Hatice Keser, Ozlem Bozkurt Girit, Selcen Aydin Abidin, Mehmet Dincer Bilgin, Ahmet Alver, İsmail Abidin
{"title":"Sensory‑motor performance and neurochemical effects in the cerebral cortex of brain‑derived neurotrophic factor heterozygous mice fed a high‑cholesterol diet.","authors":"Hatice Keser, Ozlem Bozkurt Girit, Selcen Aydin Abidin, Mehmet Dincer Bilgin, Ahmet Alver, İsmail Abidin","doi":"10.55782/ane-2023-001","DOIUrl":"https://doi.org/10.55782/ane-2023-001","url":null,"abstract":"<p><p>Reports suggest that a high‑cholesterol diet may induce neuroinflammation, oxidative stress, and neurodegeneration in brain tissue. Brain‑derived neurotrophic factor (BDNF) might play a role in protecting against changes induced by high cholesterol. We aimed to assess behavioral correlates and biochemical alterations in the motor and sensory cortices following a high‑cholesterol diet under normal and reduced BDNF concentrations. C57Bl/6 strain, wild‑type (WT) and BDNF heterozygous (+/‑) mice were used to reveal the effects of endogenous BDNF concentrations. We compared diet and genotype effects using four experimental groups: WT and BDNF heterozygous (+/‑) groups of mice were each fed a normal or high‑cholesterol diet for 16 weeks. The cylinder test and wire hanging test were performed to evaluate neuromuscular deficits and cortical sensory‑motor functions, respectively. In addition, neuroinflammation was assessed by tumor necrosis factor alpha and interleukin 6 levels measured in the somatosensory and motor areas. Additionally, MDA levels and SOD and CAT activity were evaluated as oxidative stress parameters. Results showed that a high‑cholesterol diet significantly impaired behavioral performance in the BDNF (+/‑) group. Diet did not change the levels of neuroinflammatory markers in any of the groups. However, MDA levels, an indicator of lipid peroxidation, were significantly higher in the high‑cholesterol‑fed BDNF (+/‑) mice. The results suggest that BDNF levels might be a critical factor in determining the extent of neuronal damage induced in the neocortex by a high‑cholesterol diet.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 1","pages":"1-9"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9384496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Differential local field potential oscillations in the dorsal striatum and locomotor activity induced by morphine and haloperidol in mice.","authors":"Chayaporn Reakkamnuan, Dania Cheaha, Nifareeda Samerphop, Jakkrit Nukitram, Ekkasit Kumarnsit","doi":"10.55782/ane-2023-013","DOIUrl":"https://doi.org/10.55782/ane-2023-013","url":null,"abstract":"<p><p>Dopamine (DA) depletion in the dorsal striatum underlies symptoms of basal ganglia pathologies, including Parkinson's disease (PD). Various drug compounds are used to enhance DA levels for therapeutic purposes. Understanding neural signaling and movement patterns associated with over‑ and under‑stimulation of the DA system is essential. This study investigated striatal local field potential (LFP) oscillation and locomotor activity following treatments with morphine, a DA release enhancer, and haloperidol (HAL), a DA D2 receptor (D2R) antagonist in mice. After intracranial electrodes were placed into the dorsal striatum of male Swiss albino ICR mice, intraperitoneal injections of morphine or HAL were administered. LFP signals and spontaneous motor activity were recorded simultaneously. The results showed that morphine significantly increased locomotor speed, both low (30.3-44.9 Hz) and high (60.5-95.7 Hz) LFP gamma powers and delta (1-4 Hz)‑gamma (30.3-95.7 Hz) phase‑amplitude coupling. In contrast, HAL treatments were found to significantly decrease these parameters. Moreover, regression analyses also revealed significant positive correlations between locomotor speed and high gamma powers. Taken together, these results demonstrate opposite LFP oscillations in the dorsal striatum with low and high gamma activities, and delta‑gamma couplings in response to a DA release enhancer and D2R antagonist by morphine and HAL, respectively. These parameters reflect fluctuation of neuronal activity in the dorsal striatum that might be useful for pathological research and drug discovery for PD.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 2","pages":"140-153"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9866989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Magda Helena Soratto Heitich Ferrazza, Débora Delwing-Dal Magro, Eloise Salamaia, Thales Ercole Guareschi, Luis Felipe Fernandes Erzinger, Thayná Patachini Maia, Cassiana Siebert, Tiago Marcon Dos Santos, Angela Terezinha de Souza Wyse, Gabriela Borgmann, Katherine Plautz, Daniela Delwing-de Lima
