IBRO Neuroscience Reports最新文献

{"title":"Neuroprotective effect of triptolide on neuronal inflammation in rats with mild brain injury","authors":"Zhanglu Fang ,&nbsp;Guanghong Shen ,&nbsp;Chengjian Lou ,&nbsp;Benson O.A. Botchway ,&nbsp;Qinglin Lu ,&nbsp;Qining Yang ,&nbsp;Nashwa Amin","doi":"10.1016/j.ibneur.2024.05.007","DOIUrl":"10.1016/j.ibneur.2024.05.007","url":null,"abstract":"<div><p>Concussions sustained while playing sports are a prominent cause of mild traumatic brain injury (mTBI), which is prevalent among teenagers. The early and intermediate stages of mild traumatic brain injury (mTBI) can be characterized by inflammation, neurodegeneration, and brain tissue edema, which can lead to permanent brain damage.</p><p>The present study investigated the therapeutic effects of triptolide in mTBI and brain damage recovery. After building mTBI model in male rat, triptolide administrated daily for 1 week in the treated group. On day 3 and day 7 of administration, hippocampus tissues were collected to evaluate inflammation and autophagy in the brain. The expressions of inflammatory factors interleukin (IL)-1β and tumor necrosis factor-alpha in serum were downregulated, while IL-10 expression was upregulated when compared with the mTBI group on day 3 and day 7. The expression of IL-10 on day 7 was higher than on day 3. Quantitative polymerase chain reaction (qPCR) analysis of inflammatory-related factors (i.e., <em>Il-1β</em> and nuclear factor-κB (<em>Nf-κb</em>), and western blot as well as immunofluorescence staining of autophagy-related proteins (i.e., LC3B) and aquaporin (AQP 4) showed lower expression on day 3 and day 7 in the triptolide-treated group. Moreover, NeuN immunostaining, and hematoxylin and eosin (HE) staining for hippocampus region revealed that the triptolide-treated group showed a decrease in damaged cells. Our findings emphasize the effectiveness of triptolide therapy after mild traumatic brain injury via modulating autophagy, attenuating inflammation and reduces edema by decreasing AQP 4 expression.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 13-21"},"PeriodicalIF":1.5,"publicationDate":"2024-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000514/pdfft?md5=500d812c31c058c7dc67a7709202ec39&pid=1-s2.0-S2667242124000514-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141139425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GLUT2 regulation of p38 MAPK isoform protein expression and p38 phosphorylation in male versus female rat hypothalamic primary astrocyte Cultures","authors":"Madhu Babu Pasula,&nbsp;Paul W. Sylvester,&nbsp;Karen P. Briski","doi":"10.1016/j.ibneur.2024.05.008","DOIUrl":"https://doi.org/10.1016/j.ibneur.2024.05.008","url":null,"abstract":"<div><p>Recent studies documented regulation of hypothalamic astrocyte mitogen-activated protein kinase (MAPK) pathways, including p38, by the plasma membrane glucose carrier/sensor glucose transporter-2 (GLUT2). Sex-specific GLUT2 control of p38 phosphorylation was observed, but effects on individual p38 family protein profiles were not investigated. Current research employed an established primary astrocyte culture model, gene knockdown tools, and selective primary antisera against p38-alpha, p38-beta, p38-gamma, and p38-delta isoforms to investigate whether GLUT2 governs expression of one or more of these variants in a glucose-dependent manner. Data show that GLUT2 inhibits baseline expression of each p38 protein in male cultures, yet stimulates p38-delta profiles without affecting other p38 proteins in female. Glucose starvation caused selective up-regulation of p38-delta profiles in male versus p38-alpha and -gamma proteins in female; these positive responses were amplified by GLUT2 siRNA pretreatment. GLUT2 opposes or enhances basal p38 phosphorylation in male versus female, respectively. GLUT2 siRNA pretreatment did not affect glucoprivic patterns of phospho-p38 protein expression in either sex. Outcomes document co-expression of the four principal p38 MAPK family proteins in hypothalamic astrocytes, and implicate GLUT2 in regulation of all (male) versus one (female) variant(s). Glucoprivation up-regulated expression of distinctive p38 isoforms in each sex; these stimulatory responses are evidently blunted by GLUT2. Glucoprivic-associated loss of GLUT2 gene silencing effects on p38 phosphorylation infers either that glucose status determines whether this sensor controls phosphorylation, or that decrements in screened glucose in each instance are of sufficient magnitude to abolish GLUT2 regulation of that function.