Roberto Andreatini
@ufpr.br
Pharmacology
Federal University of Paraná
RESEARCH INTERESTS
Behavioural pharmacology of anxiety and mood disorders
Scopus Publications
Scopus Publications
Thais C.S. Saldanha, William N. Sanchez, Paola Palombo, Fábio C. Cruz, José Carlos F. Galduróz, Rainer K.W. Schwarting, Roberto Andreatini, Claudio da Cunha, and José Augusto Pochapski
Elsevier BV
Nícolas Cordeiro, José Augusto Pochapski, William Sanchez Luna, Gabriel Baltazar, Rainer K. Schwarting, Roberto Andreatini, and Claudio Da Cunha
Elsevier BV
Anderson Gustavo Santos, Carlos Eduardo Kühl, Arisa Namie Higashijima, Luiz Kae Sales Kanazawa, Suzen Tortato Furtado de Souza, and Roberto Andreatini
Wiley
AbstractBackgroundAdenosinergic system has been implicated in the pathophysiology of bipolar disorder and drugs that affect adenosine neurotransmission have shown some efficacy as add‐on therapy in manic patients.ObjectiveThus, the aim of the present study was to screen adenosinergic drugs for antimanic‐like effect in methylphenidate (MPH)‐induced hyperlocomotion in mice.MethodsMale and female Swiss mice received a single allopurinol (50 and 200 mg/kg, ip), dipyridamole (20 mg/kg, ip), or inosine (50 mg/kg, ip) administration before an acute MPH challenge (5 mg/kg, sc). In experiments with repeated treatment, male mice received a daily administration of allopurinol (25 and 50 mg/kg, ip), dipyridamole (20 mg/kg, ip), or inosine (50 mg/kg, ip) for 14 days. Finally, pretreatment with aminophylline (2 mg/kg, sc), an unspecific adenosine receptor antagonist, was used to evaluate a putative adenosinergic mediation. Locomotor activity was measured in the automated activity chamber for 20 min.ResultsAcute and repeated dipyridamole reduced the increase in locomotor activity induced by MPH, while allopurinol and inosine had no effect. Aminophylline blocked the effect of dipyridamole in MPH‐induced hyperlocomotion.ConclusionThe present results suggest that dipyridamole may have an antimanic‐like effect through adenosine receptors and reinforce the proposal that the adenosine system may be an interesting target for new antimanic drugs.
Marcos K. Andrade, Leonardo C. Souza, Evellyn M. Azevedo, Ellen L. Bail, Silvio M. Zanata, Roberto Andreatini, and Maria A.B.F. Vital
Elsevier BV
Júlia Grigorini Mori Ayub, Cristina Luz Tosta, Breno Lopes Macedo, Tattyanna Fernandes Barreto, Lorena Martins Lopes, Maria Paula dos Santos Fracalossi, Roberto Andreatini, and Vanessa Beijamini
Elsevier BV
Shokouh Arjmand, Anne M. Landau, Bardia Varastehmoradi, Roberto Andreatini, Sâmia Joca, and Gregers Wegener
Springer Science and Business Media LLC
Marcela Pereira, Isadora P. Siba, Alexandra Acco, Diego Correia, Fernanda R. Lapa, Adair R.S. Santos, Ana P. Ruani, Moacir G. Pizzolatti, and Roberto Andreatini
Elsevier BV
William N. Sanchez, Jose A. Pochapski, Leticia F. Jessen, Marek Ellenberger, Rainer K. Schwarting, Donita L. Robinson, Roberto Andreatini, and Claudio Da Cunha
Wiley
BACKGROUND AND PURPOSE
Currently, no effective drug exists to treat cocaine use disorder, which affects millions of people worldwide. Benzodiazepines are potential therapeutic candidates, as microdialysis and voltammetry studies have shown that they can decrease dopamine concentrations in the nucleus accumbens of rodents and block the increase in dopamine levels and appetitive 50-kHz ultrasonic vocalizations (USV) induced by amphetamine in rats.
EXPERIMENTAL APPROACH
Here we tested whether administration of 2.5 mg·kg-1 diazepam (i.p.) in adult male rats could block the effects of 20 mg·kg-1 cocaine (i.p.) on electrically-evoked phasic dopamine signals in the nucleus accumbens measured by fast-scan cyclic voltammetry, as well as 50-kHz USV and locomotor activity.
KEY RESULTS
Cocaine injection increased evoked dopamine signals up to 3-fold within 5 min and the increase was significantly higher than baseline for at least 75 min. The injection of diazepam 5 min later attenuated the cocaine effect by nearly 50% and this attenuation was maintained for at least 40 min. Behaviorally, cocaine increased the number of appetitive 50-kHz calls by about 12-fold. Diazepam significantly blocked this effect for the entire duration of the session. Cocaine-treated rats also locomoted more compared to controls, while diazepam significantly attenuated cocaine-induced locomotion by up to 50%.
