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Passiflora incarnate extract attenuates neuronal loss and memory impairment in stressed rats 西番莲提取物能减轻应激大鼠的神经元损失和记忆损伤
IF 2.7 4区 医学 Q3 NEUROSCIENCES Pub Date : 2025-02-24 DOI: 10.1016/j.brainres.2025.149520
Mohammad Amin Dehghani , Gholam Hossein Meftahi , Elham Moghtadaei Khorasgani
The present study investigated the protective effects of hydroalcoholic Passiflora incarnate extract on memory, anxiety-like behaviors, inflammatory factors, and cell density in the brain following stress. This study randomly divided 40 adult Wistar rats into 5 groups: control, normal saline, stress, stress + Passiflora incarnata, and Passiflora incarnata groups. For 21 consecutive days, the stress group and the Passiflora incarnata + stress group were exposed to immobilizing stress for 2 h each day. The Passiflora incarnata and the stress + Passiflora incarnata groups were gavaged with Passiflora incarnata extract half an hour before stress for 21 days. One day after the last stress, the Barnes and elevated plus maze were used to measure learning, memory, and anxiety-like behavior, respectively. Additionally, the MDA (malondialdehyde), TNF-α, IL-1, and gamma-glutamyl transferase (GGT) factors in the serum, as well as the cell density in the hippocampus, amygdala, and prefrontal regions, were investigated. The results of the Barnes maze showed that immobility stress increases the number of errors and the distance traveled to reach the target hole. Administering Passiflora incarnata extract prior to stress led to fewer errors and a shorter distance covered to reach the target hole. The use of Passiflora incarnata before stress in the elevated plus maze reduced anxiety-like behaviours (less frequent entries into the open arm, reduced duration of time in the open arm) compared to the stress group. The stress group caused a significant enhance in MDA, TNF-α, and IL-1 and a decrease in GGT, while treatment with Passiflora incarnata significantly improved these factors than the stress group. The immobility stress caused a significant decrease in cell density in the hippocampus, amygdala, and prefrontal region, and treatment with Passiflora incarnata increased cell density in these areas than the stress animals. In conclusion, Passiflora incarnata improves learning and memory impairment, anxiety-like behaviors, inflammatory factors, and damage caused by stress in the hippocampus, amygdala, and prefrontal areas.
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引用次数: 0
High frequency exercise after human cranial bone-derived mesenchymal stem cells transplantation enhances motor functional recovery following traumatic brain injury in mice.
IF 2.7 4区 医学 Q3 NEUROSCIENCES Pub Date : 2025-02-20 DOI: 10.1016/j.brainres.2025.149527
Md Salimul Karim, Masataka Teranishi, Kei Nakagawa, Takafumi Mitsuhara, Tomoyuki Kurose

Traumatic brain injury (TBI) causes a neurological impairment of the central nervous system that may induce severe motor deficits. In this study, human cranial bone-derived mesenchymal stem cells (hcMSCs) were transplanted into a mouse TBI model, and the effects of differences in exercise frequency were examined as a rehabilitation approach to improve motor function after cell transplantation. Twenty-four hours after TBI induction, phosphate-buffered saline or hcMSCs were intravenously injected into mice that were divided into a non-exercise group, a low-frequency exercise group (LF Ex), and a high-frequency exercise group (HF Ex). Beam walking tests and rotarod tests were performed over time to assess motor function. Injured brain tissues were collected for mRNA and protein expression analysis on days 8 and 35 after TBI induction. On days 28 and 35 after TBI induction, significant associations were found between hcMSC transplantation (T) and exercise factors. Notably, the T + HF Ex group exhibited a significant improvement in motor function compared with the other groups. Moreover, we found that the mRNA and protein expression levels of growth associated protein 43 (GAP-43), hepatocyte growth factor (HGF), and nerve growth factor (NGF) were significantly higher in the T + HF Ex group than in other groups. Increased expression of GAP-43 enhances synaptic regeneration and promotes functional recovery. High expression of NGF accelerates neural differentiation, and HGF ensures the efficacy of hcMSCs. These data suggest that hcMSC transplantation combined with high-frequency exercise is a promising option for TBI treatment.

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引用次数: 0
Resting-state EEG alpha asymmetry predicts false belief understanding during early childhood: An exploratory longitudinal study.