{"title":"Sub‑chronic administration of lead alters markers of oxidative stress, acetylcholinesterase and Na+K+‑ATPase activities in rat brain.","authors":"Magda Helena Soratto Heitich Ferrazza, Débora Delwing-Dal Magro, Eloise Salamaia, Thales Ercole Guareschi, Luis Felipe Fernandes Erzinger, Thayná Patachini Maia, Cassiana Siebert, Tiago Marcon Dos Santos, Angela Terezinha de Souza Wyse, Gabriela Borgmann, Katherine Plautz, Daniela Delwing-de Lima","doi":"10.55782/ane-2023-019","DOIUrl":"https://doi.org/10.55782/ane-2023-019","url":null,"abstract":"<p><p>This study investigated the effects of sub‑chronic administration of lead (Pb) acetate on thiobarbituric acid reactive substances (TBA‑RS), total sulfhydryl content, protein carbonyl content, antioxidant enzymes (superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GSH‑Px]), acetylcholinesterase (AChE), and Na+K+‑ATPase in the cerebral structures of rats. Male Wistar rats aged 60 days were treated with saline (control group) or Pb (treatment group), at various doses, by gavage, once a day for 35 days. The animals were sacrificed twelve hours after the last administration, and the cerebellum, hippocampus and cerebral cortex were removed. The results showed that Pb did not alter the evaluated oxidative stress parameters. Furthermore, Pb (64 and/or 128 mg/kg) altered SOD in the cerebellum, cerebral cortex and hippocampus. Pb (128 mg/kg) altered CAT in the cerebellum and cerebral cortex and GSH‑Px in the cerebral cortex. Also, Pb (64 mg/kg and 128 mg/kg) altered GSH‑Px in the cerebellum. Moreover, Pb (128 mg/kg) increased AChE in the hippocampus and decreased Na+K+‑ATPase in the cerebellum and hippocampus. In conclusion, sub‑chronic exposure to Pb (occupational and environmental intoxication) altered antioxidant enzymes, AChE, and Na+K+‑ATPase, contributing to cerebral dysfunction.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 2","pages":"216-225"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9875744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Josiane Mann, Valter Malaguido Clímaco, Seigo Nagashima, Daniel Wolff Stanczyk, Melania Santer, Ilton Silva, Luiz Fernando Pereira
{"title":"The enriched environment prevents degeneration of cerebellum Purkinje cells layer of rats.","authors":"Josiane Mann, Valter Malaguido Clímaco, Seigo Nagashima, Daniel Wolff Stanczyk, Melania Santer, Ilton Silva, Luiz Fernando Pereira","doi":"10.55782/ane-2023-015","DOIUrl":"https://doi.org/10.55782/ane-2023-015","url":null,"abstract":"<p><p>Neurodegeneration is characterized by loss of neurons causing changes that lead individuals to debilitating conditions; the most common of this condition is the Alzheimer's disease. It has been related that enriched environment (EE) induces experience‑dependent plasticity mechanisms, improving the performance of the animals in learning and memory tests. This study evaluated the effects of EE on histological parameters of the cerebellum in rats that received intracerebroventricular streptozotocin. In the standard environment, streptozotocin (STZ) promoted a significant increase between the gaps in the Purkinje layer of approximately 20%. On the other hand, in an enriched environment, the control result (EE) was similar to the result under streptozotocin effect (STZEE). In the standard environment (SE) group a 26% significant reduction in Purkinje cell density was observed under STZ presence. By analyzing the results of the density of Purkinje cells under the effect of streptozotocin in a standard environment (STZSE) against the density of the layer of Purkinje cells also under the effect of streptozotocin in an enriched environment (STZEE), a significant reduction of approximately 76% in density was observed of Purkinje cells in standard environment (STZSE), the mean number of Purkinje cells in enriched environments was not reduced, despite of STZ. According to the results, treatment with STZ and exposure to EE did not change the cerebellum general morphology/cytoarchitecture, hence was no significant difference in the layers thickness. These facts demonstrate that the enriched environment appears to protect the Purkinje cells layer of cerebellum from possible degeneration.