CONCLUSIONS AND IMPLICATION
These results suggest that the neurochemical and psychostimulant effects of cocaine can be mitigated by diazepam.
E. Araya, Eduardo C Carvalho, R. Andreatini, G. Zamponi and J. Chichorro
Trigeminal neuropathic pain has been modeled in rodents through the constriction of the infraorbital nerve (CCI-ION). Sensory alterations, including spontaneous pain, and thermal and mechanical hyperalgesia are well characterized, but there is a notable lack of evidence about the affective pain component in this model. Evaluation of the emotional component of pain in rats has been proposed as a way to optimize potential translational value of non-clinical studies. In rats, 22 and 50 kHz ultrasonic vocalizations (USVs) are considered well-established measures of negative and positive emotional states, respectively. Thus, this study tested the hypothesis that trigeminal neuropathic pain would result, in addition to the sensory alterations, in a decrease of 50 kHz USV, which may be related to altered function of brain areas involved in emotional pain processing. CCI-ION surgery was performed on 60-day-old male Wistar rats. 15 days after surgery, von Frey filaments were applied to detect mechanical hyperalgesia, and USV was recorded. At the same timepoint, systemic treatment with d,l-amphetamine (1 mg/kg) allowed investigation of the involvement of the dopaminergic system in USV emission. Finally, brain tissue was collected to assess the change in tyrosine hydroxylase (TH) expression in the nucleus accumbens (NAc) and c-Fos expression in brain areas involved in emotional pain processing, including the prefrontal cortex (PFC), amygdala, and NAc. The results showed that CCI-ION rats presented mechanical hyperalgesia and a significant reduction of environmental-induced 50 kHz USV. Amphetamine caused a marked increase in 50 kHz USV emission in CCI-ION rats. In addition, TH expression was lower in constricted animals and c-Fos analysis revealed an increase in neuronal activation. Taken together, these data indicate that CCI-ION causes a reduction in the emission of environmental-induced appetitive calls concomitantly with facial mechanical hyperalgesia and that both changes may be related to a reduction in the mesolimbic dopaminergic activity.
Inara Fernanda Misiuta Raupp-Barcaro, Isabella Caroline da Silva Dias, Erika Meyer, Jeane Cristina Fonseca Vieira, Giovana da Silva Pereira, Arthur Ribeiro Petkowicz, Rúbia Maria Weffort de Oliveira, and Roberto Andreatini
Elsevier BV
The present study investigated the pharmacological mechanisms of the antidepressant-like effects of amantadine in mice and their influence on hippocampal neurogenesis. To improve the translational validity of preclinical results, reproducibility across laboratories and replication in other animal models and species are crucial. Single amantadine administration at doses of 50 and 75 mg/kg resulted in antidepressant-like effects in mice in the tail suspension test (TST), reflected by an increase in immobility time. The effects of amantadine were seen at doses that did not alter locomotor activity. The tyrosine hydroxylase inhibitor α-methyl-ρ-tyrosine did not influence the anti-immobility effect of amantadine in the TST. Pretreatment with the α1 adrenergic receptor antagonist prazosin, β adrenergic receptor antagonist propranolol, α2 adrenergic receptor antagonist yohimbine, and α2 adrenergic receptor agonist clonidine did not alter the antidepressant-like effect of amantadine. However, amantadine's effect was blocked by the dopamine D2 receptor antagonist haloperidol and glutamate receptor agonist N-methyl-D-aspartate (NMDA). Repeated amantadine administration (50 mg/kg) also exerted an antidepressant-like effect, paralleled by an increase in hippocampal neurogenesis. The present results demonstrate that the antidepressant-like effects of amantadine may be mediated by its actions on D2 and NMDA receptors and likely involve hippocampal neurogenesis.
Luiz K.S. Kanazawa, Débora R. Radulski, Gabriela S. Pereira, Jos Prickaerts, Rainer K.W. Schwarting, Alexandra Acco, and Roberto Andreatini
Elsevier BV
In rats, lisdexamfetamine (LDX) induces manic-like behaviors such as hyperlocomotion and increases in appetitive 50-kHz ultrasonic vocalizations (USV), which are prevented by antimanic drugs, such as lithium. Inhibition of glycogen synthase kinase 3 beta (GSK3β) and antioxidant activity have been associated with antimanic effects. Thus, the aim of the present study was to evaluate the possible antimanic-like effects of andrographolide (ANDRO), a GSK3β inhibitor, on LDX-induced hyperlocomotion and 50-kHz USV increases. In addition, the effect of ANDRO was studied on LDX-induced oxidative stress. Lithium was used as positive control. Adult Wistar rats were treated with vehicle, lithium (100 mg/kg i.p., daily) or ANDRO (2 mg/kg i.p., 3 times a week) for 21 days. On the test day, either 10 mg/kg LDX or saline was administered i.p. and USV and locomotor activity were recorded. LDX administration increased the number of 50-kHz calls, as well as locomotor activity. Repeated treatment with lithium or ANDRO prevented these effects of LDX on 50-kHz USV and locomotor activity. LDX increased lipid peroxidation (LPO) levels in rat striatum and both lithium and ANDRO prevented this effect. LPO levels in rat striatum were positively correlated with increases in 50-kHz USV emission as well as hyperlocomotion. In conclusion, the present results indicate that ANDRO has antimanic-like effects, which may be mediated by its antioxidant properties.