IF 2.7 4区 医学 Q3 NEUROSCIENCES Pub Date : 2025-02-20 DOI: 10.1016/j.brainres.2025.149523
Shuting Li, Barbara C N Müller, Jörg Meinhardt, Beate Sodian

Theory of mind (ToM), the ability to attribute mental states to others, is fundamental to human socio-cognition. In child development, a full or explicit understanding of false beliefs (FB) and their impact on action emerges around the age of 4 years. There is evidence of functional specialization of right hemispheric activity related to FB processing in adults and children. However, it remains unclear whether this specialization is the cause or the consequence of ToM development. The present exploratory study investigates the longitudinal relationship of resting-state electroencephalogram (rsEEG) alpha asymmetry measured in infancy/toddlerhood and behavioral false belief understanding (FBU) at the age of 4 years. Employing a longitudinal design, Study 1 assessed rsEEG alpha asymmetry across frontal and parietal electrode sites (N = 43), implicit FBU at 34 months (N = 38), and explicit FBU at age 4 (N = 22). Study 2 is another independent longitudinal dataset that included rsEEG alpha asymmetry at 14 months (N = 37) and explicit FBU at age 4 (N = 32). We found that superior explicit FBU at age 4 was associated with greater right frontal activity at an earlier age, and better implicit FBU was cross-sectionally related to greater right parietal activity. Given the limited sample size, these results should be viewed as preliminary and warrant replication in future studies. Interpreted cautiously, these findings may suggest that rsEEG alpha asymmetry in frontal regions may serve as an early-appearing neural marker of children's later explicit FBU.

心智理论(ToM)是将心理状态归因于他人的能力,是人类社会认知的基础。在儿童的成长过程中,对虚假信念(FB)及其对行动的影响的全面或明确理解大约出现在 4 岁左右。有证据表明,成人和儿童的右半球活动与虚假信念处理有关,具有功能特异性。然而,这种特化是 ToM 发展的原因还是结果,目前仍不清楚。本探索性研究调查了婴幼儿时期测量的静息脑电图(rsEEG)α不对称性与 4 岁时行为错误信念理解(FBU)之间的纵向关系。研究 1 采用纵向设计,评估了额叶和顶叶电极部位的 rsEEG α 不对称性(43 人)、34 个月时的内隐 FBU(38 人)和 4 岁时的外显 FBU(22 人)。研究 2 是另一个独立的纵向数据集,包括 14 个月时的 rsEEG α 不对称(37 人)和 4 岁时的显性 FBU(32 人)。我们发现,4 岁时较好的显性 FBU 与较早时较强的右额叶活动有关,而较好的隐性 FBU 与较强的右顶叶活动横截面有关。由于样本量有限,这些结果应被视为初步结果,值得在今后的研究中加以重复。谨慎地解释这些发现可能表明,额叶区域的 rsEEG α 不对称可能是儿童日后显性 FBU 的早期神经标记。
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引用次数: 0
Modeling spatio-temporal patterns in intensive binary time series eye-tracking data using Generalized Additive Mixed Models.
IF 2.7 4区 医学 Q3 NEUROSCIENCES Pub Date : 2025-02-18 DOI: 10.1016/j.brainres.2025.149511
Sarah Brown-Schmidt, Sun-Joo Cho, Kimberly Fenn, Alison M Trude

The aim of this paper is to introduce and illustrate the use of Generalized Additive Mixed Models (GAMM) for analyzing intensive binary time-series eye-tracking data. The spatio-temporal GAMM was applied to intensive binary time-series eye-tracking data. In doing so, we reveal that both fixed condition effects, as well as previouslydocumented temporal contingencies in this type of data vary over time during speech perception. Further, spatial relationships between the point of fixation and the candidate referents on screen modulate the probability of an upcoming target fixation, and this pull (and push) on fixations changes over time as the speech is being perceived. This technique provides a way to not only account for the dominant autoregressive patterns typically seen in visual-world eye-tracking data, but does so in a way that allows modeling crossed random effects (by person and item, as typical in psycholinguistics datasets), and to model complex relationships between space and time that emerge in eye-tracking data. This new technique offers ways to ask, and answer new questions in the world of language use and processing.

