Marawan Sadek, Kurt R. Stover, Xiaojing Liu, Mark A. Reed, Donald F. Weaver, Aylin Y. Reid
{"title":"IDO-1 inhibition improves outcome after fluid percussion injury in adult male rats","authors":"Marawan Sadek, Kurt R. Stover, Xiaojing Liu, Mark A. Reed, Donald F. Weaver, Aylin Y. Reid","doi":"10.1002/jnr.25338","DOIUrl":"https://doi.org/10.1002/jnr.25338","url":null,"abstract":"<p>The enzyme indoleamine 2,3 dioxygenase 1 (IDO1) catalyzes the rate-limiting step in the kynurenine pathway (KP) which produces both neuroprotective and neurotoxic metabolites. Neuroinflammatory signals produced as a result of pathological conditions can increase production of IDO1 and boost its enzymatic capacity. IDO1 and the KP have been implicated in behavioral recovery after human traumatic brain injury (TBI), but their roles in experimental models of TBI are for the most part unknown. We hypothesized there is an increase in KP activity in the fluid percussion injury (FPI) model of TBI, and that administration of an IDO1 inhibitor will improve neurological recovery. In this study, adult male Sprague Dawley rats were subjected to FPI or sham injury and received twice-daily oral administration of the IDO1 inhibitor PF-06840003 (100 mg/kg) or vehicle control. FPI resulted in a significant increase in KP activity, as demonstrated by an increased ratio of kynurenine: tryptophan, in the perilesional neocortex and ipsilateral hippocampus 3 days postinjury (DPI), which normalized by 7 DPI. The increase in KP activity was prevented by PF-06840003. IDO1 inhibition also improved memory performance as assessed in the Barnes maze and anxiety behaviors as assessed in open field testing in the first 28 DPI. These results suggest increased KP activity after FPI may mediate neurological dysfunction, and IDO1 inhibition should be further investigated as a potential therapeutic target to improve recovery.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 5","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25338","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140844764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Farzaneh Tamnanloo, Xiaoru Chen, Mariana M. Oliveira, Mélanie Tremblay, Christopher F. Rose
{"title":"Excessive intragastric alcohol administration exacerbates hepatic encephalopathy and provokes neuronal cell death in male rats with chronic liver disease","authors":"Farzaneh Tamnanloo, Xiaoru Chen, Mariana M. Oliveira, Mélanie Tremblay, Christopher F. Rose","doi":"10.1002/jnr.25337","DOIUrl":"https://doi.org/10.1002/jnr.25337","url":null,"abstract":"<p>Hepatic encephalopathy (HE) is defined as decline in neurological function during chronic liver disease (CLD). Alcohol is a major etiological factor in the pathogenesis of fibrosis/cirrhosis and has also been documented to directly impact the brain. However, the role of alcohol in the development of HE in CLD remains unclear. Here, we investigated the impact of excessive alcohol administration on neurological deterioration in rats with CLD. Starting day 7 post-BDL surgery, rats were administered alcohol twice daily (51% v/v ethanol, 3 g/kg, via gavage) for 4 weeks. Motor coordination was assessed weekly using rotarod and anxiety-like behavior was evaluated with open field and elevated plus maze at 5 weeks. Upon sacrifice, brains were collected for western blot and immunohistochemical analyses to investigate neuronal integrity and oxidative stress status. Alcohol worsened motor coordination performance and increased anxiety-like behavior in BDL rats. Impairments were associated with decreased neuronal markers of NeuN and SMI311, increased apoptotic markers of cleaved/pro-caspase-3 and Bax/Bcl2, increased necroptosis markers of pRIP3 and pMLKL, decreased total antioxidant capacity (TAC), and increased 4-hydroxynonenal (4-HNE)modified proteins in the cerebellum of BDL-alcohol rats when compared to respective controls. Immunofluorescence confirmed the colocalization of cleaved caspase-3 and pMLKL in the granular neurons of the cerebellum of BDL-alcohol rats. Excessive alcohol consumption exacerbates HE which leads to associated apoptotic and necroptotic neuronal loss in the cerebellum of BDL-alcohol rats. Additionally, higher levels of 4-HNE and decreased TAC in the cerebellum of BDL-alcohol rats suggest oxidative stress is the triggering factor of apoptotic and necroptotic neuronal loss/injury.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 5","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25337","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140808157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Luis A. Rojas-Colón, John B. Redell, Pramod K. Dash, Pedro E. Vegas, Wanda Vélez-Torres