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 2","pages":"171-178"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9875739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Consuelo Ventura-Mejía, Brandon H Nuñez-Ibarra, Laura Medina-Ceja
{"title":"An update of 4‑aminopyride as a useful model of generalized seizures for testing antiseizure drugs: in vitro and in vivo studies.","authors":"Consuelo Ventura-Mejía, Brandon H Nuñez-Ibarra, Laura Medina-Ceja","doi":"10.55782/ane-2023-007","DOIUrl":"https://doi.org/10.55782/ane-2023-007","url":null,"abstract":"<p><p>Aminopyridines constitute a drug family with the ability to enhance synaptic transmission. In particular, 4‑aminopyridine (4‑AP) has been used as a model of generalized seizures. 4‑AP is a K+ channel blocker, but its mechanism of action has not yet been fully described; some evidence has shown that it acts on the K+ channel types Kv1.1, Kv1.2, Kv1.4 and Kv4, which are localized in the axonic terminals of pyramidal neurons and interneurons. When 4‑AP blocks the K+ channels it triggers depolarization and prolongs the action potential in the neuron, which causes nonspecific neurotransmitter release. Among these neurotransmitters, glutamate is the principal excitatory neurotransmitter released in the hippocampus. Once glutamate is released, it reaches its ionotropic and metabotropic receptors continuing the neuronal depolarization chain and propagation of hyperexcitability. This brief review is focused on the use of 4‑AP as an effective seizure model for testing antiseizure drugs in relevant in vitro and in vivo studies.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 1","pages":"63-70"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9390476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Çiğdem Çantalı Öztürk, Serra Nur Ataoğlu, Ayşenur Arvas, Hamide Tokol, Havva Yaprak, Sümeyra Gürel, Hilal Nişva Levent, Dilek Akakın, Ali Şahin, Barış Çakır, Özgür Kasımay
{"title":"Weekend warrior exercise model for protection from chronic mild stress‑induced depression and ongoing cognitive impairment.","authors":"Çiğdem Çantalı Öztürk, Serra Nur Ataoğlu, Ayşenur Arvas, Hamide Tokol, Havva Yaprak, Sümeyra Gürel, Hilal Nişva Levent, Dilek Akakın, Ali Şahin, Barış Çakır, Özgür Kasımay","doi":"10.55782/ane-2023-002","DOIUrl":"https://doi.org/10.55782/ane-2023-002","url":null,"abstract":"<p><p>We aim to investigate the role and biological mechanisms of the weekend warrior (WW) exercise model on depression‑induced rats in comparison to the continuous exercise (CE) model. Sedentary, WW, and CE rats were subjected to chronic mild stress (CMS) procedure. CMS and exercise protocols continued for six weeks. Anhedonia was evaluated by sucrose preference, depressive behavior by Porsolt, cognitive functions by object recognition and passive avoidance, and anxiety levels by open field and elevated plus maze. After behavioral assessments, brain tissue myeloperoxidase (MPO) activity, malondialdehyde (MDA) levels, superoxide dismutase and catalase activities and GSH content, tumor necrosis factor‑α (TNF‑α), interleukin‑6 (IL‑6), IL‑1β, cortisol and brain‑derived neurotrophic factor levels and histological damage was assessed. CMS‑induced depression‑like outcomes with increases in anhedonia and decreases in cognitive measures that are rescued with both exercise models. The increased immobilization time in the Porsolt test was decreased with only WW. Exercise also normalized the suppression of antioxidant capacity and MPO increase induced by CMS in both exercise models. MDA levels also declined with both exercise models. Anxiety‑like behavior, cortisol levels, and histological damage scores were exacerbated with depression and improved by both exercise models. TNF‑α levels were depleted with both exercise models, and IL‑6 only with WW. WW was as protective as CE in CMS‑induced depression‑like cognitive and behavioral changes via suppressing inflammatory processes and improving antioxidant capacity.