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 635-642"},"PeriodicalIF":1.5,"publicationDate":"2024-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000538/pdfft?md5=ab8fcd18d1e11b1431501666b3817168&pid=1-s2.0-S2667242124000538-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141089831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of intrahippocampal microinjection of VU0155041, a positive allosteric modulator of mGluR4, on long term potentiation in a valproic acid-induced autistic male rat model","authors":"Zahra Ebrahimi ,&nbsp;Parsa Gholipour ,&nbsp;Reihaneh Mohammadkhani ,&nbsp;Reza Ghahremani ,&nbsp;Abdolrahman Sarihi ,&nbsp;Alireza Komaki ,&nbsp;Iraj Salehi ,&nbsp;Seyed Asaad Karimi","doi":"10.1016/j.ibneur.2024.05.005","DOIUrl":"https://doi.org/10.1016/j.ibneur.2024.05.005","url":null,"abstract":"<div><p>The precise cause of autism spectrum disorder (ASD) is not fully understood. Despite the involvement of glutamatergic dysregulation in autism, the specific contribution of mGlu4 receptors to synaptic plasticity remains unclear. Using the positive allosteric modulator VU0155041, we aimed to restore long-term potentiation (LTP) in the perforant path-dentate gyrus (PP-DG) pathway in VPA-induced autistic rat model. High-frequency stimulation was applied to the PP-DG synapse to induce LTP, while the VU0155041 was administered into the DG. Unexpectedly, VU0155041 failed to alleviate the observed LTP reduction in VPA-exposed rats, further resulting in a significant decrease in population spike LTP. This unexpected outcome prompts discussion on the complex nature of mGlu4 receptor modulation, highlighting potential interference with physiological processes underlying synaptic plasticity.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 629-634"},"PeriodicalIF":1.5,"publicationDate":"2024-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000502/pdfft?md5=52e9e71ff0c5c6d6687ddfc23f3f6062&pid=1-s2.0-S2667242124000502-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141089830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of chronic administration of ostruthin on depression-like behavior in chronically stressed mice","authors":"Masayoshi Okada ,&nbsp;Thi Thu Thuy Tran","doi":"10.1016/j.ibneur.2024.05.009","DOIUrl":"https://doi.org/10.1016/j.ibneur.2024.05.009","url":null,"abstract":"<div><p>We have previously shown that a single dose of a TREK-1 channel activator, ostruthin, exhibited antidepressant and anxiolytic effects in acute behavioral test models in mice. To assess the potential clinical application, it is essential to evaluate the effects of long-term administration of ostruthin in a chronically stressed mouse model, which is considered to be similar to the clinical condition of major depression in humans. Here, we tested the effects of a single and a 7-day administration of ostruthin on mice that were subjected to chronic unpredictable mild stress (CUMS). A single administration of ostruthin showed antidepressive effects in the tail suspension and forced swim tests of CUMS-treated mice. Unexpectedly, the 7-day administration exhibited only insignificant antidepressive and anxiolytic effects. The 7-day regimen did not affect food intake or body-weight gain, suggesting the absence of apparent cytotoxicity. The mice receiving the 7-day administration had significantly lower blood concentrations of ostruthin compared to those receiving a single dose, suggesting an upregulation of drug-metabolizing activities. These findings suggest that there is a need for stable TREK-1 channel activators that are not affected by drug metabolism.