidiol (CBD) has shown promising results in painful conditions. Then, we aimed to investigate the potential antinociceptive effect of CBD over the mechanical allodynia in streptozotocin-induced diabetic (DBT) rats, as well as its involved mechanisms. Wistar adult male diabetic rats were treated acutely or sub-chronically (for 14 days) with CBD (0.1, 0.3 or 3 mg/kg, intraperitoneal; i.p.) and had their mechanical threshold assessed using the electronic Von Frey. Acute treatment with CBD (at doses of 0.3 and 3 mg/kg) exerted a significant anti-allodynic effect, which is not associated with locomotor impairment. The antinociceptive effect of CBD (3 mg/kg) was not altered by the pre-treatment with CB or CB receptor antagonists (AM251 and AM630; respectively; both at a dose of 1 mg/kg, i.p.) nor by glycine receptor antagonist (strychnine hydrochloride, 10 μg/rat, intrathecal, i.t.). However, this effect was completely prevented by the pre-treatment with the selective 5-HT receptor antagonist WAY 100135 (3 μg/rat, i.t.). Sub-chronic treatment with CBD (0.3 or 3 mg/kg) induced a sustained attenuation of the mechanical allodynia in DBT rats. DBT rats presented significantly lower spinal cord levels of serotonin, which was prevented by the daily treatment with CBD (0.3 mg/kg). Taken together, our data suggest that CBD may be effective in the treatment of painful diabetic neuropathy and this effect seems to be potentially mediated by the serotonergic system activation through 5-HT receptors.
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http://dx.doi.org/10.1016/j.brainres.2019.03.014DOI Listing
July 2019

Antiapoptotic effects of cannabidiol in an experimental model of cognitive decline induced by brain iron overload.

Transl Psychiatry 2018 09 3;8(1):176. Epub 2018 Sep 3.

National Institute of Science and Technology for Translational Medicine (INCT-TM), Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq), Brasília, Brazil.

Iron accumulation in the brain has been recognized as a common feature of both normal aging and neurodegenerative diseases. Cognitive dysfunction has been associated to iron excess in brain regions in humans. We have previously described that iron overload leads to severe memory deficits, including spatial, recognition, and emotional memory impairments in adult rats. In the present study we investigated the effects of neonatal iron overload on proteins involved in apoptotic pathways, such as Caspase 8, Caspase 9, Caspase 3, Cytochrome c, APAF1, and PARP in the hippocampus of adult rats, in an attempt to establish a causative role of iron excess on cell death in the nervous system, leading to memory dysfunction. Cannabidiol (CBD), the main non-psychotropic component of Cannabis sativa, was examined as a potential drug to reverse iron-induced effects on the parameters analyzed. Male rats received vehicle or iron carbonyl (30 mg/kg) from the 12th to the 14th postnatal days and were treated with vehicle or CBD (10 mg/kg) for 14 days in adulthood. Iron increased Caspase 9, Cytochrome c, APAF1, Caspase 3 and cleaved PARP, without affecting cleaved Caspase 8 levels. CBD reversed iron-induced effects, recovering apoptotic proteins Caspase 9, APAF1, Caspase 3 and cleaved PARP to the levels found in controls. These results suggest that iron can trigger cell death pathways by inducing intrinsic apoptotic proteins. The reversal of iron-induced effects by CBD indicates that it has neuroprotective potential through its anti-apoptotic action.
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http://dx.doi.org/10.1038/s41398-018-0232-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6120904PMC
September 2018

Cannabinoid-Based Therapies and Brain Development: Potential Harmful Effect of Early Modulation of the Endocannabinoid System.

CNS Drugs 2018 08;32(8):697-712

Laboratory of Cellular Biochemistry, Department of Biochemistry, ICBS/UFRGS, 2600 Ramiro Barcelos St, Porto Alegre, RS, 90035-003, Brazil.