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 1","pages":"10-24"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9384490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Altered granulocyte count and erythrocyte measures in middle-aged, healthy carriers of APOE and PICALM risk genes for Alzheimer's disease.","authors":"Patrycja Dzianok, Ewa Kublik","doi":"10.55782/ane-2023-012","DOIUrl":"https://doi.org/10.55782/ane-2023-012","url":null,"abstract":"<p><p>APOE‑ε4 genotype (apolipoprotein E, epsilon 4) is the strongest genetic risk factor for Alzheimer's disease (AD). Despite years of research, it is still not known how it contributes to dementia development. APOE has been implicated in many AD pathology mechanisms, like Aβ clearance, brain metabolism, changes within microglia and other glial functions and inflammatory processes. In fact, immunological/inflammatory processes are recently discussed as an important factor in Alzheimer's development and granulocyte profiles changes are reported in patients. However, the exact link between the immune system and risk‑genes is unknown. In particular, it is not known whether and how they interact throughout the lifetime, before the disease onset. The aim of the study was to investigate the relationship between granulocyte count and the APOE/PICALM genes in healthy individuals with an increased genetic risk of AD. An exploratory analysis regarding other blood cells was also conducted. Blood samples were collected from 77 healthy middle‑aged (50-63 years old) participants, who were also asked to complete a health and life‑style questionnaires. Groups with different AD risk‑genes were compared. Differences in granulocyte profiles were found in healthy carriers of AD risk‑genes who had slightly elevated eosinophil levels as compared to non-risk carriers. An exploratory analysis showed some alteration in mean corpuscular hemoglobin content and concentration (MCH/MCHC) levels between risk‑carriers subgroups and non-risk carriers. No other differences in blood count or lipoprotein profile were found between healthy APOE/PICALM risk‑carriers and non-risk carriers. Longitudinal studies will reveal if and how those changes contribute to the development of AD pathology.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 2","pages":"127-139"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9866990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The role of neurofilament light chain in COVID‑19: A potential prognostic biomarker.","authors":"Arash Heidari, Nima Rezaei","doi":"10.55782/ane-2023-011","DOIUrl":"https://doi.org/10.55782/ane-2023-011","url":null,"abstract":"<p><p>Coronavirus disease 2019 (COVID‑19) is an unprecedented global health concern that was declared a pandemic in March 2020. Although primarily recognized by respiratory symptoms, growing evidence suggested the causal relationship between the infection with the disease agent, namely severe acute respiratory coronavirus 2 (SARS‑CoV‑2), and neurological manifestations. Given that the virus‑induced neurological involvement is associated with a poorer prognosis, persistent neurological sequelae, and a more severe form of the disease, efforts have been made to introduce a biomarker to recognize neurological abnormalities early in the course of the disease. Studies indicate a significantly higher concentration of neurofilament light chain (NFL) in cerebrospinal fluid or blood of COVID‑19 patients versus adjusted controls. It has also been reported that COVID‑19 patients suffering from the severe form of the disease had higher NFL levels than patients with mild to moderate forms. Moreover, elevated NFL levels at hospital admission in patients who did not present primarily with neurological expressions could predict the emergence of neurological symptoms during the hospital stay. The early recognition of neurological abnormalities using the NFL biomarker could lead to escalated medical care limiting the progression of SARS‑CoV‑2‑induced central nervous system pathogenesis, resulting in a significant amelioration in disease outcome. Nevertheless, NFL assessment integrated with the evaluation of other neurodegenerative biomarkers and factors indicating disease prognosis could provide a more comprehensive estimate of disease prognosis and the extent of neurological involvement.