{"title":"4R-cembranoid suppresses glial cells inflammatory phenotypes and prevents hippocampal neuronal loss in LPS-treated mice","authors":"Luis A. Rojas-Colón, John B. Redell, Pramod K. Dash, Pedro E. Vegas, Wanda Vélez-Torres","doi":"10.1002/jnr.25336","DOIUrl":"https://doi.org/10.1002/jnr.25336","url":null,"abstract":"<p>Chronic neuroinflammation has been implicated in neurodegenerative disease pathogenesis. A key feature of neuroinflammation is neuronal loss and glial activation, including microglia and astrocytes. 4R-cembranoid (4R) is a natural compound that inhibits hippocampal pro-inflammatory cytokines and increases memory function in mice. We used the lipopolysaccharide (LPS) injection model to study the effect of 4R on neuronal density and microglia and astrocyte activation. C57BL/6J wild-type mice were injected with LPS (5 mg/kg) and 2 h later received either 4R (6 mg/kg) or vehicle. Mice were sacrificed after 72 h for analysis of brain pathology. Confocal images of brain sections immunostained for microglial, astrocyte, and neuronal markers were used to quantify cellular hippocampal phenotypes and neurons. Hippocampal lysates were used to measure the expression levels of neuronal nuclear protein (NeuN), inducible nitrous oxide synthase (iNOS), arginase-1, thrombospondin-1 (THBS1), glial cell-derived neurotrophic factor (GDNF), and orosomucoid-2 (ORM2) by western blot. iNOS and arginase-1 are widely used protein markers of pro- and anti-inflammatory microglia, respectively. GDNF promotes neuronal survival, and ORM2 and THBS1 are astrocytic proteins that regulate synaptic plasticity and inhibit microglial activation. 4R administration significantly reduced neuronal loss and the number of pro-inflammatory microglia 72 h after LPS injection. It also decreased the expression of the pro-inflammatory protein iNOS while increasing arginase-1 expression, supporting its anti-inflammatory role. The protein expression of THBS1, GDNF, and ORM2 was increased by 4R. Our data show that 4R preserves the integrity of hippocampal neurons against LPS-induced neuroinflammation in mice.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 4","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25336","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140639592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fatima Aidil-Carvalho, Ana Caulino-Rocha, Joaquim Alexandre Ribeiro, Diana Cunha-Reis
{"title":"Mismatch novelty exploration training shifts VPAC1 receptor-mediated modulation of hippocampal synaptic plasticity by endogenous VIP in male rats","authors":"Fatima Aidil-Carvalho, Ana Caulino-Rocha, Joaquim Alexandre Ribeiro, Diana Cunha-Reis","doi":"10.1002/jnr.25333","DOIUrl":"https://doi.org/10.1002/jnr.25333","url":null,"abstract":"<p>Novelty influences hippocampal-dependent memory through metaplasticity. Mismatch novelty detection activates the human hippocampal CA1 area and enhances rat hippocampal-dependent learning and exploration. Remarkably, mismatch novelty training (NT) also enhances rodent hippocampal synaptic plasticity while inhibition of VIP interneurons promotes rodent exploration. Since VIP, acting on VPAC<sub>1</sub> receptors (Rs), restrains hippocampal LTP and depotentiation by modulating disinhibition, we now investigated the impact of NT on VPAC<sub>1</sub> modulation of hippocampal synaptic plasticity in male Wistar rats. NT enhanced both CA1 hippocampal LTP and depotentiation unlike exploring an empty holeboard (HT) or a fixed configuration of objects (FT). Blocking VIP VPAC<sub>1</sub>Rs with PG 97269 (100 nM) enhanced both LTP and depotentiation in naïve animals, but this effect was less effective in NT rats. Altered endogenous VIP modulation of LTP was absent in animals exposed to the empty environment (HT). HT and FT animals showed mildly enhanced synaptic VPAC<sub>1</sub>R levels, but neither VIP nor VPAC<sub>1</sub>R levels were altered in NT animals. Conversely, NT enhanced the GluA1/GluA2 AMPAR ratio and gephyrin synaptic content but not PSD-95 excitatory synaptic marker. In conclusion, NT influences hippocampal synaptic plasticity by reshaping brain circuits modulating disinhibition and its control by VIP-expressing hippocampal interneurons while upregulation of VIP VPAC<sub>1</sub>Rs is associated with the maintenance of VIP control of LTP in FT and HT animals. This suggests VIP receptor ligands may be relevant to co-adjuvate cognitive recovery therapies in aging or epilepsy, where LTP/LTD imbalance occurs.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 4","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25333","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140639590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
María Silvina Marcora, Vanesa Soledad Mattera, Pilar Goñi, Florencia Aybar, Jorge Daniel Correale, Juana Maria Pasquini
{"title":"Iron deficiency in astrocytes alters cellular status and impacts on oligodendrocyte differentiation","authors":"María Silvina Marcora, Vanesa Soledad Mattera, Pilar Goñi, Florencia Aybar, Jorge Daniel Correale, Juana Maria Pasquini","doi":"10.1002/jnr.25334","DOIUrl":"https://doi.org/10.1002/jnr.25334","url":null,"abstract":"<p>Iron deficiency (ID) has been shown to affect central nervous system (CNS) development and induce hypomyelination. Previous work from our laboratory in a gestational ID model showed that both oligodendrocyte (OLG) and astrocyte (AST) maturation was impaired. To explore the contribution of AST iron to the myelination process, we generated an in vitro ID model by silencing divalent metal transporter 1 (DMT1) in AST (siDMT1 AST) or treating AST with Fe<sup>3+</sup> chelator deferoxamine (DFX; DFX AST). siDMT1 AST showed no