NTR is another suicide gene where expression alone is not toxic, but the enzyme metabolizes systemically given prodrugs into a toxic agent. The advantage of the NTR over the suicide genes mentioned earlier is that they are not only targeted to proliferating cells, producing toxic agents that are independent of proliferation Knox et al. Khurgel et al. The depletion was accompanied by some microglial reactivity but without effects in neuronal density.
In contrast to the functional outcome after the drug-induced astrocyte ablation Khurgel et al. With this specific approach, predominantly Bergmann glia, an astrocytic subtype located in the cerebellum, were targeted in mice. The gross ablation of Bergmann glia resulted in severe developmental problems in the motor coordination of these mice, resembling a hallmark of cerebellar dysfunction.
The regional specificity of the ablation observed might be explained by how the mouse line they generated was used, as NTR-expression was detected mainly in these cells.
Shortly after tamoxifen application, mice suffered axonal degeneration accompanied by paralysis of all limbs, while the BBB remained intact. These results raise the hypothesis that a GFAP-expressing subset of astrocytes is crucial for the maintenance of neuronal health and integrity, while other astrocytes are devoted to other functions, such as the BBB maintenance.
In addition, the latter study was carried out much earlier during development at embryonic stages. This could add to the different outcomes, as these early appearing astrocytes might have other functions in the CNS than during adult stages, or because the compensation mechanisms during development are more supportive than in the adult.
L-AAA , different areas of interest spinal cord vs. Astrocytes exhibit many different morphologies and accordingly different functions depending on the CNS region Robel et al. Therefore genes expressed under the GFAP-promoter might only be displayed in a subset of astrocytes with potentially specific functions that are different from other resident astrocytes.
Moreover, these studies used different readouts in their analysis and some aspects, like the BBB closure or neuronal damage, might simply have been overlooked. Thus far, no study using genetic GFAP-driven approaches has achieved ablation of cortical astrocytes under physiological conditions in the adult brain, most likely due to the lack of promoter-expression in these cells.
To achieve ablation of cortical astrocytes, other promoters that are strongly expressed in astrocytic populations of the cerebral cortex should be considered. In summary, these studies demonstrated different methods to induce the depletion of astrocytes from at least some parts of the CNS and support the idea of astrocytes being important for neuronal and axonal integrity on a functional basis Figure 2 ; Table 2. These ablation models could be exploited in further experiments to address specific interaction points between astrocytes and neurons.
Most interestingly — in contrast to other glial cell types — no studies exist that deal with the repopulation dynamics of astrocytes after ablation or the long term effects of this ablation, which could also be a very illuminating topic of interest. Effects and dynamics of astrocyte ablation under healthy and pathological conditions.
For the astrocytes, the repopulation kinetics have not been analysed in detail yet, but these cells were also shown to repopulate the depleted area. As a functional outcome, the ablation did either not show an effect or had a negative effect on neuronal survival in the cerebellum and the spinal cord. However, with this model only the pool of proliferating astrocytes can be depleted.
The reduction of scar forming astrocytes in general had a negative outcome for the injury size and severity in spinal cord injury SCI , mechanical brain injury and EAE. It did not affect the pathology in a model of ALS, but this could be due to the low amount of proliferating astrocytes in this model. Astrogliosis displays a very broad spectrum of reactivity, the hallmarks thereof being the upregulation of structural proteins like GFAP or vimentin and the hypertrophy of both the cell body and the processes Wilhelmsson et al.
Additionally, some quiescent astrocytes re-enter the cell cycle Buffo et al. Reactive astrocytes are also known to elongate around the lesion core Wanner et al. Interestingly, as shown by repetitive in vivo imaging, astrocytes are — unlike microglia and NG2-glia — unable to migrate into the injury core after mechanical injury Bardehle et al.
Although many aspects of astrocyte-specific reactions to injury are already known, their precise role in scar formation under different pathological conditions remains unresolved. As this question has long been of great interest, studies that specifically ablate these scar forming astrocytes have already been reported almost 20 years ago. Notably, in contrast to physiological conditions, no studies have attempted to ablate astrocytes under pathological conditions using pharmacological approaches, in contrast to genetic ones that were normally used see Table 2 bottom part.
