{"title":"Evolution of Astrocyte-Neuron Interactions Across Species.","authors":"Caterina Ciani, Maria Ayub, Carmen Falcone","doi":"10.1007/978-3-031-64839-7_1","DOIUrl":"10.1007/978-3-031-64839-7_1","url":null,"abstract":"<p><p>Proper functioning of the central nervous system depends on various tightly regulated phenomena, among which astrocyte-neuron interactions are of critical importance. Various studies across the species have highlighted the diverse yet crucial roles of astrocytes in regulating the nervous system development and functions. In simpler organisms like worms or insects, astrocyte-like cells govern basic functions such as structural support to neurons or regulation of extracellular ions. As the species complexity increases, so does the functional and morphological complexity of astrocytes. For example, in fish and amphibians, these cells are involved in synaptic development and ion homeostasis, while in reptiles and birds, astrocytes regulate synaptic transmission and plasticity and are reported to be involved in complex behaviors. Other species like those belonging to mammals and, in particular, primates have a heterogeneous population of astrocytes, exhibiting region-specific functional properties. In primates, these cells are responsible for proper synaptic transmission, neurotransmitter release and metabolism, and higher cognitive functions like learning, memory, or information processing. This chapter highlights the well-established and somewhat conserved roles of astrocytes and astrocyte-neuron interactions across the evolution of both invertebrates and vertebrates.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"39 ","pages":"1-17"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142071749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eva Šimončičová, Keelin Henderson Pekarik, Haley A Vecchiarelli, Clotilde Lauro, Laura Maggi, Marie-Ève Tremblay
{"title":"Adult Neurogenesis, Learning and Memory.","authors":"Eva Šimončičová, Keelin Henderson Pekarik, Haley A Vecchiarelli, Clotilde Lauro, Laura Maggi, Marie-Ève Tremblay","doi":"10.1007/978-3-031-55529-9_13","DOIUrl":"https://doi.org/10.1007/978-3-031-55529-9_13","url":null,"abstract":"<p><p>Neural plasticity can be defined as the ability of neural circuits to be shaped by external and internal factors. It provides the brain with a capacity for functional and morphological remodelling, with many lines of evidence indicating that these changes are vital for learning and memory formation. The basis of this brain plasticity resides in activity- and experience-driven modifications of synaptic strength, including synaptic formation, elimination or weakening, as well as of modulation of neuronal population, which drive the structural reorganization of neural networks. Recent evidence indicates that brain-resident glial cells actively participate in these processes, suggesting that mechanisms underlying plasticity in the brain are multifaceted. Establishing the 'tripartite' synapse, the role of astrocytes in modulating synaptic transmission in response to neuronal activity was recognized first. Further redefinition of the synapse as 'quad-partite' followed to acknowledge the contribution of microglia which were revealed to affect numerous brain functions via dynamic interactions with synapses, acting as 'synaptic sensors' that respond to neuronal activity and neurotransmitter release, as well as crosstalk with astrocytes. Early studies identified microglial ability to dynamically survey their local brain environment and established their integral role in the active interfacing of environmental stimuli (both internal and external), with brain plasticity and remodelling. Following the introduction to neurogenesis, this chapter details the role that microglia play in regulating neurogenesis in adulthood, specifically as it relates to learning and memory, as well as factors involved in modulation of microglia. Further, a microglial perspective is introduced for the context of environmental enrichment impact on neurogenesis, learning and memory across states of stress, ageing, disease and injury.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"37 ","pages":"221-242"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142103361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eleni H Moschonas, Ellen M Annas, Jonathan Zamudio-Flores, Jessica M Jarvis, Naima Lajud, Corina O Bondi, Anthony E Kline
{"title":"Pediatric Traumatic Brain Injury: Models, Therapeutics, and Outcomes.","authors":"Eleni H Moschonas, Ellen M Annas, Jonathan Zamudio-Flores, Jessica M Jarvis, Naima Lajud, Corina O Bondi, Anthony E Kline","doi":"10.1007/978-3-031-69832-3_7","DOIUrl":"https://doi.org/10.1007/978-3-031-69832-3_7","url":null,"abstract":"<p><p>Pediatric traumatic brain injury (TBI) is a significant healthcare issue, but potential treatments are absent despite robust investigation in several clinical trials. Factors attributed to clinical TBI, such as heterogeneity of injury and single-dose pharmacological treatments as well as timing of administration, may be reasons for the negative studies. Preclinical models of TBI can reduce some of the impediments by highlighting differences in injury depending on injury severity and location and by conducting dose response studies, thus providing better therapeutic targets and pharmacological profiles for clinical use. In this chapter, there were sufficient reports to make comparisons between the models in terms of pathophysiology, behavioral dysfunction, and the efficacy of therapeutic interventions. The models used to date include controlled cortical impact (CCI), weight drop, fluid percussion, and abusive head trauma. Several therapeutics were identified after CCI injury but none in the other models, which underscores the need for studies evaluating the therapies reported after CCI injury as well as novel potential approaches.