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引用次数: 0
FusionNet: Dual input feature fusion network with ensemble based filter feature selection for enhanced brain tumor classification
IF 2.7 4区 医学 Q3 NEUROSCIENCES Pub Date : 2025-02-17 DOI: 10.1016/j.brainres.2025.149507
Akash Verma, Arun Kumar Yadav
Brain tumors pose a significant threat to human health, require a precise and quick diagnosis for effective treatment. However, achieving high diagnostic accuracy with traditional methods remains challenging due to the complex nature of brain tumors. Recent advances in deep learning have showed potential in automating brain tumor classification using brain MRI images, offering the potential to enhance diagnostic result. This paper present FusionNet, a novel approach that utilizing normal and segmented MRI images to achieve better classification accuracy. Segmented images are generated using a Dual Residual Blocks based pre-trained model. Secondly, the model uses attention based mechanism and ensemble feature selection to prioritize the relevant features for improving the classification performance. Thirdly, proposed model incorporates the feature fusion of both the images (normal and segmented) to increase the selected feature for better classification. The proposed model achieved high accuracy across multiple datasets, with an accuracy of 99.62%, 99.54%, 99.39%, and 99.57% on the Figshare, Kaggle, Sartaj, combined dataset respectively. The proposed model demonstrates notable improvements in performance on both datasets. It achieves higher accuracy, precision, recall, and F1-score compared to existing models on the both datasets. The proposed FusionNet demonstrates significant improvements in brain tumor classification performance. The utility of this study lies in its contribution to the scientific community as a robust, efficient tool that advances brain tumor classification, supporting medical professionals in achieving superior diagnostic outcomes.
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引用次数: 0
Comparison of actions of ketamine and telazol on cochlear function in a rodent model of noise-induced hearing loss
IF 2.7 4区 医学 Q3 NEUROSCIENCES Pub Date : 2025-02-15 DOI: 10.1016/j.brainres.2025.149496
Kayla Minesinger , Maria Fernanda Yepes , Suhrud M. Rajguru
Research has shown that anesthesia used in rodent models studying trauma-related changes in the peripheral auditory system can impact the results of standard functional tests like the auditory brainstem response (ABR). The anesthetic agents may also confound the effects of potential therapeutics under evaluation in the preclinical models. Ketamine, a N-methyl-D-aspartate (NMDA) receptor antagonist, is a commonly employed anesthetic in rodent models. Studies have shown that ketamine, unlike other anesthetics, exerts minimal effects on ABR measurements. Tiletamine, a compound chemically akin to ketamine, is also an NMDA antagonist. Tiletamine combined with zolazepam (Telazol) may be a substitute for ketamine given its less severe side-effects and long-acting capacity. In this study, we serially compare cochlear function in rats exposed to hazardous noise to induce noise-induced hearing loss (NIHL) under the effects of either ketamine or telazol. Awake male Brown Norway rats were exposed to octave band noise (4–8 kHz) at 110 dB SPL for 1 h. Cochlear function was assessed over multiple time points using either intramuscular injection of ketamine (44 mg/kg) and xylazine (5 mg/kg) or intraperitoneally injected telazol (20 mg/kg) and xylazine (5 mg/kg). Changes in ABR threshold, latency, and amplitude were compared to baseline (pre-NIHL) over 28 days. Functional results demonstrated that both ketamine- and telazol-anesthetized animals experience permanent changes in thresholds following noise. While both amplitude and latency were affected by noise, there were no significant differences in the changes between ketamine and telazol groups. Our findings suggest that telazol behaves similarly to ketamine and could be an alternative in rodent model experiments for the evaluations of hearing sensitivity following noise trauma.
