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Brain Sciences
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New Insights into Neuropharmacology
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New Insights into Neuropharmacology

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neuropharmacology and Neuropathology".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 10390

Special Issue Editor

Dr. Tuane B. Sampaio

E-Mail Website
Guest Editor
Graduate Program in Pharmacology, Federal University of Santa Maria, Santa Maria, Brazil
Interests: pharmacology and pathophysiology of neurodegenerative diseases

Special Issue Information

Dear Colleagues,

Neurological disorders, such as Alzheimer’s disease, epilepsy, psychiatric disturbances, Parkinson’s disease, and multiple sclerosis, are extremely common and have an increasing prevalence. Most chronic neurological illnesses have complex etiology and pathophysiology that have yet to be fully determined. Additionally, pharmacological approaches display limited efficacy. In this context, the current Special Issue aims to present recent findings within the neuropharmacology field, from new mechanistic insights—such as target molecular and signaling pathways—to putative new therapeutic strategies. Thus, we invite investigators to contribute original research articles with emerging evidence of preclinical studies on modeling, in vitro, and animal models, as well as of clinical trials and reports. In addition, relevant comprehensive reviews will be accepted. We are particularly interested in articles covering the identification of new relevant targets and/or pharmacological approaches for neurological disorders.

Dr. Tuane B. Sampaio
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • pharmacological target
  • pharmacology
  • neurodegenerative diseases
  • psychiatric disorders
  • neuroscience

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Published Papers (6 papers)

