Neuropeptides最新文献

{"title":"Changes in working memory induced by lipopolysaccharide administration in mice are associated with metabotropic glutamate receptors 5 and contrast with changes induced by cyclooxygenase-2: Involvement of postsynaptic density protein 95 and down syndrome cell adhesion molecule","authors":"Katarzyna Stachowicz ,&nbsp;Patrycja Pańczyszyn-Trzewik ,&nbsp;Magdalena Sowa-Kućma ,&nbsp;Paulina Misztak","doi":"10.1016/j.npep.2023.102347","DOIUrl":"10.1016/j.npep.2023.102347","url":null,"abstract":"<div><p><span>The strength and quality of the signal propagated by the glutamate<span><span> synapse (Glu) depend, among other things, on the structure of the postsynaptic part and the quality of adhesion between the interacting components of the synapse. Postsynaptic density protein 95 (PSD95), </span>mammalian target of rapamycin<span> (mTOR), and Down syndrome cell adhesion molecule<span><span> (DSCAM) are components of the proper functioning of an excitatory synapse. PSD95 is a member of the membrane-associated </span>guanylate kinases protein family, mainly located at the postsynaptic density of the excitatory synapse. PSD95, via direct interaction, regulates the clustering and functionality of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and </span></span></span></span><em>N</em><span><span><span>-methyl-D-aspartic acid (NMDA) receptors at a synapse. Here, the effects of treatment with an antagonist of mGluR5 (MTEP) and </span>NS398<span><span> (cyclooxygenase-2, COX-2 inhibitor) on PSD95, mTOR, and DSCAM in the hippocampus<span> (HC) of C57B1/6 J mice using Western blots in the context of learning were examined. Moreover, the sensitivity of selected proteins to </span></span>lipopolysaccharide (LPS) was monitored. </span></span>MTEP injected for seven days induced upregulation of PSD95 in HC of mice. The observed effect was regulated by a COX-2 inhibitor and concurrently by LPS. Accompanying alterations in DSCAM protein were found, suggesting changes in adhesion strength after modulation of glutamatergic (Glu) synapse via tested compounds.</span></p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"100 ","pages":"Article 102347"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10126371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intrathecal administration of botulinum toxin type a antagonizes neuropathic pain by countering increased vesicular nucleotide transporter expression in the spinal cord of chronic constriction injury of the sciatic nerve rats","authors":"Yongqiang Shi ,&nbsp;Chaoyang Gong ,&nbsp;Wei Nan ,&nbsp;Wenming Zhou ,&nbsp;Zeyuan Lei ,&nbsp;Kaisheng Zhou ,&nbsp;Linna Wang ,&nbsp;Guanghai Zhao ,&nbsp;Haihong Zhang","doi":"10.1016/j.npep.2023.102346","DOIUrl":"10.1016/j.npep.2023.102346","url":null,"abstract":"<div><p><span><span><span>Botulinum toxin type A (BoNT/A) induces direct </span>analgesic effects<span><span> in neuropathic pain by inhibiting the release of substance P, calcitonin gene-related peptide (CGRP) and </span>glutamate<span>. Vesicular nucleotide transporter<span> (VNUT) was responsible for the storage and release of ATP in vivo, and one of the mechanisms underlying neuropathic pain is VNUT-dependent release of extracellular ATP from dorsal horn neurons. However, the analgesic effect of BoNT/A by affecting the expression of VNUT remained largely unknown. Thus, in this study, we aimed to elucidate the antinociceptive potency and analgesic mechanism of BoNT/A in </span></span></span></span>chronic constriction injury<span> of the sciatic nerve (CCI) induced neuropathic pain. Our results showed that a single </span></span>intrathecal<span><span> injection of 0.1 U BoNT/A seven days after CCI surgery produced significant analgesic activity and decreased the expression of VNUT in the spinal cord of CCI rats. Similarly, BoNT/A inhibited the CCI-induced increase in ATP content in the rat spinal cord. Overexpression of VNUT in the spinal cord of CCI-induced rats markedly reversed the antinociceptive effect of BoNT/A. Furthermore, 33 U/mL BoNT/A dramatically reduced the expression of VNUT in pheochromocytoma (PC12) cells but overexpressing SNAP-25 increased VNUT expression in </span>PC12 cells. Our current study is the first to demonstrate that BoNT/A is involved in neuropathic pain by regulating the expression of VNUT in the spinal cord in rats.