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引用次数: 0
Rhythmic deep-brain magnetic stimulation promotes angiogenesis and inhibits apoptosis by regulating the JAK2/STAT3 pathway in rats with superior sagittal sinus thrombosis
IF 2.7 4区 医学 Q3 NEUROSCIENCES Pub Date : 2025-02-15 DOI: 10.1016/j.brainres.2025.149509
Min Li , Jiahao Chen , Ran Meng , Xunming Ji
The purpose of this study is to investigate the therapeutic value of rhythmic deep-brain magnetic stimulation (rDMS) and its potential mechanisms in Sprague-Dawley rats with superior sagittal sinus thrombosis (SSST). Rats were randomly allocated into Sham, SSST, SSST + rDMS and SSST + rDMS + AG490 group (N = 27 each). After 2 weeks of rDMS treatment, the motor function of rats was assessed using the open field, rotarod, and beam balance tests. Triphenyltetrazolium chloride (TTC) staining was used to determine the infarct volume. Magnetic resonance venography (MRV) and hematoxylin and eosin (H&E) staining were used to assess the recanalization of the superior sagittal sinus. The protein expression levels of JAK2, p-JAK2, STAT3, p-STAT3, VEGF-A, Bcl-2, Bax, and caspase-3 was analyzed by Western blotting. The mRNA expression of VEGF-A was determined by quantitative real-time polymerase chain reaction (qPCR). Immunofluorescence staining was used to evaluate the protein expression of the capillary marker CD31. Rats with SSST exhibited motor dysfunction compared to sham rats. rDMS therapy alleviated the motor dysfunction as indicated by increased move distance (p < 0.001), move time (p = 0.046) and latency to fall (p = 0.042), and decreased balance latency (p = 0.024) in rats with SSST. Remarkably, rDMS treatment reduced the infarction volume (p = 0.010) in the parasagittal sinus cortex without promoting recanalization of the superior sagittal sinus. rDMS therapy increased the expression of p-JAK2 (p = 0.006) and p-STAT3 (p < 0.001) in rats with SSST, but had no effect on the expression of JAK2 and STAT3. rDMS therapy also increased the mRNA and protein expression of VEGF-A (p = 0.002; p = 0.030) and the density of CD31-positive capillaries (p < 0.001) in rats with SSST. In addition, rDMS treatment increased the expression of Bcl-2 (p < 0.001) and decreased the expression of Caspase-3 (p < 0.001) and Bax (p < 0.001) in rats with SSST. AG490, an inhibitor of JAK2, eliminated the therapeutic effect of rDMS. In conclusion, rDMS therapy improves motor dysfunction, reduces parasagittal infarct, promotes angiogenesis, and suppresses apoptosis in rats with SSST by activating the JAK2/STAT3 signaling pathway.
{"title":"Rhythmic deep-brain magnetic stimulation promotes angiogenesis and inhibits apoptosis by regulating the JAK2/STAT3 pathway in rats with superior sagittal sinus thrombosis","authors":"Min Li ,&nbsp;Jiahao Chen ,&nbsp;Ran Meng ,&nbsp;Xunming Ji","doi":"10.1016/j.brainres.2025.149509","DOIUrl":"10.1016/j.brainres.2025.149509","url":null,"abstract":"<div><div>The purpose of this study is to investigate the therapeutic value of rhythmic deep-brain magnetic stimulation (rDMS) and its potential mechanisms in Sprague-Dawley rats with superior sagittal sinus thrombosis (SSST). Rats were randomly allocated into Sham, SSST, SSST + rDMS and SSST + rDMS + AG490 group (N = 27 each). After 2 weeks of rDMS treatment, the motor function of rats was assessed using the open field, rotarod, and beam balance tests. Triphenyltetrazolium chloride (TTC) staining was used to determine the infarct volume. Magnetic resonance venography (MRV) and hematoxylin and eosin (H&amp;E) staining were used to assess the recanalization of the superior sagittal sinus. The protein expression levels of JAK2, p-JAK2, STAT3, p-STAT3, VEGF-A, Bcl-2, Bax, and caspase-3 was analyzed by Western blotting. The mRNA expression of VEGF-A was determined by quantitative real-time polymerase chain reaction (qPCR). Immunofluorescence staining was used to evaluate the protein expression of the capillary marker CD31. Rats with SSST exhibited motor dysfunction compared to sham rats. rDMS therapy alleviated the motor dysfunction as indicated by increased move distance (p &lt; 0.001), move time (p = 0.046) and latency to fall (p = 0.042), and decreased balance latency (p = 0.024) in rats with SSST. Remarkably, rDMS treatment reduced the infarction volume (p = 0.010) in the parasagittal sinus cortex without promoting recanalization of the superior sagittal sinus. rDMS therapy increased the expression of p-JAK2 (p = 0.006) and p-STAT3 (p &lt; 0.001) in rats with SSST, but had no effect on the expression of JAK2 and STAT3. rDMS therapy also increased the mRNA and protein expression of VEGF-A (p = 0.002; p = 0.030) and the density of CD31-positive capillaries (p &lt; 0.001) in rats with SSST. In addition, rDMS treatment increased the expression of Bcl-2 (p &lt; 0.001) and decreased the expression of Caspase-3 (p &lt; 0.001) and Bax (p &lt; 0.001) in rats with SSST. AG490, an inhibitor of JAK2, eliminated the therapeutic effect of rDMS. In conclusion, rDMS therapy improves motor dysfunction, reduces parasagittal infarct, promotes angiogenesis, and suppresses apoptosis in rats with SSST by activating the JAK2/STAT3 signaling pathway.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1852 ","pages":"Article 149509"},"PeriodicalIF":2.7,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143432619","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}