The population targeted when utilizing the GFAP-promoter in pathological conditions is predicted to be much higher and might even go beyond the specific subset of cells observed in healthy tissue. This is because a huge proportion of cortical astrocytes upregulate GFAP upon any changes in brain homeostasis Takamiya et al.
The pathological conditions examined with this approach spanned a broad range from neurodegenerative diseases to traumatic brain injury. With this ablation model, already within 1 week a myelin oligodendrocyte glycoprotein MOG -induced model of EAE, which mainly shows pathology in the spinal cord, showed robust astrocytic death that resulted in a failure of tissue scar formation, increased immune cell infiltration as well as a worsened clinical score Voskuhl et al.
Mechanical injury to the brain identified similar findings to studies in the spinal cord, but with greater effect. The brain suffered more detrimental injury and greater damage, which was induced by robust astrocyte ablation after 7 days of ganciclovir treatment Bush et al.
All these studies — independent of the pathological conditions — presented an exacerbation of the disease outcome after the ablation of astrocytes, with only two exceptions presenting contradictory results. Skripuletz et al.
In contrast to the other studies, less immune cell activation — in this case specifically microglia — could be observed, resulting in less efficient myelin clearance. One explanation for this different outcome could be due to the cell types involved: while all other pathological models include the recruitment of peripheral immune cells for debris clearance, the cuprizone model mainly relies on resident brain cells Kipp et al.
Moreover, astrocytes might play different roles in diverse pathological conditions. Along the same line, no effect could be found on disease onset, duration, neuronal loss or motor function in astrocyte ablated mice for two different models of neurodegenerative diseases injection of the neuroadapted Sindbis virus NSV inducing neuronal death as well as in a genetic model of ALS Lepore et al.
However, the number of proliferating astrocytes in these neurodegenerative disease models is relatively low in comparison to the other models of pathology. These contradictory results might simply be an effect of low numbers of ablated astrocytes and more remaining ones that are able to react, rather than of their function. In summary, the ablation of astrocytes under pathological conditions has given a clear functional readout for the first time: astrocytes play a crucial role in the maintenance of the diseased tissue and in the inhibition of secondary tissue damage by blocking inflammation Figure 2 ; Table 2.
This interpretation has to be taken with care, as only proliferating astrocytes were ablated in all the approaches described above, while the non-proliferating cells retained normal function that might be different or even opposing to that of the proliferating ones.
Moreover, it is now textbook knowledge that although scar forming astrocytes are beneficial to injury, they also have detrimental effects on tissue regeneration Pekny and Pekna, ; Sofroniew, These aspects were only slightly addressed in the experiments mentioned above, giving space for further ablation approaches in the future.
Although NG2-glia are precursors of mature oligodendrocytes within the oligodendrocyte lineage, they are often considered an independent glial population due to their additional characteristics. In relation to the long history of neuroscience, NG2-glia are a relatively young cell type in terms of discovery with identification only 30 years ago ffrench-Constant and Raff, Although a great amount of work has been performed on these cells, the cellular function of NG2-glia — at least in the adult brain — remains largely a mystery.
However, many cellular characteristics have been described: NG2-glia are part of the oligodendrocyte lineage and keep generating mature myelinating oligodendrocytes throughout lifetime Dimou et al. Most interestingly NG2-glia in the adult rodent brain form a tight homeostatic network in which the cell numbers are maintained under physiological conditions. As soon as one cell has been lost due to either differentiation or cell death, the remaining gap is immediately replaced by a neighboring cell Hughes et al.
Furthermore, NG2-glia are the only highly proliferative cells in the brain parenchyma Dimou et al. The most curious aspect of NG2-glia is their ability to form functional synapses with neurons, originally discovered in the hippocampus Bergles et al. The function of these synapses is not well understood. One interesting aspect of these synapses is the directionality, as NG2-glia are only able to receive neuronal signals but cannot create action potentials on their own and propagate them further De Biase et al.
The ablation approaches that are discussed in this section give some insight in the role s of NG2-glia in the adult brain. Further on in the lineage, the function of mature oligodendrocytes is clear: they are the myelin-producing cells that insulate axons to allow a rapid saltatory conduction and give trophic support to axons reviewed in Nave, But as high numbers of presumably non-myelinating oligodendrocytes are also present in sparsely myelinated brain regions like the gray matter of the cerebral cortex, some functional aspects may have been overlooked.
