Cell proliferation in the repairing adult insect central nervous system: incorporation of the thymidine analogue 5-bromo-2-deoxyuridine in vivo

1990 ◽  
Vol 95 (4) ◽  
pp. 599-604
Author(s):  
P.J. Smith ◽  
E.A. Howes ◽  
J.E. Treherne

Uptake of the thymidine analogue 5-bromo-2-deoxyuridine into non-neuronal cells of the insect central nervous system has been examined following a controlled lesioning of the glial elements. The pattern of BUdR labelling along the penultimate abdominal connective was examined over a period of 17 days. Cell proliferation occurred in and immediately around the site of damage in both perineurial and subperineurial glial cells but at different times post-lesion for the two regions. Proliferation in the perineurial zone was maximal at 6–8 days post-lesion but continued for at least 17 days. Subperineurial proliferation was less dramatic and peaked between days 8–11 post-lesion. In both areas division appears to be confined to the reactive glial cells. These results are discussed in the context of past research on this system, particularly with regard to the restoration of the blood-brain barrier.

2006 ◽  
Vol 83 (8) ◽  
pp. 1425-1431 ◽  
Author(s):  
Robert P. Lisak ◽  
Beverly Bealmear ◽  
Liljana Nedelkoska ◽  
Joyce A. Benjamins

2018 ◽  
Vol 283 ◽  
pp. 126-134 ◽  
Author(s):  
Satoshi Zeniya ◽  
Hiroya Kuwahara ◽  
Kaiichi Daizo ◽  
Akihiro Watari ◽  
Masuo Kondoh ◽  
...  

1992 ◽  
Vol 116 (6) ◽  
pp. 1455-1464 ◽  
Author(s):  
R Curtis ◽  
H J Stewart ◽  
S M Hall ◽  
G P Wilkin ◽  
R Mirsky ◽  
...  

Recently it has been demonstrated that the growth-associated protein GAP-43 is not confined to neurons but is also expressed by certain central nervous system glial cells in tissue culture and in vivo. This study has extended these observations to the major class of glial cells in the peripheral nervous system, Schwann cells. Using immunohistochemical techniques, we show that GAP-43 immunoreactivity is present in Schwann cell precursors and in mature non-myelin-forming Schwann cells both in vitro and in vivo. This immunoreactivity is shown by Western blotting to be a membrane-associated protein that comigrates with purified central nervous system GAP-43. Furthermore, metabolic labeling experiments demonstrate definitively that Schwann cells in culture can synthesize GAP-43. Mature myelin-forming Schwann cells do not express GAP-43 but when Schwann cells are removed from axonal contact in vivo by nerve transection GAP-43 expression is upregulated in nearly all Schwann cells of the distal stump by 4 wk after denervation. In contrast, in cultured Schwann cells GAP-43 is not rapidly upregulated in cells that have been making myelin in vivo. Thus the regulation of GAP-43 appears to be complex and different from that of other proteins associated with nonmyelin-forming Schwann cells such as N-CAM, glial fibrillary acidic protein, A5E3, and nerve growth factor receptor, which are rapidly upregulated in myelin-forming cells after loss of axonal contact. These observations suggest that GAP-43 may play a more general role in the nervous system than previously supposed.


1987 ◽  
Vol 132 (1) ◽  
pp. 59-78 ◽  
Author(s):  
P. J. Smith ◽  
E. A. Howes ◽  
J. E. Treherne

As in other repairing systems, glial regeneration in insect central nervous connectives, following selective chemical lesioning, involves both exogenous and endogenous elements. Our current evidence, including that obtained with monoclonal antibodies, indicates that the reactive, granule-containing cells are derived from a sub-population of circulating haemocytes which, within 24 h, invade, and are restricted to, the lesion zone. The granule-containing cells are involved in the initial repair of the perineurial region. They also contribute to the first stage in the restoration of the blood-brain barrier and are responsible for recruiting reactive endogenous glia, apparently from the vicinity of the anterior abdominal ganglion. The granule-containing cells transform into or are replaced by functional glia between 3 and 5 days after selective glial disruption, coincident with the appearance in the lesion zone of dividing reactive cells.