</span></p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"100 ","pages":"Article 102346"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9749394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin promotes Schwann cell remyelination, preserves neural tissue and improves functional recovery after spinal cord injury","authors":"Zucheng Huang ,&nbsp;Junyu Lin (1,) ,&nbsp;Hui Jiang ,&nbsp;Wanrong Lin ,&nbsp;Zhiping Huang ,&nbsp;Jiayu Chen ,&nbsp;Wende Xiao ,&nbsp;Qiong Lin ,&nbsp;Jun Wang ,&nbsp;Shifeng Wen ,&nbsp;Qingan Zhu ,&nbsp;Junhao Liu","doi":"10.1016/j.npep.2023.102348","DOIUrl":"10.1016/j.npep.2023.102348","url":null,"abstract":"<div><p><span><span>Patients with a spinal cord injury (SCI) usually suffer lifelong disability as a result. Considering this, SCI </span>treatment<span> and pathology study are urgently needed. Metformin, a widely used </span></span>hypoglycemic drug<span><span><span>, has been indicated for its important role in central nervous system diseases<span>. This study aimed to investigate the potential effect of metformin on remyelination after SCI. In the present study, we established a cervical contusion SCI model and metformin treatment was applied after SCI. Biomechanical parameters and behavioral assessment were used to evaluate the </span></span>severity of injury<span> and the improvement of functional recovery after SCI, respectively. The immunofluorescence and </span></span>western blot<span> were performed at the terminal time point. Our results showed that treating with metformin after SCI improved functional recovery by reducing the white matter loss and promoting Schwann cell<span><span> remyelination, and the Nrg1/ErbB signaling pathway may be involved in promoting remyelination mediated by </span>oligodendrocytes and Schwann cells. In addition, the area of spared tissues was significantly increased in the metformin group. However, metformin had no significant effects on the glial scar and inflammation after SCI. In summary, these findings indicated that the role of metformin in Schwann cell remyelination after SCI was probably related to the regulation of the Nrg1/ErbB pathway. It is, therefore, possible to suggest that metformin may be a potential therapy for SCI.</span></span></span></p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"100 ","pages":"Article 102348"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10108683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effect of Prolactin releasing peptide against 1,2-diacetylbenzene -induced neuroinflammation","authors":"Ngoc Minh Hong Hoang,&nbsp;Wonhee Jo,&nbsp;Min-Sun Kim","doi":"10.1016/j.npep.2023.102349","DOIUrl":"10.1016/j.npep.2023.102349","url":null,"abstract":"<div><p><span>Prolactin-releasing peptide (PrRP) has been investigated as a potential therapeutic for diabetes by the effect of food intake reduction, increasing leptin signaling, and insulin tolerance. Recent studies focused on its </span>synaptogenesis<span><span><span><span> and protective effects against neurodegeneration. Whereas 1,2-diacetylbenzene (DAB), a common metabolite of a neurotoxicant 1,2-diethyl benzene, causes memory impairment and </span>neurotoxicity<span> partly through the inflammatory process. Our present study assessed the effect of PrRP in microglia and its action in balancing the inflammation to protect against DAB. We observed that PrRP modulated </span></span>NADPH oxidase - regulated NLRP3 </span>inflammasome<span> and PRL signaling pathways differently between physical and toxic conditions in microglia.</span></span></p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"100 ","pages":"Article 102349"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10126418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Arginine vasopressin effects on membrane potentials of preoptic area temperature-sensitive and -insensitive neurons in rat hypothalamic tissue slices","authors":"Yu Tang ,&nbsp;Siyuan Liu ,&nbsp;Lingzhi Xu ,&nbsp;Min Huang ,&nbsp;Ke Zhang","doi":"10.1016/j.npep.2023.102344","DOIUrl":"10.1016/j.npep.2023.102344","url":null,"abstract":"<div><p><span>Arginine vasopressin<span><span> (AVP) plays a hypothermic regulatory role in thermoregulation and is an important </span>endogenous mediator<span> in this mechanism. In the preoptic area (POA), AVP increases the spontaneous firing and thermosensitivity of warm-sensitive neurons and