To address this question, specific oligodendrocyte ablation approaches may deepen our understanding of the functions of these cells. Although NG2-glia were only discovered a short time ago ffrench-Constant and Raff, , several approaches to deplete these cells from the adult brain have already been developed. As NG2-glia are well characterized on the cellular level, these approaches mainly aimed to clarify the physiological function of these cells.
However, most of these approaches have been rather disappointing until recently, both in terms of achieving a NG2-glia-free brain as well as in identifying the physiological function of these cells. The ablation of NG2-glia proved to be more difficult in comparison with other glial cell populations: due to their tightly regulated homeostasis Hughes et al. So far no method has successfully ablated all NG2-glia over a long period of time, as can be achieved successfully for microglia compare Table 3 and Figure 3.
Although technically quite different, all of the ablation approaches for NG2-glia commonly demonstrated the highly efficient repopulation capacity of resident NG2-glia, ranging from two to 6 weeks depending on the study. Two-photon in vivo imaging demonstrated the mechanism by which these cells become aware of their need for proliferation: they are able to sense cell-free gaps with their fine filopodia, triggering their migration or proliferation in order to fill the gap Hughes et al.
Interestingly, these repopulating cells seem to be less branched and occupy a smaller surface area Birey and Aguirre, However, this could change over time as the cells re-grow and re-gain their original cellular complexity. TABLE 3. NG2-glia ablation and differentiation block approaches under healthy conditions.
Effects and dynamics of NG2-glia ablation under healthy conditions. The very efficient repopulation occurred either immediately or between 2 and 6 weeks after the ablation, depending on the study. Although the function of NG2-glia has long been a mystery, recent studies showed that the NG2-glia ablation negatively affects the leptin-dependent energy metabolism and leads to a depression like behavior. Although the repopulation capacity of NG2-glia — independent of the ablation approach — has fundamentally proven to be fast, it declines with aging Chari et al.
In correlation with their slowing physiological cycling behavior, the cell cycle length increases with aging Psachoulia et al. Early studies depleting NG2-glia both in the spinal cord as well as in the brain with high-dose X-irradiation demonstrated an efficient repopulation within four to 6 weeks following the ablation treatment Chari and Blakemore, ; Irvine and Blakemore, The nature of these regional differences might either lie in a different cell cycle length of NG2-glia, as X-irradiation mainly affects fast cycling cells, or it may be an issue of different developmental origins or regional heterogeneity of those cells Kessaris et al.
The use of a single cell type-specific antibody to estimate the efficiency of depletion can lead to an overestimation since some proteins might be down-regulated upon a change in brain homeostasis, as shown for neurons after injury Pignataro et al. If this also holds true for NG2-glia, the X-irradiation method would solely lead to a failure to detect these cells with the use of an anti-NG2 antibody although they are still present.
NG2-glia are known to be the only proliferating cells outside the neurogenic niches in the healthy adult brain and therefore suspected to be the only cell type responding to X-irradiation. However, after a mild irradiation injury, other cells like microglia and astrocytes become reactive upon any cellular death, potentially triggering their proliferation in response to damage.
This would make them sensitive to irradiation-induced cellular death, hence weakening the cell type specificity of this method. A more specific and therefore more elegant way to follow the dynamics of ablation and repopulation of NG2-glia in vivo by overcoming the pitfalls of detection with different antibodies, is the use of genetically modified mouse lines to intrinsically label NG2-glia.
As this tamoxifen-inducible marker is permanently expressed under the ubiquitous Rosapromoter, the downregulation of this locus is very unlikely to happen.
Combining this mouse line with the intraventricular administration of AraC, a toxic agent interfering with the cellular DNA synthesis and inducing cell death in fast cycling but not slow or non-cycling cells Doetsch et al. This ablation was then followed by a subsequent, complete repopulation within 2 weeks. Furthermore, with the use of BrdU-labeling experiments, insights were provided that the repopulation of NG2-glia exclusively occurs through proliferation of surviving adjacent NG2-glia located in an area without AraC diffusion, but not from a NG2-negative stem cell source.