引用次数: 0
Outlook of SNCA (α-synuclein) transgenic fly models in delineating the sequel of mitochondrial dysfunction in Parkinson’s disease
IF 2.7 4区 医学 Q3 NEUROSCIENCES Pub Date : 2025-02-13 DOI: 10.1016/j.brainres.2025.149505
Jennifer Sally Samson , Kalyanaraman Rajagopal , Venkatachalam Deepa Parvathi
Parkinson’s disease (PD) is a progressive neurodegenerative disorder associated with mechanisms that results in loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) region of the brain. Being a complex heterogeneous disorder, there is a requisite in discovering the underlying molecular signatures that could potentially help in resolving challenges associated with diagnosis as well as therapeutic management. SNCA gene that encodes for the protein α-synuclein is widely known for its indispensable role in aggravating the progression of sporadic and familial PD, upon mutations. Likewise, mitochondrial dysfunction is inferred to be playing a central role in both forms of PD. Observations from experimental models and human PD cases displayed strong evidence for disruption of mitochondrial dynamics, inhibition of mitochondrial complex I protein’s function and elevation in reactive oxygen species (ROS) by the toxic aggregation of α-synuclein. Further, recent studies have raised the possibility of an underlying relationship, where the α-synuclein toxicity is exacerbated by the mutant mitochondrial complex proteins and vice-versa. In this review, we provide an overview of mechanisms influencing α-synuclein-related neurodegeneration, particularly, emphasizing the role of SNCA (α-synuclein) gene in leading to altered mitochondrial biogenesis during PD. We have described how transgenic Drosophila models were reliable at recapitulating some of the essential characteristics of PD. In addition, we highlight the capability of utilizing transgenic fly models in deciphering the altered α-synuclein toxicity and mitochondrial dysfunction, as induced by defects in the mitochondrial DNA.
{"title":"Outlook of SNCA (α-synuclein) transgenic fly models in delineating the sequel of mitochondrial dysfunction in Parkinson’s disease","authors":"Jennifer Sally Samson ,&nbsp;Kalyanaraman Rajagopal ,&nbsp;Venkatachalam Deepa Parvathi","doi":"10.1016/j.brainres.2025.149505","DOIUrl":"10.1016/j.brainres.2025.149505","url":null,"abstract":"<div><div>Parkinson’s disease (PD) is a progressive neurodegenerative disorder associated with mechanisms that results in loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) region of the brain. Being a complex heterogeneous disorder, there is a requisite in discovering the underlying molecular signatures that could potentially help in resolving challenges associated with diagnosis as well as therapeutic management. <em>SNCA</em> gene that encodes for the protein α-synuclein is widely known for its indispensable role in aggravating the progression of sporadic and familial PD, upon mutations. Likewise, mitochondrial dysfunction is inferred to be playing a central role in both forms of PD. Observations from experimental models and human PD cases displayed strong evidence for disruption of mitochondrial dynamics, inhibition of mitochondrial complex I protein’s function and elevation in reactive oxygen species (ROS) by the toxic aggregation of α-synuclein. Further, recent studies have raised the possibility of an underlying relationship, where the α-synuclein toxicity is exacerbated by the mutant mitochondrial complex proteins and vice-versa. In this review, we provide an overview of mechanisms influencing α-synuclein-related neurodegeneration, particularly, emphasizing the role of <em>SNCA</em> (α-synuclein) gene in leading to altered mitochondrial biogenesis during PD. We have described how transgenic <em>Drosophila</em> models were reliable at recapitulating some of the essential characteristics of PD. In addition, we highlight the capability of utilizing transgenic fly models in deciphering the altered α-synuclein toxicity and mitochondrial dysfunction, as induced by defects in the mitochondrial DNA.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1852 ","pages":"Article 149505"},"PeriodicalIF":2.7,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143422347","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}
引用次数: 0
Habituation to novel stimuli alters hippocampal plasticity associated with morphine tolerance in male Wistar rats.