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 2","pages":"111-126"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9866991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Fasudil alleviates cerebral ischemia‑reperfusion injury by inhibiting inflammation and improving neurotrophic factor expression in rats.","authors":"Min-Fang Guo, Hui-Yu Zhang, Pei-Jun Zhang, Yi-Jin Zhao, Jing-Wen Yu, Tao Meng, Meng-Di Li, Na Li, Cun-Gen Ma, Li-Juan Song, Jie-Zhong Yu","doi":"10.55782/ane-2023-010","DOIUrl":"https://doi.org/10.55782/ane-2023-010","url":null,"abstract":"<p><p>The Rho kinase inhibitor fasudil exerts neuroprotective effects. We previously showed that fasudil can regulate M1/M2 microglia polarization and inhibit neuroinflammation. Here, the therapeutic effect of fasudil on cerebral ischemia‑reperfusion (I/R) injury was investigated using the middle cerebral artery occlusion and reperfusion (MCAO/R) model in Sprague‑Dawley rats. The effect of fasudil on the phenotype of microglia and neurotrophic factors in the I/R brain and its potential molecular mechanism was also explored. It was found that fasudil ameliorated neurological deficits, neuronal apoptosis, and inflammatory response in rats with cerebral I/R injury. Fasudil also promoted the polarization of microglia into the M2 phenotype, in turn promoting the secretion of neurotrophic factors. Furthermore, fasudil significantly inhibited the expression of TLR4 and NF‑κB. These findings suggest that fasudil could inhibit the neuroinflammatory response and reduce brain injury after I/R injury by regulating the shift of microglia from an inflammatory M1 phenotype to an anti‑inflammatory M2 phenotype, which may be related to the regulation of the TLR4/ NF‑κB signal pathway.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 1","pages":"97-110"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9378665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The effect of nicotine on antidepressant and anxiolytic responses induced by citalopram and citicoline in mice.","authors":"Fatemeh Khakpai, Mohammad-Reza Zarrindast","doi":"10.55782/ane-2023-017","DOIUrl":"https://doi.org/10.55782/ane-2023-017","url":null,"abstract":"<p><p>The effect of nicotine on both anxiety and depression has been broadly studied. Moreover, citalopram and citicoline play a role in the modulation of anxiety and depression. This study was designed to examine the effects of nicotine on the antidepressant and anxiolytic responses induced by citalopram and citicoline in mice. Anxiety‑ and depression‑related behaviors were assessed with the elevated plus maze and forced swim test, respectively. The results showed that subcutaneous administration of nicotine decreased open‑arm time (OAT) and open‑arm entries (OAE) but increased immobility time, suggesting anxiogenic‑like and depressive‑like effects. Intraperitoneal administration of citalopram increased OAT but decreased immobility time, indicating that citalopram induced anxiolytic‑like and antidepressant‑like responses. Additionally, an injection of citicoline increased OAE but decreased immobility time, revealing anxiolytic‑like and antidepressant‑like effects. Interestingly, the subthreshold dose of nicotine potentiated the citalopram and citicoline effects on OAT and immobility time, which revealed anxiolytic‑like and antidepressant‑like behaviors. Locomotor activity was not significantly changed by any doses of the drugs. In conclusion, these findings suggest that interactions between nicotine and citalopram or citicoline occur upon induction of anxiolytic and antidepressant responses in mice.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 2","pages":"194-202"},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9875742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}