These first ablation studies fundamentally characterized the repopulation capacity of NG2-glia, but did not answer the question about the NG2-glia function in the adult brain. Two recently published NG2-glia ablation studies have so far directly addressed the functional outcome of an at least transient lack of NG2-glia Birey et al. Birey et al. This work therefore indicates that NG2-glia have a direct influence on the functionality and the properties of the neuronal network.
The mechanisms of this interaction still remains, however, a speculation. Djogo et al. In this work, it could be demonstrated that under physiological conditions NG2-glia in the hypothalamus contact dendritic processes of leptin receptor neurons which degenerate upon NG2-glia ablation, reducing leptin signaling. Hence, NG2-glia are essential to maintain the function of leptin receptor neurons in the hypothalamus, therefore proving for the first time a direct role for NG2-glia in the maintenance of the thalamic energy metabolism.
The need for these newly generated oligodendrocytes in the adulthood remains, however, not well understood.
A recent study tested the hypothesis whether chronic NG2-glia ablation also influences the oligodendrocyte differentiation and assessed potential functional consequences Schneider et al. This study took advantage of the above mentioned genetic ablation model in which the deletion of the cell cycle protein Esco2 driven by the Soxpromoter induces apoptosis of proliferating NG2-glia. This depletion of recombined cells yielded a reduced oligodendrogenesis that further resulted in an elongation of the nodes of Ranvier, reduction of the saltatory nerve conduction as well as in motor dysfunctions, therefore demonstrating the importance of constant oligodendrogenesis in the adult brain.
In line with the above mentioned study, it could be demonstrated that the lifelong oligodendrogenesis is required for physiological function of the brain — in this case in the very early stages of complex motor skill learning.
While the functional outcome of a NG2-glia ablation is just at the beginning of being understood, the role of oligodendrocytes and their ablation in the adult brain has been subjected to studies for several years compare Table 4 and Figure 4 , not only in the rodent CNS Vanderluit et al. Furthermore, a broad variety of demyelination models that are used to study Multiple Sclerosis MS like, e.
Effects and dynamics of oligodendrocyte ablation under healthy conditions. Very commonly, although very diverse in the use of promoters and suicide genes, these approaches induced oligodendrocyte death that in most cases resulted in primary demyelination followed by secondary induced neuronal damage.
These observations were in most cases accompanied by a behavioral phenotype resulting from demyelination. This phenotype could, however, take up to 50 weeks to appear, depending on the model. After a longer time, demyelination was followed by a spontaneous remyelination. Only one study observed axonal damage without global demyelination that could be due to the loss of trophic axonal support.
Since oligodendrocytes do not have particular unique features like being proliferative, all of the used approaches are taking advantage of a toxin-induced ablation system amongst which the DTA-system is the most common one in combination with promoters that are specific for oligodendrocytes summarized in Table 4.
DTA toxicity in oligodendrocytes was, e. This was accompanied with the development of an autoimmune response against myelin Traka et al. Already some time ago, Vanderluit et al. This LacZ-system approach allows the focal ablation of cells that can even be controlled in size, while all the other described studies used systemic drug application and hence targeted and ablated oligodendrocytes in the complete CNS.
However, this study did not report any functional outcome of the ablation but might be a good tool for future experiments. Despite the differences in the ablation approach and possibly the functional readout, all studies have in common that the death of myelinating oligodendrocytes leads to a primary demyelination with a persisting secondary induced axonal damage and a subsequent spontaneous remyelination Figure 4.
In most of the studies the demyelination and the axonal damage are accompanied by severe motor dysfunctions like tremor, ataxia as well as weight loss or even the development of seizures. Although there is a severe loss of myelin and an accumulation of myelin debris, one study reported about the absence of the development of an autoimmune-response, what is generally thought to happen during MS pathology Locatelli et al. Due to the widespread myelin loss, the biology of these models all together creates a perfect tool for studying remyelination besides analyzing the outcome of oligodendrocyte death.
Interestingly, Oluich et al. In summary, the specific ablation of both NG2-glia as well as oligodendrocytes using different approaches proved to be similarly effective than for the other glial cell types; in case of the NG2-glia at least transiently as they repopulate very fast see Table 3.