The endocannabinoid retrograde signaling pathway is widely expressed in the central nervous system, where it plays major roles in regulating synaptic plasticity (excitatory and inhibitory) through long-term potentiation and long-term depression. The endocannabinoid system (ECS) components-cannabinoid receptors, endocannabinoids and synthesis/degradation enzymes-are expressed and are functional from early developmental stages and throughout adolescent cortical development, regulating progenitor cell fate, neural differentiation, migration and survival. This may potentially confer increased vulnerability to adverse outcomes from early cannabinoid exposure. Cannabidiol (CBD) is one of the most studied exogenous cannabinoids, and CBD-enriched Cannabis extracts have been widely (and successfully) used as adjuvants to treat children with refractory epilepsy, and there is even a Food and Drug Administration (FDA)-approved drug with purified CBD derived from Cannabis. However, there is insufficient information on possible long-term changes in the central nervous system caused by cannabinoid treatments during early childhood. Like the majority of cannabinoids, CBD is able to exert its effects directly and indirectly through the ECS, which can perturb the regulatory processes mediated by this system. In addition, CBD has a large number of non-endocannabinoid targets, which can explain CBD's effects. Here, we review the current knowledge about CBD-based therapies-pure and CBD-enriched Cannabis extracts-in studies with pediatric patients, their side effects, and their mechanisms of action regarding the central nervous system and neurodevelopment aspects. Since Cannabis extracts contain Δ-tetrahydrocannabinol (Δ-THC), we consider that pure CBD is possibly safer for young patients. Nevertheless, CBD, as well as other natural and/or synthetic cannabinoids, should be studied in more detail as a therapeutic alternative to CBD-enriched Cannabis extracts for young patients.
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http://dx.doi.org/10.1007/s40263-018-0550-4DOI Listing
August 2018

Cannabidiol did not induce teratogenicity or neurotoxicity in exposed zebrafish embryos.

Chem Biol Interact 2018 Aug 11;291:81-86. Epub 2018 Jun 11.

School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, 14040-903, Ribeirão Preto, São Paulo, Brazil; National Institute of Science and Technology for Detection, Toxicological Evaluation and Removal of Emerging and Radioactive Contaminants (INCT-DATREM), Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq), Brasília, Brazil.

Cannabidiol (CBD) is a non-psychotomimetic compound of the Cannabis sativa that has been used for the treatment of severe epilepsy as well as other diseases of nervous system. However, toxicity studies of CBD have great relevance to guarantee the patients safety. In this context, morphological analyses of zebrafish can contribute to evaluate the teratogenic potential, as well as evaluation of acetylcholinesterase activity and motor activity of zebrafish are valuable tools to verify the neurotoxicity potential. In the present work, we use this methodology to test the toxicity of CBD to zebrafish embryos. No malformation was observed in morphological analysis of embryos exposed to all tested concentrations of CBD. Although, twenty per cent of embryos exposed to maximal dose of CBD (300 μg/L) hatched after 96hpf, while embryos in control solution had already hatched in this period. Embryos exposed to CBD did not show differences in acetylcholinesterase activity, but embryos exposed to CBD 20-300 μg/L were 1.4 up to 1.7-fold more active when compared to the control. Despite that, at 48 hpf, motor activity returned to control values. Our results suggest that the effects observed after CBD exposure are intimately related to CB1 receptor that is present in zebrafish since early stages of development. The present work showed early light effects induced by CBD exposure in concentrations that did not alter biochemical activity.
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http://dx.doi.org/10.1016/j.cbi.2018.06.008DOI Listing
August 2018

Novel insights into mitochondrial molecular targets of iron-induced neurodegeneration: Reversal by cannabidiol.

Brain Res Bull 2018 05 31;139:1-8. Epub 2018 Jan 31.