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Research

14 pages, 2492 KiB  
Article
The Role of Ion Channels and Intracellular Signaling Cascades in the Inhibitory Action of WIN 55,212-2 upon Hyperexcitation
by Sergei A. Maiorov, Denis P. Laryushkin, Kristina A. Kritskaya, Valery P. Zinchenko, Sergei G. Gaidin and Artem M. Kosenkov
Brain Sci. 2024, 14(7), 668; https://doi.org/10.3390/brainsci14070668 - 29 Jun 2024
Viewed by 929
Abstract
Gi-coupled receptors, particularly cannabinoid receptors (CBRs), are considered perspective targets for treating brain pathologies, including epilepsy. However, the precise mechanism of the anticonvulsant effect of the CBR agonists remains unknown. We have found that WIN 55,212-2 (a CBR agonist) suppresses the synchronous oscillations [...] Read more.
Gi-coupled receptors, particularly cannabinoid receptors (CBRs), are considered perspective targets for treating brain pathologies, including epilepsy. However, the precise mechanism of the anticonvulsant effect of the CBR agonists remains unknown. We have found that WIN 55,212-2 (a CBR agonist) suppresses the synchronous oscillations of the intracellular concentration of Ca2+ ions (epileptiform activity) induced in the neurons of rat hippocampal neuron-glial cultures by bicuculline or NH4Cl. As we have demonstrated, the WIN 55,212-2 effect is mediated by CB1R receptors. The agonist suppresses Ca2+ inflow mediated by the voltage-gated calcium channels but does not alter the inflow mediated by NMDA, AMPA, and kainate receptors. We have also found that phospholipase C (PLC), protein kinase C (PKC), and G-protein-coupled inwardly rectifying K+ channels (GIRK channels) are involved in the molecular mechanism underlying the inhibitory action of CB1R activation against epileptiform activity. Thus, our results demonstrate that the antiepileptic action of CB1R agonists is mediated by different intracellular signaling cascades, including non-canonical PLC/PKC-associated pathways. Full article
(This article belongs to the Special Issue New Insights into Neuropharmacology)
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17 pages, 4249 KiB  
Article
Nanoencapsulated Curcumin: Enhanced Efficacy in Reversing Memory Loss in An Alzheimer Disease Model
by Anne Suély Pinto Savall, Jhuly Dorneles de Mello, Eduarda Monteiro Fidelis, Antonio Alvenir Comis-Neto, Maria Regina Nepomuceno, Camila de Oliveira Pacheco, Sandra Elisa Haas and Simone Pinton
Brain Sci. 2024, 14(2), 130; https://doi.org/10.3390/brainsci14020130 - 26 Jan 2024
Cited by 3 | Viewed by 1849
Abstract
Investigating new drugs or formulations that target Alzheimer disease (AD) is critical for advancing therapeutic interventions. Therefore, this study aimed to assess the effectiveness of nanoencapsulated curcumin (NC Curc) in alleviating memory impairment, oxidative stress, and neuroinflammation in a validated AD model. Male [...] Read more.
Investigating new drugs or formulations that target Alzheimer disease (AD) is critical for advancing therapeutic interventions. Therefore, this study aimed to assess the effectiveness of nanoencapsulated curcumin (NC Curc) in alleviating memory impairment, oxidative stress, and neuroinflammation in a validated AD model. Male Wistar rats were given bilateral intracerebroventricular injections of either saline or streptozotocin (STZ) (3 mg/3 µL/site) to establish the AD model (day 0). On day 22, daily oral administrations of curcumin (6 mg/kg), NC Curc (6 mg/kg), or a vehicle (unloaded NC) were initiated and continued for 14 days. NC Curc significantly reversed memory deficits in object recognition and inhibitory avoidance tests induced by STZ. Both formulations of curcumin attenuated elevated acetylcholinesterase activity caused by STZ. Importantly, NC Curc alone effectively mitigated STZ-induced oxidative stress. Additionally, NC Curc treatment normalized GFAP levels, suggesting a potential reduction in neuroinflammation in STZ-treated rats. Our findings indicate that NC Curc improves memory in an AD rat model, highlighting its enhanced therapeutic effects compared to unencapsulated curcumin. This research significantly contributes to understanding the therapeutic and neurorestorative potential of NC Curc in AD, particularly in reversing pathophysiological changes. Full article
(This article belongs to the Special Issue New Insights into Neuropharmacology)
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20 pages, 3232 KiB  
Article
Development and In Vivo Assessment of 4-Phenyltellanyl-7-chloroquinoline-loaded Polymeric Nanocapsules in Alzheimer’s Disease Models
by Ana Cláudia Funguetto-Ribeiro, Kelly Ayumi Nakama, Mikaela Peglow Pinz, Renata Leivas de Oliveira, Manoela do Sacramento, Flávia S. Oliveira Pereira, Simone Pinton, Ethel Antunes Wilhelm, Cristiane Luchese, Diego Alves, Daiana Silva Ávila and Sandra Elisa Haas
Brain Sci. 2023, 13(7), 999; https://doi.org/10.3390/brainsci13070999 - 28 Jun 2023
Cited by 2 | Viewed by 1558
Abstract
Alzheimer’s disease (AD) is the most common form of dementia in older people, and available treatments are palliative and produce undesirable side effects. The 4-phenyltellanyl-7-chloroquinoline (TQ) is an organochalcogen compound studied due to its pharmacological properties, particularly its antioxidant potential. However, TQ possesses [...] Read more.
Alzheimer’s disease (AD) is the most common form of dementia in older people, and available treatments are palliative and produce undesirable side effects. The 4-phenyltellanyl-7-chloroquinoline (TQ) is an organochalcogen compound studied due to its pharmacological properties, particularly its antioxidant potential. However, TQ possesses some drawbacks such as low aqueous solubility and high toxicity, thus warranting the search for tools that improve the safety and effectiveness of new compounds. Here, we developed and investigated the biological effects of TQ-loaded polymeric nanocapsules (NCTQ) in an AD model in transgenic Caenorhabditis elegans expressing human Aβ1–42 in their body–wall muscles and Swiss mice injected with Aβ25–35. The NCTQ displayed good physicochemical properties, including nanometer size and maximum encapsulation capacity. The treatment showed low toxicity, reduced Aβ peptide-induced paralysis, and activated an endoplasmic reticulum chaperone in the C. elegans model. The Aβ injection in mice caused memory impairment, which NCTQ mitigated by improving working, long-term, and aversive memory. Additionally, no changes in biochemical markers were evidenced in mice, demonstrating that there was no hepatotoxicity in the tested doses. Altogether, these findings provide insights into the neuroprotective effects of TQ and indicate that NCTQ is a promising candidate for AD treatment. Full article
(This article belongs to the Special Issue New Insights into Neuropharmacology)
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14 pages, 1397 KiB  
Article
Kinins’ Contribution to Postoperative Pain in an Experimental Animal Model and Its Implications