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"42 ","pages":"147-163"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142455764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Dementia and Depression Among Older Adults Following Traumatic Brain Injury.","authors":"Mira H Ghneim, Meaghan Broderick, Deborah M Stein","doi":"10.1007/978-3-031-69832-3_5","DOIUrl":"https://doi.org/10.1007/978-3-031-69832-3_5","url":null,"abstract":"<p><p>Traumatic brain injuries are increasingly common in older adults and represent a substantial source of morbidity and mortality for this population. In addition to the impact from the primary insult, TBI can lead to a variety of chronic neurocognitive conditions including dementia, depression, and sleep disturbances. When caused by TBI, these conditions differ importantly from their non-TBI-related counterparts. Much about how TBI relates to the development of these conditions is unknown, and more research is needed to further elucidate optimal treatment strategies.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"42 ","pages":"99-118"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142455760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Engrams of Fear Memory Attenuation.","authors":"Johannes Gräff","doi":"10.1007/978-3-031-62983-9_9","DOIUrl":"https://doi.org/10.1007/978-3-031-62983-9_9","url":null,"abstract":"<p><p>Fear attenuation is an etiologically relevant process for animal survival, since once acquired information needs to be continuously updated in the face of changing environmental contingencies. Thus, when situations are encountered that were originally perceived as fearful but are no longer so, fear must be attenuated, otherwise, it risks becoming maladaptive. But what happens to the original memory trace of fear during fear attenuation? In this chapter, we review the studies that have started to approach this question from an engram perspective. We find evidence pointing to both the original memory trace of fear being suppressed, as well as it being updated towards safety. These seemingly conflicting results reflect a well-established dichotomy in the field of fear memory attenuation, namely whether fear attenuation is mediated by an inhibitory mechanism that suppresses fear expression, called extinction, or by an updating mechanism that allows the fear memory to reconsolidate in a different form, called reconsolidation-updating. Which of these scenarios takes the upper hand is ultimately influenced by the behavioral paradigms used to induce fear attenuation, but is an important area for further study as the precise cell populations underlying fear attenuation and the molecular mechanisms therein can now be understood at unprecedented resolution.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"38 ","pages":"149-161"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141615640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Adult Neurogenesis, Context Encoding, and Pattern Separation: A Pathway for Treating Overgeneralization.","authors":"Wei-Li Chang, Rene Hen","doi":"10.1007/978-3-031-62983-9_10","DOIUrl":"https://doi.org/10.1007/978-3-031-62983-9_10","url":null,"abstract":"<p><p>In mammals, the subgranular zone of the dentate gyrus is one of two brain regions (with the subventricular zone of the olfactory bulb) that continues to generate new neurons throughout adulthood, a phenomenon known as adult hippocampal neurogenesis (AHN) (Eriksson et al., Nat Med 4:1313-1317, 1998; García-Verdugo et al., J Neurobiol 36:234-248, 1998). The integration of these new neurons into the dentate gyrus (DG) has implications for memory encoding, with unique firing and wiring properties of immature neurons that affect how the hippocampal network encodes and stores attributes of memory. In this chapter, we will describe the process of AHN and properties of adult-born cells as they integrate into the hippocampal circuit and mature. Then, we will discuss some methodological considerations before we review evidence for the role of AHN in two major processes supporting memory that are performed by the DG. First, we will discuss encoding of contextual information for episodic memories and how this is facilitated by AHN. Second, will discuss pattern separation, a major role of the DG that reduces interference for the formation of new memories. Finally, we will review clinical and translational considerations, suggesting that stimulation of AHN may help decrease overgeneralization-a common endophenotype of mood, anxiety, trauma-related, and age-related disorders.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"38 ","pages":"163-193"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141615623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sylvana Stephano Zuniga, Marcela Rodriguez Flores, Adriana Albu