decreases those of cold-sensitive and temperature-insensitive neurons. Because POA neurons play a crucial role in precise thermoregulatory responses, these findings indicate that there is an association between the hypothermia and changes in the firing activity of AVP-induced POA neurons. However, the electrophysiological mechanisms by which AVP controls this firing activity remain unclear. Therefore, in the present study, using in vitro hypothalamic brain slices and whole-cell recordings, we elucidated the membrane potential responses of temperature-sensitive and –insensitive POA neurons to identify the applications of AVP or V</span></span></span>_1a<span> vasopressin receptor antagonists. By monitoring changes in the resting potential and membrane potential thermosensitivity of the neurons before and during experimental perfusion, we observed that AVP increased the changes in the resting potential of 50% of temperature-insensitive neurons but reduced them in others. These changes are because AVP enhances the membrane potential thermosensitivity of nearly 50% of the temperature-insensitive neurons. On the other hand, AVP changes both the resting potential and membrane potential thermosensitivity of temperature-sensitive neurons, with no differences between the warm- and cold-sensitive neurons. Before and during AVP or V</span>_1a vasopressin receptor antagonist perfusion, no correlation was observed between changes in the thermosensitivity and membrane potential of all neurons. Furthermore, no correlation was observed between the thermosensitivity and membrane potential thermosensitivity of the neurons during experimental perfusion. In the present study, we found that AVP induction did not result in any changes in resting potential, which is unique to temperature-sensitive neurons. The study results suggest that AVP-induced changes in the firing activity and firing rate thermosensitivity of POA neurons are not controlled by resting potentials.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"100 ","pages":"Article 102344"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9750152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effects of Zishen Huoxue recipe against neuronal injury in the neurovascular unit of rats with vascular dementia by interfering with inflammatory cascade-induced pyroptosis","authors":"Ting Yao ,&nbsp;Le Xie ,&nbsp;Yao Xie ,&nbsp;Jinlin Jiang ,&nbsp;Qian Deng ,&nbsp;Jie Wang ,&nbsp;Lu Liu ,&nbsp;Dahua Wu","doi":"10.1016/j.npep.2023.102358","DOIUrl":"10.1016/j.npep.2023.102358","url":null,"abstract":"<div><h3>Objective</h3><p>Chinese herbal formulas show considerable therapeutic benefits in dementia. This study specifically explored the protective action of Zishen Huoxue recipe on the neurovascular unit (NVU) of rats with vascular dementia (VD).</p></div><div><h3>Methods</h3><p><span>VD rat models were established by permanent bilateral common carotid artery occlusion and treated with Zishen Huoxue recipe. </span><em>In vitro</em><span><span><span> glucose‑oxygen deprivation (OGD)-injured NVU models were established and treated with miR-124-3p agomir or rat medicated serum. The neurological damage, histopathological changes, and neuronal injury in the rat hippocampus were assessed using Morris </span>water maze test and histological </span>stainings<span><span><span><span>. Expression of miR-124-3p was determined using RT-qPCR. The blood-brain barrier/NVU injury, cell pyroptosis, </span>NLRP3 </span>inflammasome<span> activation, and release of inflammatory factors were analyzed mainly by immunofluorescence analysis, </span></span>TUNEL<span> staining, Western blot<span>, and ELISA. QS-21 (an NLRP3 activator) was used to verify the role of miR-124-3p/NLRP3.</span></span></span></span></p></div><div><h3>Results</h3><p>Zishen Huoxue recipe ameliorated the learning/memory deficits, neuronal injury, NVU insults, cell pyroptosis, activation of NLRP3 inflammasome, and extensive secretion of lactate dehydrogenase/IL-1β/IL-18 in VD rats. miR-124-3p was downregulated in VD rats but upregulated after treatment of this recipe. miR-124-3p overexpression ameliorated NVU insults, reduced cell pyroptosis, lowered NLRP3 inflammasome activation, and suppressed inflammatory responses in OGD-injured NVU models. NLRP3 inflammasome activation partly counteracted the amelioration effect of miR-124-3p on pyroptosis. Zishen Huoxue recipe could upregulate miR-124-3p to suppress pyroptosis and protect NVU function.