While for the oligodendrocytes the functional outcome of myelin loss and axonal damage seemed to be quite foreseeable Table 4 , the role of NG2-glia in the adult brain remains open and further ablation studies could give a deeper insight.
Many cellular characteristics of NG2-glia and their activation upon different pathologies have been well described. Like astrocytes and microglia, NG2-glia were shown to react to various kinds of pathological insults, however, only when accompanied with an opening of the BBB Rhodes et al. Two-photon in vivo imaging studies even revealed a very heterogeneous reaction of NG2-glia to injury: cell migration, proliferation, hypertrophy, and even combined reactions are possible Hughes et al.
Moreover, it became clear that NG2-glia strongly increase in number and align around the lesion site as part of the glial scar Levine et al. Besides these observations, the cellular role of NG2-glia under pathological conditions remains unresolved — comparable to the healthy brain.
Interestingly, unlike the other glial cell types, so far there are no published studies that specifically ablate NG2-glia under pathological conditions. However, as the ablation approaches under healthy conditions are quite successful — at least transiently — they seem to be a very promising tool to further tackle the functional role of these cells in pathology. In a similar way, there are also no studies where mature and myelinating oligodendrocytes have been specifically depleted from the adult brain under pathological conditions.
Probably these experiments are also very unlikely to be performed in the future, as oligodendrocytes were not shown to react to different kinds of injury besides providing new myelin during tissue repair, but remain rather stable. Furthermore, the death of oligodendrocytes induces global demyelination as well as axonal defects already under healthy conditions Vanderluit et al.
Summarizing this section, nothing has been published regarding ablation studies of oligodendrocyte lineage cells under pathological conditions. However, as especially for NG2-glia the already established methods have proven to be effective, very promising studies during pathological conditions will likely be investigated in the future.
This review summarizes the tremendous work of the last decades on the various ablation approaches in all types of glial cells in the adult brain see also Tables 1 — 4.
Although these methods especially under healthy conditions seem quite similar at first sight, the nature of the cells requires different methodologies. Using the DTA or DTR-system under a cell type specific promoter is a commonly shared and frequently used approach between all glial cell populations.
This method has the advantage that it does not require specific features like the expression of a uniquely expressed surface receptor that can be targeted by a drug or being a uniquely mitotically active cell population, but can be applied to all cell types in a similar fashion when used with a specific promoter. The side effects of this method also seem to be rather low and the efficiency quite high, wherefore this method is a very good candidate to be used for future ablation studies of any cell type.
The use of cell specific pharmacological drugs is still an applicable and successful method to ablate cells, but has been so far only exploited for microglia Elmore et al. Nervous systems throughout the animal kingdom vary in structure and complexity, as illustrated by the variety of animals shown in Figure Some organisms, like sea sponges, lack a true nervous system.
The insect nervous system is more complex but also fairly decentralized. It contains a brain, ventral nerve cord, and ganglia clusters of connected neurons. These ganglia can control movements and behaviors without input from the brain. Octopi may have the most complicated of invertebrate nervous systems—they have neurons that are organized in specialized lobes and eyes that are structurally similar to vertebrate species.
Compared to invertebrates, vertebrate nervous systems are more complex, centralized, and specialized. While there is great diversity among different vertebrate nervous systems, they all share a basic structure: a CNS that contains a brain and spinal cord and a PNS made up of peripheral sensory and motor nerves. One interesting difference between the nervous systems of invertebrates and vertebrates is that the nerve cords of many invertebrates are located ventrally whereas the vertebrate spinal cords are located dorsally.
The nervous system is made up of neurons , specialized cells that can receive and transmit chemical or electrical signals, and glia , cells that provide support functions for the neurons by playing an information processing role that is complementary to neurons.
A neuron can be compared to an electrical wire—it transmits a signal from one place to another. Glia can be compared to the workers at the electric company who make sure wires go to the right places, maintain the wires, and take down wires that are broken.
Although glia have been compared to workers, recent evidence suggests that also usurp some of the signaling functions of neurons. There is great diversity in the types of neurons and glia that are present in different parts of the nervous system. There are four major types of neurons, and they share several important cellular components. The nervous system of the common laboratory fly, Drosophila melanogaster , contains around , neurons, the same number as a lobster.