changes in proliferation but remained immature. Co-cultures of oligodendrocyte precursors cells (OPC) with siDMT1 AST and OPC cultures incubated with siDMT1 AST-conditioned media (ACM) rendered a reduction in OPC maturation. These findings correlated with a decrease in the expression of AST-secreted factors IGF-1, NRG-1, and LIF, known to promote OPC differentiation. siDMT1 AST also displayed increased mitochondrial number and reduced mitochondrial size as compared to control cells. DFX AST also remained immature and DFX AST-conditioned media also hampered OPC maturation in culture, in keeping with a decrease in the expression of AST-secreted growth factors IGF-1, NRG-1, LIF, and CNTF. DFX AST mitochondrial morphology and number showed results similar to those observed in siDMT1 AST. In sum, our results show that ID, induced through two different methods, impacts AST maturation and mitochondrial functioning, which in turn hampers OPC differentiation.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 4","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140639591","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}
J. Manuel Herrera-Zamora, Fernando Osuna-Lopez, Miriam E. Reyes-Méndez, Ramon E. Valadez-Lemus, Enrique A. Sánchez-Pastor, Ricardo A. Navarro-Polanco, Eloy G. Moreno-Galindo, Javier Alamilla
{"title":"Increased glutamatergic neurotransmission between the retinohypothalamic tract and the suprachiasmatic nucleus of old mice","authors":"J. Manuel Herrera-Zamora, Fernando Osuna-Lopez, Miriam E. Reyes-Méndez, Ramon E. Valadez-Lemus, Enrique A. Sánchez-Pastor, Ricardo A. Navarro-Polanco, Eloy G. Moreno-Galindo, Javier Alamilla","doi":"10.1002/jnr.25331","DOIUrl":"https://doi.org/10.1002/jnr.25331","url":null,"abstract":"<p>Circadian rhythms synchronize to light through the retinohypothalamic tract (RHT), which is a bundle of axons coming from melanopsin retinal ganglion cells, whose synaptic terminals release glutamate to the ventral suprachiasmatic nucleus (SCN). Activation of AMPA–kainate and NMDA postsynaptic receptors elicits the increase in intracellular calcium required for triggering the signaling cascade that ends in phase shifts. During aging, there is a decline in the synchronization of circadian rhythms to light. With electrophysiological (whole-cell patch-clamp) and immunohistochemical assays, in this work, we studied pre- and postsynaptic properties between the RHT and ventral SCN neurons in young adult (P90–120) and old (P540–650) C57BL/6J mice. Incremental stimulation intensities (applied on the optic chiasm) induced much lesser AMPA–kainate postsynaptic responses in old animals, implying a lower recruitment of RHT fibers. Conversely, a higher proportion of old SCN neurons exhibited synaptic facilitation, and variance–mean analysis indicated an increase in the probability of release in RHT terminals. Moreover, both spontaneous and miniature postsynaptic events displayed larger amplitudes in neurons from aged mice, whereas analysis of the NMDA and AMPA–kainate components (evoked by RHT electrical stimulation) disclosed no difference between the two ages studied. Immunohistochemistry revealed a bigger size in the puncta of vGluT2, GluN2B, and GluN2A of elderly animals, and the number of immunopositive particles was increased, but that of PSD-95 was reduced. All these synaptic adaptations could be part of compensatory mechanisms in the glutamatergic signaling to ameliorate the loss of RHT terminals in old animals.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 4","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140633830","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}
Deepak Kumbhare, George Weistroffer, Sofia Goyanaga, Zi Ling Huang, Jacob Blagg, Mark S. Baron
{"title":"Parkinsonism originates in a discrete secondary and dystonia in a primary motor cortical-basal ganglia subcircuit","authors":"Deepak Kumbhare, George Weistroffer, Sofia Goyanaga, Zi Ling Huang, Jacob Blagg, Mark S. Baron","doi":"10.1002/jnr.25328","DOIUrl":"https://doi.org/10.1002/jnr.25328","url":null,"abstract":"<p>Although manifesting contrasting phenotypes, Parkinson's disease and dystonia, the two most common movement disorders, can originate from similar pathophysiology. Previously, we demonstrated that lesioning (silencing) of a discrete dorsal region in the globus pallidus (rodent equivalent to globus pallidus externa) in rats and produced parkinsonism, while lesioning a nearby ventral hotspot-induced dystonia. Presently, we injected fluorescent-tagged multi-synaptic tracers into these pallidal hotspots (<i>n</i> = 36 Long Evans rats) and permitted 4 days for the viruses to travel along restricted connecting pathways and reach the motor cortex before sacrificing the animals. Viral injections in the Parkinson's hotspot fluorescent labeled a circumscribed region in the secondary motor cortex, while injections in the dystonia hotspot labeled within the primary motor cortex. Custom probability mapping and N200 staining affirmed the segregation of the cortical territories for Parkinsonism and dystonia to the secondary and primary motor cortices. Intracortical microstimulation localized territories specifically to their respective rostral and caudal microexcitable zones. Parkinsonian features are thus explained by pathological signaling within a secondary motor subcircuit normally responsible for initiation and scaling of movement, while dystonia is explained by abnormal (and excessive) basal ganglia signaling directed at primary motor corticospinal transmission.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 4","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25328","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140633829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Swetha B. M. Gowda, Ayesha Banu, Sadam Hussain, Farhan Mohammad