2021 ◽  
Vol 3 ◽  
Author(s):  
Vasco Meneghini ◽  
Marco Peviani ◽  
Marco Luciani ◽  
Giada Zambonini ◽  
Angela Gritti

Glial cells (astrocytes, oligodendrocytes, and microglia) are emerging as key players in several physiological and pathological processes of the central nervous system (CNS). Astrocytes and oligodendrocytes are not only supportive cells that release trophic factors or regulate energy metabolism, but they also actively modulate critical neuronal processes and functions in the tripartite synapse. Microglia are defined as CNS-resident cells that provide immune surveillance; however, they also actively contribute to shaping the neuronal microenvironment by scavenging cell debris or regulating synaptogenesis and pruning. Given the many interconnected processes coordinated by glial cells, it is not surprising that both acute and chronic CNS insults not only cause neuronal damage but also trigger complex multifaceted responses, including neuroinflammation, which can critically contribute to the disease progression and worsening of symptoms in several neurodegenerative diseases. Overall, this makes glial cells excellent candidates for targeted therapies to treat CNS disorders. In recent years, the application of gene editing technologies has redefined therapeutic strategies to treat genetic and age-related neurological diseases. In this review, we discuss the advantages and limitations of clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9-based gene editing in the treatment of neurodegenerative disorders, focusing on the development of viral- and nanoparticle-based delivery methods for in vivo glial cell targeting.


Author(s):  
Alexandria N. Hughes

Building a functional nervous system requires the coordinated actions of many glial cells. In the vertebrate central nervous system (CNS), oligodendrocytes myelinate neuronal axons to increase conduction velocity and provide trophic support. Myelination can be modified by local signaling at the axon-myelin interface, potentially adapting sheaths to support the metabolic needs and physiology of individual neurons. However, neurons and oligodendrocytes are not wholly responsible for crafting the myelination patterns seen in vivo. Other cell types of the CNS, including microglia and astrocytes, modify myelination. In this review, I cover the contributions of non-neuronal, non-oligodendroglial cells to the formation, maintenance, and pruning of myelin sheaths. I address ways that these cell types interact with the oligodendrocyte lineage throughout development to modify myelination. Additionally, I discuss mechanisms by which these cells may indirectly tune myelination by regulating neuronal activity. Understanding how glial-glial interactions regulate myelination is essential for understanding how the brain functions as a whole and for developing strategies to repair myelin in disease.


2021 ◽  
Author(s):  
Elif S. Seven ◽  
Yasin B. Seven ◽  
Yiqun Zhou ◽  
Sijan Poudel-Sharma ◽  
Juan J. Diaz Rucco ◽  
...  

The blood-brain barrier (BBB) is a major obstacle for drug delivery to the central nervous system (CNS) such that most therapeutics lack efficacy against brain tumors or neurological disorders due...


2021 ◽  
Author(s):  
Amélie Barthelemy ◽  
Valérie Demais ◽  
Izabela-Cristina Stancu ◽  
Eugeniu Vasile ◽  
Tom Houben ◽  
...  

AbstractNiemann-Pick type C (NPC) disease is a rare and fatal lysosomal storage disorder presenting severe neurovisceral symptoms. Disease-causing mutations in genes encoding either NPC1 or NPC2 protein provoke accumulation of cholesterol and other lipids in specific structures of the endosomal-lysosomal system and degeneration of specific cells, notably neurons in the central nervous system (CNS). 2-hydroxypropyl-beta-cyclodextrin (CD) emerged as potential therapeutic approach based on animal studies and clinical data, but the mechanism of action on neurons has remained unclear. To address this topic in vivo, we took advantage of the retina as highly accessible part of the (CNS) and intravitreal injections as mode of drug administration. We find that CD enters the endosomal-lysosomal system of neurons and enables the release of lipid-laden lamellar inclusions, which are then removed from the extracellular space by specific types of glial cells. Thus, CD triggers a concerted action of neurons and glial cells to restore lipid homeostasis in the central nervous system.


Author(s):  
Sarah A. Neely ◽  
David A. Lyons

The term glia describes a heterogenous collection of distinct cell types that make up a large proportion of our nervous system. Although once considered the glue of the nervous system, the study of glial cells has evolved significantly in recent years, with a large body of literature now highlighting their complex and diverse roles in development and throughout life. This progress is due, in part, to advances in animal models in which the molecular and cellular mechanisms of glial cell development and function as well as neuron-glial cell interactions can be directly studied in vivo in real time, in intact neural circuits. In this review we highlight the instrumental role that zebrafish have played as a vertebrate model system for the study of glial cells, and discuss how the experimental advantages of the zebrafish lend themselves to investigate glial cell interactions and diversity. We focus in particular on recent studies that have provided insight into the formation and function of the major glial cell types in the central nervous system in zebrafish.


2018 ◽  
Vol 216 (1) ◽  
pp. 71-83 ◽  
Author(s):  
Kevin A. Guttenplan ◽  
Shane A. Liddelow

Glial cells serve as fundamental regulators of the central nervous system in development, homeostasis, and disease. Discoveries into the function of these cells have fueled excitement in glial research, with enthusiastic researchers addressing fundamental questions about glial biology and producing new scientific tools for the community. Here, we outline the pros and cons of in vivo and in vitro techniques to study astrocytes and microglia with the goal of helping researchers quickly identify the best approach for a given research question in the context of glial biology. It is truly a great time to be a glial biologist.


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