Neurobiology and Developmental Biology Laboratory, Faculty of Biosciences, Pontifical Catholic University of Rio Grande do Sul, 90619-900 Porto Alegre, RS, Brazil; National Institute of Science and Technology for Translational Medicine (INCT-TM), Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq), Brasília, Brazil. Electronic address:

Evidence has demonstrated iron accumulation in specific brain regions of patients suffering from neurodegenerative disorders, and this metal has been recognized as a contributing factor for neurodegeneration. Using an experimental model of brain iron accumulation, we have shown that iron induces severe memory deficits that are accompanied by oxidative stress, increased apoptotic markers, and decreased synaptophysin in the hippocampus of rats. The present study aims to characterize iron loading effects as well as to determine the molecular targets of cannabidiol (CBD), the main non-psychomimetic compound of Cannabis sativa, on mitochondria. Rats received iron in the neonatal period and CBD for 14 days in adulthood. Iron induced mitochondrial DNA (mtDNA) deletions, decreased epigenetic modulation of mtDNA, mitochondrial ferritin levels, and succinate dehydrogenase activity. CBD rescued mitochondrial ferritin and epigenetic modulation of mtDNA, and restored succinate dehydrogenase activity in iron-treated rats. These findings provide new insights into molecular targets of iron neurotoxicity and give support for the use of CBD as a disease modifying agent in the treatment of neurodegenerative diseases.
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http://dx.doi.org/10.1016/j.brainresbull.2018.01.014DOI Listing
May 2018

Impact of different approaches of primary care mental health on the prevalence of mental disorders.

Prim Health Care Res Dev 2018 05 5;19(3):256-263. Epub 2017 Dec 5.

2Department of Neurosciences and Behavioral Sciences,Ribeirão Preto Medical School,University of São Paulo,São Paulo,Brazil.

AimTo compare the impact of three different approaches to primary care mental health on the prevalence of mental disorders.

Background: Millions of people suffer from mental disorders. As entry point into the health service, primary healthcare plays an important role in providing mental health prevention and treatment.

Methods: Random sample of households in three different areas of the city of Ribeirão Preto (state of São Paulo, Brazil) were selected, and 20 trained medical students conducted interviews using a mental health screening instrument, the Mini-Screening of Mental Disorders, and a socio-demographic datasheet. Primary care mental health was provided in each area through a specific approach. The influence of the area of residence and the socio-demographic variables on the prevalence of mental disorder was explored and analyzed by univariate binary logistic regression and then by a multiple logistic regression model.FindingsA total of 1545 subjects were interviewed. Comparison between the three areas showed a significantly higher number of people with mental disorders in the area covered by the primary care team that did not have physicians with specific primary care mental health training, even when this association was adjusted for the influence of age, education, and socio-economic status.Our results suggest that residing in areas with family physicians with mental health training is associated with a lower prevalence of mental disorders.
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http://dx.doi.org/10.1017/S1463423617000743DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6452967PMC
May 2018

A Conversion of Oral Cannabidiol to Delta9-Tetrahydrocannabinol Seems Not to Occur in Humans.

Cannabis Cannabinoid Res 2017 1;2(1):81-86. Epub 2017 May 1.

Department of Neuroscience and Behavior, University of São Paulo Ribeirão Preto, Brazil and Instituto Nacional de Ciência e Tecnologia Translacional em Medicina (INCT-TM).

Cannabidiol (CBD), a major cannabinoid of hemp, does not bind to CB1 receptors and is therefore devoid of psychotomimetic properties. Under acidic conditions, CBD can be transformed to delta9-tetrahydrocannabinol (THC) and other cannabinoids. It has been argued that this may occur also after oral administration in humans. However, the experimental conversion of CBD to THC and delta8-THC in simulated gastric fluid (SGF) is a highly artificial approach that deviates significantly from physiological conditions in the stomach; therefore, SGF does not allow an extrapolation to conditions. Unsurprisingly, the conversion of oral CBD to THC and its metabolites has not been observed to occur , even after high doses of oral CBD. In addition, the typical spectrum of side effects of THC, or of the very similar synthetic cannabinoid nabilone, as listed in the official Summary of Product Characteristics (e.g., dizziness, euphoria/high, thinking abnormal/concentration difficulties, nausea, tachycardia) has not been observed after treatment with CBD in double-blind, randomized, controlled clinical trials. In conclusion, the conversion of CBD to THC in SGF seems to be an artifact.
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http://dx.doi.org/10.1089/can.2017.0009DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5510776PMC
May 2017

Even High Doses of Oral Cannabidol Do Not Cause THC-Like Effects in Humans: Comment on Merrick et al. 2016;1(1):102-112; DOI: 10.1089/can.2015.0004.