by Indiara Brusco, Cássia Regina Silva, Juliano Ferreira and Sara Marchesan Oliveira
Brain Sci. 2023, 13(6), 941; https://doi.org/10.3390/brainsci13060941 - 12 Jun 2023
Cited by 1 | Viewed by 1418
Abstract
Postoperative pain causes discomfort and disability, besides high medical costs. The search for better treatments for this pain is essential to improve recovery and reduce morbidity and risk of chronic postoperative pain. Kinins and their receptors contribute to different painful conditions and are [...] Read more.
Postoperative pain causes discomfort and disability, besides high medical costs. The search for better treatments for this pain is essential to improve recovery and reduce morbidity and risk of chronic postoperative pain. Kinins and their receptors contribute to different painful conditions and are among the main painful inflammatory mediators. We investigated the kinin’s role in a postoperative pain model in mice and reviewed data associating kinins with this painful condition. The postoperative pain model was induced by an incision in the mice’s paw’s skin and fascia with the underlying muscle’s elevation. Kinin levels were evaluated by enzyme immunoassays in sham or operated animals. Kinin’s role in surgical procedure-associated mechanical allodynia was investigated using systemic or local administration of antagonists of the kinin B1 receptor (DALBk or SSR240612) or B2 receptor (Icatibant or FR173657) and a kallikrein inhibitor (aprotinin). Kinin levels increased in mice’s serum and plantar tissue after the surgical procedure. All kinin B1 or B2 receptor antagonists and aprotinin reduced incision-induced mechanical allodynia. Although controversial, kinins contribute mainly to the initial phase of postoperative pain. The kallikrein–kinin system can be targeted to relieve this pain, but more investigations are necessary, especially associations with other pharmacologic targets. Full article
(This article belongs to the Special Issue New Insights into Neuropharmacology)
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13 pages, 1011 KiB  
Article
Intermittent Exposure to Aflatoxin B1 Did Not Affect Neurobehavioral Parameters and Biochemical Markers of Oxidative Stress
by Ana Claudia Monteiro Braga, Naieli Schiefelbein Souto, Fernanda Licker Cabral, Micheli Dassi, Érica Vanessa Furlan Rosa, Naiara dos Santos Guarda, Luiz Fernando Freire Royes, Michele Rechia Fighera, Rafael Noal Moresco, Mauro Schneider Oliveira, Marcel Henrique Marcondes Sari and Ana Flávia Furian
Brain Sci. 2023, 13(3), 386; https://doi.org/10.3390/brainsci13030386 - 23 Feb 2023
Cited by 4 | Viewed by 1984
Abstract
Aflatoxin B1 (AFB1) is the most common toxic mycotoxin that contaminates food. The treatment of its intoxication and the management of contaminations are a constant subject of health agendas worldwide. However, such efforts are not always enough to avoid population [...] Read more.
Aflatoxin B1 (AFB1) is the most common toxic mycotoxin that contaminates food. The treatment of its intoxication and the management of contaminations are a constant subject of health agendas worldwide. However, such efforts are not always enough to avoid population intoxication. Our objective was to investigate whether intermittent exposure to AFB1 would cause any impairment in biochemical and behavioral parameters, intending to simulate an irregular consumption. Male Wistar rats received four AFB1 administrations (250 μg/kg) by intragastric route separated by a 96-h interval. Toxicity was evaluated using behavioral tests (open field, object recognition, nest construction, marble burying, and splash test), biochemical markers of oxidative stress (cerebral cortex, hippocampus, liver, and kidneys), and plasma parameters of hepatic and renal functions. The intermittent exposure caused no modification in body weight gain as well as in organ weight. Both control and AFB1 groups presented similar profiles of behavior to all tests performed. Furthermore, AFB1 administrations alter neither antioxidant defenses nor markers of oxidation in all assayed tissues and in the plasma markers of hepatic and renal functions. Therefore, AFB1 intermittent administration did not cause its common damage from exposure to this toxicant, which must be avoided, and additional studies are required. Full article
(This article belongs to the Special Issue New Insights into Neuropharmacology)
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11 pages, 1052 KiB  
Article
Beneficial Effects of Rosmarinic Acid In Vitro and In Vivo Models of Epileptiform Activity Induced by Pilocarpine
by Bruna Neuberger, Fernanda Kulinski Mello, Michele Pereira Mallmann, Karine Gabriela da Costa Sobral, Michele Rechia Fighera, Luiz Fernando Freire Royes, Ana Flávia Furian, Tuane Bazanella Sampaio and Mauro Schneider Oliveira
Brain Sci. 2023, 13(2), 289; https://doi.org/10.3390/brainsci13020289 - 8 Feb 2023
Cited by 3 | Viewed by 1704
Abstract
Epilepsy is characterized by a predisposition to generate recurrent and spontaneous seizures; it affects millions of people worldwide. Status epilepticus (SE) is a severe type of seizure. In this context, screening potential treatments is very important. In the present study, we evaluated the [...] Read more.
Epilepsy is characterized by a predisposition to generate recurrent and spontaneous seizures; it affects millions of people worldwide. Status epilepticus (SE) is a severe type of seizure. In this context, screening potential treatments is very important. In the present study, we evaluated the beneficial effects of rosmarinic acid (RA) in pilocarpine-induced in vitro and in vivo models of epileptiform activity. Using an in vitro model in combined entorhinal cortex–hippocampal from Wistar rats we evaluated the effects of RA (10 µg/mL) on the lactate release and a glucose fluorescent analogue, 2-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose (2-NDBG), after incubation in high potassium aCSF supplemented or not with pilocarpine. In the in vivo model, SE was induced in male C57BL/6 mice by pilocarpine. At 1, 24, and 48 h after the end of SE mice were treated with RA (30 mg/kg/v.o.). We evaluated the neuromotor impairment by neuroscore tests and protein carbonyl levels in the cerebral cortex. In both in vitro models, RA was able to decrease the stimulated lactate release, while no effect on 2-NBDG uptake was found. RA has beneficial effects in models of epileptiform activity in vivo and in vitro. We found that RA treatment attenuated SE-induced neuromotor impairment at the 48 h timepoint. Moreover, post-SE treatment with RA decreased levels of protein carbonyls in the cerebral cortex of mice when compared to their vehicle-treated counterparts. Importantly, RA was effective in a model of SE which is relevant for the human condition. The present data add to the literature on the biological effects of RA, which could be a good candidate for add-on therapy in epilepsy. Full article
(This article belongs to the Special Issue New Insights into Neuropharmacology)
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