Débora Dalla Vecchia, Luiz Kae Sales Kanazawa, Etiéli Wendler, Palloma de Almeida Soares Hocayen, Maria Aparecida Barbato Frazão Vital, Reinaldo Naoto Takahashi, Claudio Da Cunha, Edmar Miyoshi, and Roberto Andreatini
Elsevier BV
The most common features of Parkinson's disease (PD) are motor impairments, but many patients also present depression and memory impairment. Ketamine, an N-methyl-d-aspartate (NMDA) receptor antagonist, has been shown to be effective in patients with treatment-resistant major depression. Thus, the present study evaluated the action of ketamine on memory impairment and depressive-like behavior in an animal model of PD. Male Wistar rats received a bilateral infusion of 6 μg/side 6-hydroxydopamine (6-OHDA) into the substantia nigra pars compacta (SNc). Short-term memory was evaluated by the social recognition test, and depressive-like behaviors were evaluated by the sucrose preference and forced swimming tests (FST). Drug treatments included vehicle (i.p., once a week); ketamine (5, 10 and 15 mg/kg, i.p., once a week); and imipramine (20 mg/kg, i.p., daily). The treatments were administered 21 days after the SNc lesion and lasted for 28 days. The SNc lesion impaired short-term social memory, and all ketamine doses reversed the memory impairment and anhedonia (reduction of sucrose preference) induced by 6-OHDA. In the FST, 6-OHDA increased immobility, and all doses of ketamine and imipramine reversed this effect. The anti-immobility effect of ketamine was associated with an increase in swimming but not in climbing, suggesting a serotonergic effect. Ketamine and imipramine did not reverse the 6-OHDA-induced reduction in tyrosine hydroxylase immunohistochemistry in the SNc. In conclusion, ketamine reversed depressive-like behaviors and short-term memory impairment in rats with SNc bilateral lesions, indicating a promising profile for its use in PD patients.
Erika Ivanna Araya, Darciane Favero Baggio, Laura de Oliveira Koren, Roberto Andreatini, Rainer K. W. Schwarting, Gerald W. Zamponi, and Juliana Geremias Chichorro
Ovid Technologies (Wolters Kluwer Health)
Pedro Felipe Pereira Chaves, Palloma de Almeida S. Hocayen, Jorge Luiz Dallazen, Maria Fernanda de Paula Werner, Marcello Iacomini, Roberto Andreatini, and Lucimara M.C. Cordeiro
Elsevier BV
Thiago Rodrigues da Silva, Ana Maria Raymundi, Leandro José Bertoglio, Roberto Andreatini, and Cristina A. Stern
Springer Science and Business Media LLC
Thiago Rodrigues da Silva, Jeferson Machado Batista Sohn, Roberto Andreatini, and Cristina Aparecida Stern
Cold Spring Harbor Laboratory
Gabriela P. Silote, Sabrina F.S. de Oliveira, Deidiane E. Ribeiro, Mayara S. Machado, Roberto Andreatini, Sâmia R.L. Joca, and Vanessa Beijamini
Elsevier BV
Amanda Ribeiro Barroso, Erika Ivanna Araya, Camila Pasquini de Souza, Roberto Andreatini, and Juliana Geremias Chichorro
Elsevier BV
Meira Maria Forcelini Machado, Taysa Bervian Bassani, Valentín Cóppola-Segovia, Eric Luiz Rossa Moura, Silvio Marques Zanata, Roberto Andreatini, and Maria Aparecida Barbato Frazão Vital
Springer Science and Business Media LLC
Palloma de A.S. Hocayen, Etiele Wendler, Débora D. Vecchia, Luiz K.S. Kanazawa, Ana Carolina Issy, Elaine Del Bel, and Roberto Andreatini
Wiley
Etieli Wendler, Camila Pasquini de Souza, Ana Paula Segantine Dornellas, Luis Eduardo Santos, Sergio T. Ferreira, José Carlos Fernandes Galduróz, Markus Wöhr, Rainer K.W. Schwarting, and Roberto Andreatini
Elsevier BV
Cristina Luz Tosta, Gabriela Pandini Silote, Maria Paula Fracalossi, Ariandra Guerini Sartim, Roberto Andreatini, Sâmia Regiane Lourenço Joca, and Vanessa Beijamini
Elsevier BV
Moria D. Braun, Theresa M. Kisko, Débora Dalla Vecchia, Roberto Andreatini, Rainer K.W. Schwarting, and Markus Wöhr
Elsevier BV
Inara F. Raupp-Barcaro, Maria A. Vital, José C. Galduróz, and Roberto Andreatini
FapUNIFESP (SciELO)