IF 2.7 4区 医学 Q3 NEUROSCIENCES Pub Date : 2025-02-13 DOI: 10.1016/j.brainres.2025.149508
Ghazaleh Ghamkharinejad, Francesca Mottarlini, Zohreh Tavassoli, Lucia Caffino, Fabio Fumagalli, Judith R Homberg, Yaghoub Fathollahi

Chronic morphine exposure affects neuroplasticity in the hippocampus, a key area for learning and memory. Since, novelty exploration influence rodent hippocampal plasticity, the aim of this study was to investigate the effects of habituation to novel contexts and odors on hippocampal plasticity in morphine-tolerant rats. For this purpose, neurogenesis markers, dendritic spine density and mRNA levels for various genes encoding neurotrophic factors were evaluated in the hippocampus tissue (ventral, vH vs. dorsal, dH) of male rats. Habituation to the new environment was established using animal models of morphine tolerance. Following multiple exposures to a novel context (open field habituation, OFH) or a series of novel odors (odor habituation, OH), markers (Ki67 or DCX) associated with neurogenesis were found to be lower in the morphine-tolerant rats that underwent habituation than the non-habituated morphine-tolerant rats, with specific regions (dH, vH), being differently influenced by specific type of habituation (OFH, OH, respectively). Further results showed subregion and habituation specific effects on the number of dendritic spines per spine type or levels of neurotropic factors including BDNF and TrkB mRNA levels in the dH and vH in morphine-tolerant rats that underwent habituation as compared to the non-habituated morphine-tolerant rats. We provide new evidence that habituation to novel contexts and novel odors appears to affect hippocampal plasticity in morphine-tolerant rats and that pro-plasticity molecules appear to mediate habituation effects on morphine tolerance plasticity.

{"title":"Habituation to novel stimuli alters hippocampal plasticity associated with morphine tolerance in male Wistar rats.","authors":"Ghazaleh Ghamkharinejad, Francesca Mottarlini, Zohreh Tavassoli, Lucia Caffino, Fabio Fumagalli, Judith R Homberg, Yaghoub Fathollahi","doi":"10.1016/j.brainres.2025.149508","DOIUrl":"https://doi.org/10.1016/j.brainres.2025.149508","url":null,"abstract":"<p><p>Chronic morphine exposure affects neuroplasticity in the hippocampus, a key area for learning and memory. Since, novelty exploration influence rodent hippocampal plasticity, the aim of this study was to investigate the effects of habituation to novel contexts and odors on hippocampal plasticity in morphine-tolerant rats. For this purpose, neurogenesis markers, dendritic spine density and mRNA levels for various genes encoding neurotrophic factors were evaluated in the hippocampus tissue (ventral, vH vs. dorsal, dH) of male rats. Habituation to the new environment was established using animal models of morphine tolerance. Following multiple exposures to a novel context (open field habituation, OFH) or a series of novel odors (odor habituation, OH), markers (Ki67 or DCX) associated with neurogenesis were found to be lower in the morphine-tolerant rats that underwent habituation than the non-habituated morphine-tolerant rats, with specific regions (dH, vH), being differently influenced by specific type of habituation (OFH, OH, respectively). Further results showed subregion and habituation specific effects on the number of dendritic spines per spine type or levels of neurotropic factors including BDNF and TrkB mRNA levels in the dH and vH in morphine-tolerant rats that underwent habituation as compared to the non-habituated morphine-tolerant rats. We provide new evidence that habituation to novel contexts and novel odors appears to affect hippocampal plasticity in morphine-tolerant rats and that pro-plasticity molecules appear to mediate habituation effects on morphine tolerance plasticity.</p>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":" ","pages":"149508"},"PeriodicalIF":2.7,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424588","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}
引用次数: 0