Cannabis Cannabinoid Res 2017 1;2(1):1-4. Epub 2017 Jan 1.

Medical School-University of São Paulo, Ribeirão Preto, Brazil.

This short communication examines the question whether the experimental data presented in a study by Merrick et al. are of clinical relevance. These authors found that cannabidiol (CBD), a major cannabinoid of the cannabis plant devoid of psychotropic effects and of great interest for therapeutic use in several medical conditions, may be converted in gastric fluid into the psychoactive cannabinoids delta-8-THC and delta-9-THC to a relevant degree. They concluded that "the acidic environment during normal gastrointestinal transit can expose orally CBD-treated patients to levels of THC and other psychoactive cannabinoids that may exceed the threshold for a positive physiological response." They issued a warning concerning oral use of CBD and recommend the development of other delivery methods. However, the available clinical data do not support this conclusion and recommendation, since even high doses of oral CBD do not cause psychological, psychomotor, cognitive, or physical effects that are characteristic for THC or cannabis rich in THC. On the contrary, in the past decades and by several groups, high doses of oral CBD were consistently shown to cause opposite effects to those of THC in clinical studies. In addition, administration of CBD did not result in detectable THC blood concentrations. Thus, there is no reason to avoid oral use of CBD, which has been demonstrated to be a safe means of administration of CBD, even at very high doses.
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http://dx.doi.org/10.1089/can.2016.0036DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5531368PMC
January 2017

Selective post-training time window for memory consolidation interference of cannabidiol into the prefrontal cortex: Reduced dopaminergic modulation and immediate gene expression in limbic circuits.

Neuroscience 2017 05 24;350:85-93. Epub 2017 Mar 24.

Brain Institute, Federal University of Rio Grande do Norte, Natal - RN, Brazil. Electronic address:

The prefrontal cortex (PFC), amygdala and hippocampus display a coordinated activity during acquisition of associative fear memories. Evidence indicates that PFC engagement in aversive memory formation does not progress linearly as previously thought. Instead, it seems to be recruited at specific time windows after memory acquisition, which has implications for the treatment of post-traumatic stress disorders. Cannabidiol (CBD), the major non-psychotomimetic phytocannabinoid of the Cannabis sativa plant, is known to modulate contextual fear memory acquisition in rodents. However, it is still not clear how CBD interferes with PFC-dependent processes during post-training memory consolidation. Here, we tested whether intra-PFC infusions of CBD immediately after or 5h following contextual fear conditioning was able to interfere with memory consolidation. Neurochemical and cellular correlates of the CBD treatment were evaluated by the quantification of extracellular levels of dopamine (DA), serotonin, and their metabolites in the PFC and by measuring the cellular expression of activity-dependent transcription factors in cortical and limbic regions. Our results indicate that bilateral intra-PFC CBD infusion impaired contextual fear memory consolidation when applied 5h after conditioning, but had no effect when applied immediately after it. This effect was associated with a reduction in DA turnover in the PFC following retrieval 5days after training. We also observed that post-conditioning infusion of CBD reduced c-fos and zif-268 protein expression in the hippocampus, PFC, and thalamus. Our findings support that CBD interferes with contextual fear memory consolidation by reducing PFC influence on cortico-limbic circuits.
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http://dx.doi.org/10.1016/j.neuroscience.2017.03.019DOI Listing
May 2017

Impact of length of stay for first psychiatric admissions on the ratio of readmissions in subsequent years in a large Brazilian catchment area.

Soc Psychiatry Psychiatr Epidemiol 2016 Apr 22;51(4):575-87. Epub 2016 Jan 22.