{"title":"Neuronal mechanisms regulating locomotion in adult Drosophila","authors":"Swetha B. M. Gowda, Ayesha Banu, Sadam Hussain, Farhan Mohammad","doi":"10.1002/jnr.25332","DOIUrl":"https://doi.org/10.1002/jnr.25332","url":null,"abstract":"<p>The coordinated action of multiple leg joints and muscles is required even for the simplest movements. Understanding the neuronal circuits and mechanisms that generate precise movements is essential for comprehending the neuronal basis of the locomotion and to infer the neuronal mechanisms underlying several locomotor-related diseases. <i>Drosophila melanogaster</i> provides an excellent model system for investigating the neuronal circuits underlying motor behaviors due to its simple nervous system and genetic accessibility. This review discusses current genetic methods for studying locomotor circuits and their function in adult <i>Drosophila</i>. We highlight recently identified neuronal pathways that modulate distinct forward and backward locomotion and describe the underlying neuronal control of leg swing and stance phases in freely moving flies. We also report various automated leg tracking methods to measure leg motion parameters and define inter-leg coordination, gait and locomotor speed of freely moving adult flies. Finally, we emphasize the role of leg proprioceptive signals to central motor circuits in leg coordination. Together, this review highlights the utility of adult <i>Drosophila</i> as a model to uncover underlying motor circuitry and the functional organization of the leg motor system that governs correct movement.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 4","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140632041","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":"Correction to Increased hippocampal cannabinoid 1 receptor expression is associated with protection from severe seizures in pregnant mice with reduced uterine perfusion pressure","authors":"","doi":"10.1002/jnr.25326","DOIUrl":"https://doi.org/10.1002/jnr.25326","url":null,"abstract":"<p>Jones-Muhammad, M., Pryor, T., Shao, Q., Freeman, K. B., & Warrington, J. P. (2023). Increased hippocampal cannabinoid 1 receptor expression is associated with protection from severe seizures in pregnant mice with reduced uterine perfusion pressure. <i>Journal of Neuroscience Research</i>, <i>101</i>, 1884–1899. https://doi.org/10.1002/jnr.25244</p><p>In this article, the pregnancy dates were incorrectly counted, leading to an error where all listed gestational days are 1 day later than they actually were. For example, the gestational day for the Sham and RUPP surgery was GD 12.5 instead of 13.5 as stated. Additionally, the date for the seizure induction and analysis, and tissue harvest occurred on GD 17.5 instead of 18.5 as stated in the original article. We have now corrected the gestational days wherever they appeared in the article. The gestational age error does not change the major conclusions of this research.</p><p>We apologize for this error.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 4","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25326","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140559492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Coralie Mignot, Susanne Weise, Dino Podlesek, Georg Leonhardt, Moustafa Bensafi, Thomas Hummel
{"title":"What do brain oscillations tell about the human sense of smell?","authors":"Coralie Mignot, Susanne Weise, Dino Podlesek, Georg Leonhardt, Moustafa Bensafi, Thomas Hummel","doi":"10.1002/jnr.25335","DOIUrl":"https://doi.org/10.1002/jnr.25335","url":null,"abstract":"<p>Brain activity may manifest itself as oscillations which are repetitive rhythms of neuronal firing. These local field potentials can be measured via intracranial electroencephalography (iEEG). This review focuses on iEEG used to map human brain structures involved in olfaction. After presenting the methodology of the review, a summary of the brain structures involved in olfaction is given, followed by a review of the literature on human olfactory oscillations in different contexts. A single case is provided as an illustration of the olfactory oscillations. Overall, the timing and sequence of oscillations found in the different structures of the olfactory system seem to play an important role for olfactory perception.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 4","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25335","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140606246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}