</p></div><div><h3>Conclusion</h3><p>Zishen Huoxue recipe can upregulate miR-124-3p expression to repress the inflammatory cascade-evoked pyroptosis, thereby protecting against neuronal injury in the NVU of VD rats.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"102 ","pages":"Article 102358"},"PeriodicalIF":2.9,"publicationDate":"2023-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10028094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effect of TNIP2 on the inflammatory response of microglia after spinal cord injury in rats","authors":"J. Fu, Chunshuai Wu, Guanhua Xu, Jinlong Zhang, Jia-jia Chen, Chu Chen, H. Hong, pengfei xue, Jiawei Jiang, Jiayi Huang, Chunyan Ji, Zhiming Cui","doi":"10.2139/ssrn.4355105","DOIUrl":"https://doi.org/10.2139/ssrn.4355105","url":null,"abstract":"BACKGROUND\u0000Spinal cord injury (SCI) is a devastating disease that can lead to tissue loss and neurological dysfunction. TNIP2 is a negative regulator of NF-κB signaling due to its capacity to bind A20 and suppress inflammatory cytokines-induced NF-κB activation. However, the anti-inflammatory role of TNIP2 in SCI remains unclear. Our study's intention was to evaluate the effect of TNIP2 on the inflammatory response of microglia after spinal cord injury in rats.\u0000\u0000\u0000METHODS\u0000HE staining and Nissl staining were performed on day 3 following SCI to analyze the histological changes. To further investigate the functional changes of TNIP2 after SCI, we performed immunofluorescence staining experiments. The effect of LPS on TNIP2 expression in BV2 cells was examined by western blot. The levels of TNF-α, IL-1β, and IL-6 in spinal cord tissues of rats with SCI and in BV2 cells with LPS were measured by using qPCR.\u0000\u0000\u0000RESULTS\u0000TNIP2 expression was closely associated with the pathophysiology of SCI in rats, and TNIP2 was involved in regulating functional changes in microglia. TNIP2 expression was increased during SCI in rats and that overexpression of TNIP2 inhibited M1 polarization and pro-inflammatory cytokine production in microglia, which might ultimately protect against inflammatory responses through the MAPK and NF-κB signaling pathways.\u0000\u0000\u0000CONCLUSIONS\u0000The present study provides evidence for a role of TNIP2 in the regulation of inflammation in SCI and suggests that induction of TNIP2 expression alleviated the inflammatory response of microglia.","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"101 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43014924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PACAP inhibition alleviates neuropathic pain by modulating Nav1.7 through the MAPK/ERK signaling pathway in a rat model of chronic constriction injury","authors":"Mingzheng Liu ,&nbsp;Fan He ,&nbsp;Mengci Shao ,&nbsp;Tianyuan Li ,&nbsp;Liecheng Wang ,&nbsp;Yuanyin Wang ,&nbsp;Wenhua Xu","doi":"10.1016/j.npep.2023.102327","DOIUrl":"10.1016/j.npep.2023.102327","url":null,"abstract":"<div><h3>Background</h3><p>Trigeminal neuralgia is a common chronic maxillofacial neuropathic pain disorder, and voltage-gated sodium channels (VSGCs) are likely involved in its pathology. Prior studies report that pituitary adenylate cyclase-activating polypeptide (PACAP), a neuropeptide highly expressed in the trigeminal ganglion, may contribute to dorsal root ganglion neuron excitability by modulating the Nav1.7.</p></div><div><h3>Objective</h3><p>We investigated whether PACAP can regulate Nav1.7 through the mitogen-activated protein kinase/ERK kinase/extracellular-signal-regulated kinase (MEK/ERK) pathway in the trigeminal ganglion after chronic constriction injury of the infraorbital nerve (ION-CCI) in rats.</p></div><div><h3>Study design</h3><p>Sprague-Dawley rats underwent ION-CCI, followed by intrathecal injection of PACAP 6–38 (PAC1 receptor antagonist) and PD98059 (MEK/ERK antagonist). Quantitative real-time PCR and western blot were used to quantify ATF3, PACAP, ERK, p-ERK, and Nav1.7 expression.