Departamento de Neurociências e Ciências do Comportamento, Faculdade de Medicina de Ribeirão Preto-USP, Ribeirão Preto Medical School, University of São Paulo, Avenida Bandeirantes 3900, Ribeirão Preto, SP, CEP: 14048-900, Brazil.

Purpose: This study aims to verify the impact that the length of stay has on the rates of readmission for patients who were first admitted to various inpatient psychiatric units in a large catchment area in a middle-income country.

Methods: The study included all patients who were first admitted to the 108 acute psychiatric beds available in the catchment area of Ribeirão Preto, Brazil, for a period of 8 years. Demographic features, inpatient unit of discharge, diagnosis and length of stay were assessed by bivariate analysis. An analysis of the time span between first admission and readmission was also conducted using survival curves estimated by the Kaplan-Meier formula. For the analyses of the risk of readmissions, a logistic regression analysis was conducted.

Results: From a total of 6261 patients admitted in the period of the survey, approximately one-third (2006) had at least one other readmission during the follow-up period. The rates per year of early readmission (within 90 days after discharge) varied from 16.1 to 20.9 %. The risk of readmission was higher immediately after discharge. The survival analysis showed that ultrashort length of stay (1-2 days) was associated with reduced odds of readmission, but multivariate logistic analysis showed no association between length of stay and the odds of readmissions. The predictors of early readmission included the diagnosis of depressive, bipolar, psychotic, and non-alcohol-related disorders, younger ages and unemployment.

Conclusions: Duration of the first psychiatric admission was not associated with a higher risk of readmissions. Predictors for early readmissions of first-time-admitted psychiatric patients seem to be more related to the severity of the psychiatric diagnosis and demographic characteristics.
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http://dx.doi.org/10.1007/s00127-016-1175-xDOI Listing
April 2016

Evaluation of the role of the cannabidiol system in an animal model of ischemia/reperfusion kidney injury.

Rev Bras Ter Intensiva 2015 Oct-Dec;27(4):383-9

Laboratório de Fisiopatologia Experimental, Programa de Graduação em Ciências da Saúde, Unidade de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil.

Objective: This work aimed to investigate the effects of the administration of cannabidiol in a kidney ischemia/reperfusion animal model.

Methods: Kidney injury was induced by 45 minutes of renal ischemia followed by reperfusion. Cannabidiol (5mg/kg) was administered immediately after reperfusion.

Results: Ischemia/reperfusion increased the IL-1 and TNF levels, and these levels were attenuated by cannabidiol treatment. Additionally, cannabidiol was able to decrease lipid and protein oxidative damage, but not the nitrite/nitrate levels. Kidney injury after ischemia/reperfusion seemed to be independent of the cannabidiol receptor 1 and cannabidiol receptor 2 (CB1 and CB2) expression levels, as there was no significant increase in these receptors after reperfusion.

Conclusion: The cannabidiol treatment had a protective effect against inflammation and oxidative damage in the kidney ischemia/reperfusion model. These effects seemed to be independent of CB1/CB2 receptor activation.
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http://dx.doi.org/10.5935/0103-507X.20150064DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4738825PMC
December 2016

Reprint of "Caffeine protects against memory loss induced by high and non-anxiolytic dose of cannabidiol in adult zebrafish (Danio rerio)".

Pharmacol Biochem Behav 2015 Dec 18;139 Pt B:134-40. Epub 2015 Nov 18.

Laboratório de Neuroquímica e Psicofarmacologia, Departamento de Biologia Celular e Molecular, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul, Avenida Ipiranga, 6681, Caixa Postal 1429, 90619-900 Porto Alegre, RS, Brazil; Instituto Nacional de Ciência e Tecnologia Translacional em Medicina (INCT-TM), 90035-003 Porto Alegre, RS, Brazil. Electronic address:

Cannabidiol (CBD) has been investigated in a wide spectrum of clinical approaches due to its psychopharmacological properties. CBD has low affinity for cannabinoid neuroreceptors and agonistic properties to 5-HT receptors. An interaction between cannabinoid and purinergic receptor systems has been proposed. The purpose of this study is to evaluate CBD properties on memory behavioral and locomotor parameters and the effects of pre-treatment of adenosine receptor blockers on CBD impacts on memory using adult zebrafish. CBD (0.1, 0.5, 5, and 10mg/kg) was tested in the avoidance inhibitory paradigm and anxiety task. We analyzed the effect of a long-term caffeine pre-treatment (~20mg/L - four months). Also, acute block of adenosine receptors was performed in co-administration with CBD exposure in the memory assessment. CBD promoted an inverted U-shaped dose-response curve in the anxiety task; in the memory assessment, CBD in the dose of 5mg/Kg promoted the strongest effects without interfering with social and aggressive behavior. Caffeine treatment was able to prevent CBD (5mg/kg) effects on memory when CBD was given after the training session. CBD effects on memory were partially prevented by co-treatment with a specific A2A adenosine receptor antagonist when given prior to or after the training session, while CBD effects after the training session were fully prevented by adenosine A1 receptor antagonist. These results indicated that zebrafish have responses to CBD anxiolytic properties that are comparable to other animal models, and high doses changed memory retention in a way dependent on adenosine.
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http://dx.doi.org/10.1016/j.pbb.2015.11.002DOI Listing
December 2015

Cannabidiol and Sodium Nitroprusside: Two Novel Neuromodulatory Pharmacological Interventions to Treat and Prevent Psychosis.

CNS Neurol Disord Drug Targets 2015 ;14(8):970-8

Hospital das Clinicas - Terceiro Andar; Av. Bandeirantes, 3900; RibeiraoPreto -Sao Paulo, CEP - 14049-900, Brazil.

Since most patients with schizophrenia do not respond properly to treatment, scientific effort has been driven to the development of new compounds acting on pharmacological targets beyond the dopaminergic system. Therefore, the aim is to review basic and clinical research findings from studies evaluating the effects of cannabidiol (CBD), an inhibitor of the reuptake and metabolism of anandamide and several other effects on nervous system, and sodium nitroprusside, a nitric oxide donor, on the prevention and treatment of psychosis. Animal and human research supports that CBD and sodium nitroprusside might be effective in the prevention and treatment of psychosis in general and especially in schizophrenia. The evidence available to date shows that CBD and sodium nitroprusside act in pathways associated with psychotic symptoms and that they may be important agents in the management of prodromal psychotic states and psychosis. This underscores the relevance of further research on the effects of these agents and others that mediate the activity of the cannabinoid system and of nitric oxide, as well as comparative studies of their antipsychotic effects and those of other antipsychotic drugs currently used to treat schizophrenia.
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http://dx.doi.org/10.2174/1871527314666150909113930DOI Listing
July 2016

Evaluation of Serum Cytokines Levels and the Role of Cannabidiol Treatment in Animal Model of Asthma.

Mediators Inflamm 2015 25;2015:538670. Epub 2015 May 25.

Laboratório de Fisiopatologia Experimental, Programa de Pós-Graduação em Ciências da Saúde, Universidade do Extremo Sul Catarinense, 88806000 Criciúma, SC, Brazil.

Asthma represents a public health problem and traditionally is classified as an atopic disease, where the allergen can induce clinical airway inflammation, bronchial hyperresponsiveness, and reversible obstruction of airways. Studies have demonstrated the presence of T-helper 2 lymphocytes in the lung of patients with asthma. These cells are involved in cytokine production that regulates immunoglobulin synthesis. Recognizing that T cell interaction with antigens/allergens is key to the development of inflammatory diseases, the aim of this study is to evaluate the anti-inflammatory potential of cannabidiol (CBD) in this setting. Asthma was induced in 8-week-old Wistar rats by ovalbumin (OVA). In the last 2 days of OVA challenge animals received CBD (5 mg/kg, i.p.) and were killed 24 hours after. The levels of IL-4, IL-5, IL-13, IL-6, IL-10, and TNF-α were determinate in the serum. CBD treatment was able to decrease the serum levels of all analyzed cytokines except for IL-10 levels. CBD seems to be a potential new drug to modulate inflammatory response in asthma.
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http://dx.doi.org/10.1155/2015/538670DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4458548PMC
May 2016

Caffeine protects against memory loss induced by high and non-anxiolytic dose of cannabidiol in adult zebrafish (Danio rerio).