Olfactory deprivation promotes amyloid β deposition in a mouse model of Alzheimer’s disease
IF 2.7 4区 医学 Q3 NEUROSCIENCES Pub Date : 2025-02-07 DOI: 10.1016/j.brainres.2025.149500
Xirun Zhao , Qing Zhou , Huan Zhang , Munenori Ono , Takafumi Furuyama , Ryo Yamamoto , Tomoko Ishikura , Masami Kumai , Yukari Nakamura , Hideaki Shiga , Takaki Miwa , Nobuo Kato
Olfactory dysfunction is regarded as an early marker for Alzheimer’s disease (AD). Slowly progressing AD pathology is interpreted to impair cognition and olfactory sensation independently, while olfactory deficits emerge earlier. The present experiments tested the possibility that olfactory impairment may worsen cognition or AD pathology using 3xTg AD model mice with olfactory bulbectomy (OBX). In open-field tests, OBX was shown to increase anxiety-like behavior in both wild-type (WT) and AD model mice, and hyperactivity was induced in WT mice only. Spatial memory, assessed by the Morris water maze (MWM) test, was impaired in WT but not AD mice. Object memory, assessed by the novel object recognition test, was not changed by OBX either in WT or AD mice. Densitometry of Aβ plaques stained with 6E10 and anti-Aβ42 antibodies was carried out in sections containing the hippocampal formation obtained from AD mice aged 12 and 18 months. The plaque area was larger in the OBX than in the sham group at 12 months. At 18 months, there was also difference in the plaque area. Given that Aβ plaques emerge in 3xTg mice relatively later (>9 months of age) than in other models, OBX in 3xTg mice appears to exacerbate Aβ pathology at the early phase of Aβ emergence, implying a causative link of smell loss to AD pathogenesis. The accelerated Aβ plaque formation by OBX was accompanied by microglial activation. Early intervention to smell loss may be beneficial for AD control.
{"title":"Olfactory deprivation promotes amyloid β deposition in a mouse model of Alzheimer’s disease","authors":"Xirun Zhao ,&nbsp;Qing Zhou ,&nbsp;Huan Zhang ,&nbsp;Munenori Ono ,&nbsp;Takafumi Furuyama ,&nbsp;Ryo Yamamoto ,&nbsp;Tomoko Ishikura ,&nbsp;Masami Kumai ,&nbsp;Yukari Nakamura ,&nbsp;Hideaki Shiga ,&nbsp;Takaki Miwa ,&nbsp;Nobuo Kato","doi":"10.1016/j.brainres.2025.149500","DOIUrl":"10.1016/j.brainres.2025.149500","url":null,"abstract":"<div><div>Olfactory dysfunction is regarded as an early marker for Alzheimer’s disease (AD). Slowly progressing AD pathology is interpreted to impair cognition and olfactory sensation independently, while olfactory deficits emerge earlier. The present experiments tested the possibility that olfactory impairment may worsen cognition or AD pathology using 3xTg AD model mice with olfactory bulbectomy (OBX). In open-field tests, OBX was shown to increase anxiety-like behavior in both wild-type (WT) and AD model mice, and hyperactivity was induced in WT mice only. Spatial memory, assessed by the Morris water maze (MWM) test, was impaired in WT but not AD mice. Object memory, assessed by the novel object recognition test, was not changed by OBX either in WT or AD mice. Densitometry of Aβ plaques stained with 6E10 and anti-Aβ42 antibodies was carried out in sections containing the hippocampal formation obtained from AD mice aged 12 and 18 months. The plaque area was larger in the OBX than in the sham group at 12 months. At 18 months, there was also difference in the plaque area. Given that Aβ plaques emerge in 3xTg mice relatively later (&gt;9 months of age) than in other models, OBX in 3xTg mice appears to exacerbate Aβ pathology at the early phase of Aβ emergence, implying a causative link of smell loss to AD pathogenesis. The accelerated Aβ plaque formation by OBX was accompanied by microglial activation. Early intervention to smell loss may be beneficial for AD control.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1851 ","pages":"Article 149500"},"PeriodicalIF":2.7,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143373776","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}
引用次数: 0
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Brain Research
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