</p></div><div><h3>Results</h3><p>The mechanical pain threshold decreased from day 3 to day 21 after ION-CCI and reached the lowest testing value by day 14; however, it increased after PACAP 6–38 and PD98059 injections. Additionally, ION-CCI surgery increased ATF3, PACAP, and p-ERK expression in the rat trigeminal ganglion and decreased Nav1.7 and PAC1 receptor expression; however, there was no difference in ERK expression. PACAP 6–38 injection significantly decreased PACAP, p-ERK, and Nav1.7 expression and increased the PAC1 receptor expression, with no change in ERK expression. Moreover, PD98059 injection decreased PACAP, p-ERK, and Nav1.7 expression and increased the expression of PAC1 receptor.</p></div><div><h3>Conclusion</h3><p>After ION-CCI, PACAP in the rat trigeminal ganglion can modulate Nav1.7 through the MEK/ERK pathway via the PAC1 receptor. Further, PACAP inhibition alleviates allodynia in ION-CCI rats.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"99 ","pages":"Article 102327"},"PeriodicalIF":2.9,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9435439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 sensory and sympathetic nerves in craniofacial bone regeneration","authors":"Freshet Assefa","doi":"10.1016/j.npep.2023.102328","DOIUrl":"10.1016/j.npep.2023.102328","url":null,"abstract":"<div><p><span>Multiple factors regulate the regeneration of craniofacial bone defects. The </span>nervous system<span><span> is recognized as one of the critical regulators of bone mass, thereby suggesting a role for neuronal pathways in bone regeneration<span><span><span>. However, in the context of craniofacial bone regeneration, little is known about the interplay between the nervous system and craniofacial bone. Sensory and sympathetic nerves interact with the bone through their neuropeptides, </span>neurotransmitters<span>, proteins, peptides, and amino acid derivates. The neuron-derived factors, such as </span></span>semaphorin<span> 3A (SEMA3A), substance P (SP), calcitonin gene-related peptide (CGRP), neuropeptide Y<span><span> (NPY), and vasoactive intestinal peptide (VIP), possess a remarkable role in craniofacial regeneration. This review summarizes the roles of these factors and recently published factors such as </span>secretoneurin<span> (SN) and spexin (SPX) in the osteoblast and </span></span></span></span></span>osteoclast<span><span> differentiation, bone metabolism, growth, remodeling and discusses the novel application of nerve-based craniofacial bone regeneration. Moreover, the review will facilitate understanding the mechanism of action and provide potential </span>treatment direction for the craniofacial bone defect.</span></span></p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"99 ","pages":"Article 102328"},"PeriodicalIF":2.9,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9437094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Several neuropeptides involved in parkinsonian neuroprotection modulate the firing properties of nigral dopaminergic neurons","authors":"Lei Chen ,&nbsp;Cui Liu ,&nbsp;Yan Xue ,&nbsp;Xin-Yi Chen","doi":"10.1016/j.npep.2023.102337","DOIUrl":"10.1016/j.npep.2023.102337","url":null,"abstract":"<div><p><span><span>Parkinson's disease<span><span> is characterized by progressive degeneration of dopaminergic neurons in the </span>substantia nigra pars compacta. The surviving nigral dopaminergic neurons display altered spontaneous firing activity in Parkinson's disease. The firing rate of nigral dopaminergic neurons decreases long before complete </span></span>neuronal death<span> and the appearance of parkinsonian symptoms. A mild stimulation could rescue dopaminergic neurons from death and in turn play neuroprotective<span><span> effects. Several neuropeptides, including </span>cholecystokinin<span> (CCK), ghrelin, </span></span></span></span>neurotensin<span><span>, orexin<span>, tachykinins<span> and apelin, within the substantia nigra pars compacta play important roles in the modulation of spontaneous firing activity of dopaminergic neurons and therefore involve motor control and </span></span></span>motor disorders. Here, we review neuropeptide-induced modulation of the firing properties of nigral dopaminergic neurons. This review may provide a background to guide further investigations into the involvement of neuropeptides in movement control by modulating firing activity of nigral dopaminergic neurons in Parkinson's disease.</span></p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"99 ","pages":"Article 102337"},"PeriodicalIF":2.9,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9442092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}