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 622-628"},"PeriodicalIF":1.5,"publicationDate":"2024-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000526/pdfft?md5=3fdb3efea334e5d53b3f721fd3411e08&pid=1-s2.0-S2667242124000526-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141090280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polarization of organoids by bioengineered symmetry breaking","authors":"Jae Ryun Ryu ,&nbsp;Kahee Ko ,&nbsp;Woong Sun","doi":"10.1016/j.ibneur.2024.05.002","DOIUrl":"10.1016/j.ibneur.2024.05.002","url":null,"abstract":"<div><p>Symmetry breaking leading to axis formation and spatial patterning is crucial for achieving more accurate recapitulation of human development in organoids. While these processes can occur spontaneously by self-organizing capabilities of pluripotent stem cells, they can often result in variation in structure and composition of cell types within organoids. To address this limitation, bioengineering techniques that utilize geometric, topological and stiffness factors are increasingly employed to enhance control and consistency. Here, we review how spontaneous manners and engineering tools such as micropattern, microfluidics, biomaterials, <em>etc.</em> can facilitate the process of symmetry breaking leading to germ layer patterning and the formation of anteroposterior and dorsoventral axes in blastoids, gastruloids, neuruloids and neural organoids. Furthermore, brain assembloids, which are composed of multiple brain regions through fusion processes are discussed. The overview of organoid polarization in terms of patterning tools can offer valuable insights for enhancing the physiological relevance of organoid system.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 22-31"},"PeriodicalIF":1.5,"publicationDate":"2024-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000460/pdfft?md5=1a5c211344e28cb582a7e19548d79481&pid=1-s2.0-S2667242124000460-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141141574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The additive effect between citalopram and muscimol upon induction of antinociceptive effect in male mice","authors":"Taha Shokrnejad-namin ,&nbsp;Elnaz Amini ,&nbsp;Fatemeh Khakpai ,&nbsp;Mohammad-Reza Zarrindast","doi":"10.1016/j.ibneur.2024.05.003","DOIUrl":"10.1016/j.ibneur.2024.05.003","url":null,"abstract":"<div><p>Previous investigations have revealed the role of GABAergic and serotonergic systems in the modulation of pain behavior. This research aimed to examine the effects of intracerebroventricular (i.c.v.) infusion of GABA_A receptor agonist and antagonist as well as citalopram on pain behavior in male mice. For i.c.v. microinjection, a guide cannula was surgically implanted in the left lateral ventricle of male mice. Pain behavior was evaluated using a tail-flick test. Tail flick latency was measured in each experimental group of mice every 15 min (for 60 min). I.c.v. microinjection of muscimol (0.5 and 1 µg/mouse; GABA_A receptor agonist) into the left lateral ventricle dose-dependently induced an antinociceptive effect. On the other hand, i.c.v. infusion of bicuculline (1 µg/mouse; GABA_A receptor antagonist) induced a hyperalgesia response. Moreover, intraperitoneally (i.p.) administration of citalopram (8 mg/kg) produced an antinociceptive effect. Co-treatment of citalopram (8 mg/kg) along with muscimol (0.25 µg/mouse) or bicuculline (0.25 µg/mouse) potentiated the antinociceptive effect produced by citalopram. We found an additive antinociceptive effect of citalopram and muscimol in male mice. In conclusion, our results suggested an interaction between citalopram and GABAergic agents on the modulation of pain behavior in male mice.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 58-64"},"PeriodicalIF":1.5,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000472/pdfft?md5=2e897424261be5d41af55ff0dec10a42&pid=1-s2.0-S2667242124000472-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141057222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Focal brain cooling suppresses spreading depolarization and reduces endothelial nitric oxide synthase expression in rats","authors":"Yuya Hirayama ,&nbsp;Hiroyuki Kida ,&nbsp;Takao Inoue ,&nbsp;Kazutaka Sugimoto ,&nbsp;Fumiaki Oka ,&nbsp;Satoshi Shirao ,&nbsp;Hirochika Imoto ,&nbsp;Sadahiro Nomura ,&nbsp;Michiyasu Suzuki","doi":"10.1016/j.ibneur.2024.05.001","DOIUrl":"10.1016/j.ibneur.2024.05.001","url":null,"abstract":"<div><p>This study aimed to investigate the effects