{"title":"Role of Endogenous Opioids in the Pathophysiology of Obesity and Eating Disorders.","authors":"Sylvana Stephano Zuniga, Marcela Rodriguez Flores, Adriana Albu","doi":"10.1007/978-3-031-45493-6_17","DOIUrl":"10.1007/978-3-031-45493-6_17","url":null,"abstract":"<p><p>This second chapter in our trilogy reviews and critically appraises the scientific evidence for the role of endogenous opioid system (EOS) activity in the onset and progression of both obesity and eating disorders. Defining features of normative eating and maladaptive eating behaviors are discussed as a foundation. We review the scientific literature pertaining to the predisposing risk factors and pathophysiology for obesity and eating disorders. Research targeting the association between obesity, disordered eating, and psychiatric comorbidities is reviewed. We conclude by discussing the involvement of endogenous opioids in neurobiological and behavior traits, and the clinical evidence for the role of the EOS in obesity and eating disorders.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"35 ","pages":"329-356"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141316492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nicholas J Felicione, Melissa D Blank, Casey D Wright, Daniel W McNeil
{"title":"Pain, Fear, Anxiety, and Stress: Relations to the Endogenous Opioid System.","authors":"Nicholas J Felicione, Melissa D Blank, Casey D Wright, Daniel W McNeil","doi":"10.1007/978-3-031-45493-6_9","DOIUrl":"10.1007/978-3-031-45493-6_9","url":null,"abstract":"<p><p>Pain, fear, stress, and anxiety are separate yet interrelated phenomena. Each of these concepts has an extensive individual body of research, with some more recent work focusing on points of conceptual overlap. The role of the endogenous opioid system in each of these phenomena is only beginning to be examined and understood. Research examining the ways in which endogenous opioids (e.g., beta-endorphin; βE) may mediate the relations among pain, fear, stress, and anxiety is even more nascent. This chapter explores the extant evidence for endogenous opioid activity as an underpinning mechanism of these related constructs, with an emphasis on research examining βE.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"35 ","pages":"157-182"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141316490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Multilayer Analysis of RNA Sequencing Data in Alzheimer's Disease to Unravel Molecular Mysteries.","authors":"Dilara Uzuner, Atılay İlgün, Elif Düz, Fatma Betül Bozkurt, Tunahan Çakır","doi":"10.1007/978-3-031-69188-1_9","DOIUrl":"https://doi.org/10.1007/978-3-031-69188-1_9","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a complex disease, and numerous cellular events may be involved in etiology. RNAseq-based transcriptome data hold multilayer information content, which could be crucial in unraveling molecular mysteries of AD. It enables quantification of gene expression levels, identification of genomic variants, and elucidation of splicing anomalies such as exon skipping and intron retention. Additional integration of this information into protein-protein interaction networks and genome-scale metabolic models from the literature has potential to decipher functional modules and affected mechanisms for complex scenarios such as AD. In this chapter, we review the application areas of the multilayer content of RNAseq and associated integrative approaches available, with a special focus on AD.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"41 ","pages":"219-246"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142714778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Alzheimer's Disease from Modeling to Mechanism Research.","authors":"Xiaoyan Sun, Weiqi Zhang","doi":"10.1007/978-3-031-69188-1_7","DOIUrl":"https://doi.org/10.1007/978-3-031-69188-1_7","url":null,"abstract":"<p><p>As our population continues to age, the search for effective therapeutic strategies to combat neurodegenerative diseases, particularly Alzheimer's disease (AD), has become more pressing than ever. For over a decade, researchers have focused on the amyloid cascade hypothesis in their pursuit of new drugs for AD. However, with numerous drugs targeting this hypothesis failing in clinical trials, it is clear that AD's pathogenesis is complex, and each individual may display significant heterogeneity. Consequently, treatment has shifted to focus on multiple targets and early AD detection. Furthermore, there is an urgent need to develop new models that address the shortcomings of current rodent models, which have species differences. The organoid model, a newly developed model, appears to be the future direction, but it must overcome some system immaturity problems.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"41 ","pages":"153-170"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142714839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}