Pharmacol Biochem Behav 2015 Aug 20;135:210-6. Epub 2015 Jun 20.

Laboratório de Neuroquímica e Psicofarmacologia, Departamento de Biologia Celular e Molecular, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul, Avenida Ipiranga, 6681, Caixa Postal 1429, 90619-900 Porto Alegre, RS, Brazil; Instituto Nacional de Ciência e Tecnologia Translacional em Medicina (INCT-TM), 90035-003 Porto Alegre, RS, Brazil. Electronic address:

Cannabidiol (CBD) has been investigated in a wide spectrum of clinical approaches due to its psychopharmacological properties. CBD has low affinity for cannabinoid neuroreceptors and agonistic properties to 5-HT receptors. An interaction between cannabinoid and purinergic receptor systems has been proposed. The purpose of this study is to evaluate CBD properties on memory behavioral and locomotor parameters and the effects of pre-treatment of adenosine receptor blockers on CBD impacts on memory using adult zebrafish. CBD (0.1, 0.5, 5, and 10mg/kg) was tested in the avoidance inhibitory paradigm and anxiety task. We analyzed the effect of a long-term caffeine pre-treatment (~20mg/L - four months). Also, acute block of adenosine receptors was performed in co-administration with CBD exposure in the memory assessment. CBD promoted an inverted U-shaped dose-response curve in the anxiety task; in the memory assessment, CBD in the dose of 5mg/Kg promoted the strongest effects without interfering with social and aggressive behavior. Caffeine treatment was able to prevent CBD (5mg/kg) effects on memory when CBD was given after the training session. CBD effects on memory were partially prevented by co-treatment with a specific A2A adenosine receptor antagonist when given prior to or after the training session, while CBD effects after the training session were fully prevented by adenosine A1 receptor antagonist. These results indicated that zebrafish have responses to CBD anxiolytic properties that are comparable to other animal models, and high doses changed memory retention in a way dependent on adenosine.
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http://dx.doi.org/10.1016/j.pbb.2015.06.008DOI Listing
August 2015

Dissociation between the panicolytic effect of cannabidiol microinjected into the substantia nigra, pars reticulata, and fear-induced antinociception elicited by bicuculline administration in deep layers of the superior colliculus: The role of CB1-cannabinoid receptor in the ventral mesencephalon.

Eur J Pharmacol 2015 Jul 2;758:153-63. Epub 2015 Apr 2.

Laboratory of Neuroanatomy and Neuropsychobiology, Department of Pharmacology, Ribeirão Preto School of Medicine of the University of São Paulo (FMRP-USP), Av Bandeirantes, 3900, Ribeirão Preto 14049-900, São Paulo, Brazil; Behavioural Neurosciences Institute (INeC), Av. do Café, 2450, Monte Alegre, Ribeirão Preto 14050-220, São Paulo, Brazil; Neurobiology of Emotions Research Centre (NAP-USP-NuPNE), Ribeirão Preto School of Medicine of the University of São Paulo (FMRP-USP), Av. dos Bandeirantes, 3900, Ribeirão Preto, São Paulo 14049-900, São Paulo, Brazil. Electronic address:

Many studies suggest that the substantia nigra, pars reticulata (SNpr), a tegmental mesencephalic structure rich in γ-aminobutyric acid (GABA)- and cannabinoid receptor-containing neurons, is involved in the complex control of defensive responses through the neostriatum-nigral disinhibitory and nigro-tectal inhibitory GABAergic pathways during imminently dangerous situations. The aim of the present work was to investigate the role played by CB1-cannabinoid receptor of GABAergic pathways terminal boutons in the SNpr or of SNpr-endocannabinoid receptor-containing interneurons on the effect of intra-nigral microinjections of cannabidiol in the activity of nigro-tectal inhibitory pathways. GABAA receptor blockade in the deep layers of the superior colliculus (dlSC) elicited vigorous defensive behaviour. This explosive escape behaviour was followed by significant antinociception. Cannabidiol microinjection into the SNpr had a clear anti-aversive effect, decreasing the duration of defensive alertness, the frequency and duration of defensive immobility, and the frequency and duration of explosive escape behaviour, expressed by running and jumps, elicited by transitory GABAergic dysfunction in dlSC. However, the innate fear induced-antinociception was not significantly changed. The blockade of CB1 endocannabinoid receptor in the SNpr decreased the anti-aversive effect of canabidiol based on the frequency and duration of defensive immobility, the frequency of escape expressed by running, and both the frequency and duration of escape expressed by jumps. These findings suggest a CB1 mediated endocannabinoid signalling in cannabidiol modulation of panic-like defensive behaviour, but not of innate fear-induced antinociception evoked by GABAA receptor blockade with bicuculline microinjection into the superior colliculus, with a putative activity in nigro-collicular GABAergic pathways.
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http://dx.doi.org/10.1016/j.ejphar.2015.03.051DOI Listing
July 2015

Oxytocin does not improve performance of patients with schizophrenia and healthy volunteers in a facial emotion matching task.

Psychiatry Res 2014 Dec 9;220(1-2):125-8. Epub 2014 Aug 9.

Department of Neuroscience and Behavior of Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.

The neuropeptide oxytocin improves the performance in facial emotion recognition tests in healthy volunteers and in individuals with schizophrenia. Different paradigms are used in emotion recognition tasks, engaging different neurobiological bases. To date, the effects of oxytocin in facial emotion matching tasks have not been studied. The objective of this study was to evaluate the effects of intranasal oxytocin in a facial emotion matching task in patients with schizophrenia and healthy volunteers. Twenty patients and 20 healthy volunteers received 48 IU intranasal oxytocin and placebo in a double-blind, randomized, placebo-controlled, within subjects design. Fifty minutes after treatment, subjects completed a facial emotion matching task and three control tests. Oxytocin failed to improve facial affect processing, in contrast with previous results. Possible explanations are the fact that we used a facial emotion matching paradigm instead of emotion labeling tasks and a higher dose of oxytocin than the one used in most similar studies.
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http://dx.doi.org/10.1016/j.psychres.2014.07.082DOI Listing
December 2014

Human experimental anxiety: actual public speaking induces more intense physiological responses than simulated public speaking.

Braz J Psychiatry 2013 Jul-Sep;35(3):248-53

Universidade de São Paulo, Department of Neuroscience and Behavioral Science, School of Medicine, Ribeirão PretoSP, Brazil.

Objectives: a) To perform a systematic and meta-analytic review to verify whether the Simulated Public Speaking Task (SPST) leads to a greater increase in self-rated anxiety than in physiological correlates of anxiety; and b) to compare the results obtained with the SPST with an actual public speaking task involving healthy volunteers.

Methods: a) The PubMed and ISI Web of Knowledge databases were searched for studies involving the SPST prior to 2012. Eleven publications were eligible and provided data from 143 healthy volunteers for meta-analysis; b) 48 university students without somatic or psychiatric disorders were divided into three experimental groups of 16 subjects to undergo one of the following: SPST, real-world public speaking task (real-world), and control situation (control).

Results: The meta-analysis showed that the SPST induced a significant increase in the Visual Analogue Mood Scale (VAMS) anxiety factor, but no significant increases in systolic blood pressure or heart rate. The empirical study showed that the real-world public speaking task increased heart rate, systolic blood pressure and diastolic blood pressure significantly more than the control and SPST conditions.

Conclusions: These results suggest that real public speaking might be better than SPST in inducing experimental anxiety.
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http://dx.doi.org/10.1590/1516-4446-2012-0930DOI Listing
May 2014
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