of focal brain cooling (FBC) on spreading depolarization (SD), which is associated with several neurological disorders. Although it has been studied from various aspects, no medication has been developed that can effectively control SD. As FBC can reduce neuronal damage and promote functional recovery in pathological conditions such as epilepsy, cerebral ischemia, and traumatic brain injury, it may also potentially suppress the onset and progression of SD. We created an experimental rat model of SD by administering 1 M potassium chloride (KCl) to the cortical surface. Changes in neuronal and vascular modalities were evaluated using multimodal recording, which simultaneously recorded brain temperature (BrT), wide range electrocorticogram, and two-dimensional cerebral blood flow. The rats were divided into two groups (cooling [CL] and non-cooling [NC]). Warm or cold saline was perfused on the surface of one hemisphere to maintain BrT at 37°C or 15°C in the NC and CL groups, respectively. Western blot analysis was performed to determine the effects of FBC on endothelial nitric oxide synthase (eNOS) expression. In the NC group, KCl administration triggered repetitive SDs (mean frequency = 11.57/h). In the CL group, FBC increased the duration of all KCl-induced events and gradually reduced their frequency. Additionally, eNOS expression decreased in the cooled brain regions compared to the non-cooled contralateral hemisphere. The results obtained by multimodal recording suggest that FBC suppresses SD and decreases eNOS expression. This study may contribute to developing new treatments for SD and related neurological disorders.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 609-621"},"PeriodicalIF":1.5,"publicationDate":"2024-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000459/pdfft?md5=8c737a71ea1abf2d651a0c0d007e60c7&pid=1-s2.0-S2667242124000459-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141056982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progressive Supranuclear Palsy Syndrome: An Overview","authors":"Eduardo Ichikawa-Escamilla,&nbsp;Rodrigo A. Velasco-Martínez,&nbsp;Laura Adalid-Peralta","doi":"10.1016/j.ibneur.2024.04.008","DOIUrl":"https://doi.org/10.1016/j.ibneur.2024.04.008","url":null,"abstract":"<div><p>Progressive supranuclear palsy (PSP) is a neurodegenerative disease, commonly observed as a movement disorder in the group of parkinsonian diseases. The term PSP usually refers to PSP-Richardson’s syndrome (PSP-RS), the most typical clinical presentation. However, the broad concept of progressive supranuclear palsy syndrome (PSP-S) applies to a set of clinical entities that share a pathophysiological origin and some symptoms. According to its clinical predominance, PSP-S is divided into subtypes. PSP-S has clinical similarities with Parkinson's disease, and both pathologies are classified in the group of parkinsonisms, but they do not share pathophysiological traits. By contrast, the pathophysiology of corticobasal syndrome (CBS) depends on tau expression and shares similarities with PSP-S in both pathophysiology and clinical picture. An involvement of the immune system has been proposed as a cause of neurodegeneration. The role of neuroinflammation in PSP-S has been studied by neuroimaging, among other methods. As it is the case in other neurodegenerative pathologies, microglial cells have been attributed a major role in PSP-S. While various studies have explored the detection and use of possible inflammatory biomarkers in PSP-S, no significant advances have been made in this regard. This review is aimed at highlighting the most relevant information on neuroinflammation and peripheral inflammation in the development and progression of PSP-S, to lay the groundwork for further research on the pathophysiology, potential biomarkers, and therapeutic strategies for PSP-S.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 598-608"},"PeriodicalIF":1.5,"publicationDate":"2024-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000411/pdfft?md5=baed6a1e62b2eba18612caf78dc4a236&pid=1-s2.0-S2667242124000411-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140948668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"East Asian perspective of responsible research and innovation in neurotechnology","authors":"Tamami Fukushi","doi":"10.1016/j.ibneur.2024.04.009","DOIUrl":"https://doi.org/10.1016/j.ibneur.2024.04.009","url":null,"abstract":"<div><p>After more than half a century of research and development (R&amp;D), Brain–computer interface (BCI)-based Neurotechnology continues to progress as one of the leading technologies of the 2020 s worldwide. Various reports and academic literature in Europe and the United States (U.S.) have outlined the trends in the R&amp;D of neurotechnology and the consideration of ethical issues, and the importance of the formulation of ethical principles, guidance and industrial standards as well as the development of relevant human resources has been discussed. However, limited number studies have focused on neurotechnology R&amp;D, the dissemination of neuroethics related to the academic foundation advancing the discussion on ethical principles, guidance and standards or human resource development in the Asian region. This study fills in this gap in understanding of Eastern Asian (China, Korea and Japan) situation based on the participation in activities to develop ethical principles, guidance, and industrial standards for appropriate use of neurotechnology, in addition to literature survey and clinical registries’ search investigation reflecting the trends in neurotechnology R&amp;D as well as its social implication in Asian region. The current study compared the results with the situation in Europa and the U.S. and discussed issues that need to be addressed in the future and discussed the significance and potential of corporate consortium initiatives in Japan and examples of ethics and governance activities in Asian Countries.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 582-597"},"PeriodicalIF":1.5,"publicationDate":"2024-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000435/pdfft?md5=ae4cc5e479c07d468b5cf2c902b8d093&pid=1-s2.0-S2667242124000435-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140910102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of spexin injection and its interaction with nitric oxide, serotonin, and corticotropin receptors on the central regulation of food intake in broilers","authors":"Mohaya Farzin ,&nbsp;Shahin Hassanpour ,&nbsp;Morteza Zendehdel ,&nbsp;Bita vazir ,&nbsp;Ahmad Asghari","doi":"10.1016/j.ibneur.2024.04.010","DOIUrl":"https://doi.org/10.1016/j.ibneur.2024.04.010","url":null,"abstract":"<div><p>Complex homeostatic control mechanisms are tools to adjust the food birds eat and their appetite. Birds and mammals differ in several ways considering food intake regulation. Therefore, this study aimed to investigate the special effects of the intracerebroventricular (ICV) injection of spexin and its interaction with nitric oxide, serotonin and corticotropin receptors on central food intake regulation in broilers. In the test 1, Broilers received ICV injection of saline, PCPA (p-chlorophenylalanine,1.25 µg), spexin (10 nmol) and PCPA+spexin. In test 2–7, 8-OH-DPAT, SB-242084 (5-HT2C, 1.5 µg), L-arginine (Precursor of nitric oxide, 200 nmol), L-NAME (nitric oxide synthetize inhibitor, 100 nmol), Astressin-B (30 µg) and Astressin2-B (30 µg) were injected to Broilers instead of the PCPA. Then, the amount of food received was measured up to 2 h after the injection. The food consumption was significantly decreased by Spexin (10 nmol) (P&lt;0.05). Concomitant injection of SB-242084+spexin attenuated spexin-induced hypophagia (P&lt;0.05). Co-injection of L-arginine+spexin enhanced spexin-induced hypophagia and this effect was reversed by L-NAME (P&lt;0.05). Also, concomitant injection of Astressin-B + spexin or Astressin2-B + spexin enhanced spexin-induced hypophagia (P&lt;0.05). Founded on these observations, spexin-induced hypophagia may be mediated by nitric oxide and 5-HT2C, CRF1, and CRF2 receptors in neonatal broilers.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 542-549"},"PeriodicalIF":1.5,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000447/pdfft?md5=8f374f3b2adae40ffd7c8b7a227995bf&pid=1-s2.0-S2667242124000447-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140880342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}