This number compares to 75 million in the mouse and million in the octopus. A human brain contains around 86 billion neurons. Despite these very different numbers, the nervous systems of these animals control many of the same behaviors—from basic reflexes to more complicated behaviors like finding food and courting mates.
The ability of neurons to communicate with each other as well as with other types of cells underlies all of these behaviors. Most neurons share the same cellular components. But neurons are also highly specialized—different types of neurons have different sizes and shapes that relate to their functional roles. Like other cells, each neuron has a cell body or soma that contains a nucleus, smooth and rough endoplasmic reticulum, Golgi apparatus, mitochondria, and other cellular components.
Neurons also contain unique structures, illustrated in Figure Dendrites are tree-like structures that extend away from the cell body to receive messages from other neurons at specialized junctions called synapses.
Although some neurons do not have any dendrites, some types of neurons have multiple dendrites. Dendrites can have small protrusions called dendritic spines, which further increase surface area for possible synaptic connections.
Once a signal is received by the dendrite, it then travels passively to the cell body. The cell body contains a specialized structure, the axon hillock that integrates signals from multiple synapses and serves as a junction between the cell body and an axon. An axon is a tube-like structure that propagates the integrated signal to specialized endings called axon terminals.
Without myelin, the electrical impulses going down the axon would be a lot slower, resulting in delayed and disrupted signals. As such, oligodendrocytes are essential for providing support to neurons for quicker signaling. Microglial are small cells with an oval shaped cell body and many small branches projecting out of it to enable them to move about.
The main function of these cells is to respond to any injuries or diseases in the CNS. When injury and disease are detected, the microglial are alerted and respond by moving to the injury site in order to either clear away any dead cells or to remove any harmful toxins or pathogens that may be present.
The cells are therefore especially important for maintaining the health of the CNS and are known as immune cells. Microglia also play a role in the development of the brain. Typically, far more synapses are created than are needed, when only the strongest and most important ones need to survive. Microglia directly contribute to removing synapses that are deemed as unnecessary, a process known as synaptic pruning.
Ependymal cells are located in the CNS that are column shaped and typically line up together to form a membrane. This membrane is called the ependyma, which is a thin membrane lining the spinal cord and ventricles of the brain.
In the ventricles, these cells have tiny hairlike structures on them called cilia, which face the open space of the cavities they line. Cilia move in a coordinated pattern to encourage the directional flow of cerebrospinal fluid, which they also produce. Cerebrospinal fluid works by allowing nutrients and other substances to reach the neurons as well as filtering out any harmful molecules.
It also works as a cushion and shock absorber between the brain and the skull, as well as maintaining homeostasis of the brain such as regulating temperature. A final type of glial in the CNS to discuss are radial glial.
Radial glia is believed to be a type of stem cell, meaning they can generate other cells. These cells are able to make neurons as well as other types of glial such as astrocytes and oligodendrocytes. Their role as stem cells, especially as being creators of neurons, makes them a target of interest for researchers who are looking into how to repair brain damage from injury and illness, or their role as the brain ages.
Schwann cells work in a similar fashion to oligodendrocytes as they also produce myelin sheath for the axons of neurons, however, they are located in the PNS. The plasma membrane of these Schwann cells spirals around the axons of neurons to form the fatty insulation that is required for faster transmission of electrical signals. Schwann cells can be either myelinating or non-myelinating. Whilst myelinating Schwann cells wrap around the axons of neurons, non-myelinating Schwann cells do not wrap around the axons, but they still provide support and cushioning to them.
Also, each Schwann cell form a single myelin sheath around an axon, whereas oligodendrocytes form myelin sheaths for multiple surrounding axons.
In addition to insulating axons, Schwann cells are critical in response to axon damage within the PNS as they can help in regenerating these damaged axons. When any type of injury occurs, the Schwann cells are sent to the injury site to remove the dead cells.
Other diseases believed to be associated with oligodendrocyte dysfunction include:. Some research suggests that oligodendrocytes may be damaged by the neurotransmitter glutamate , which, among other functions, stimulates areas of your brain so you can focus and learn new information.
However, in high levels, glutamate is considered an "excitotoxin," which means that it can overstimulate cells until they die. As their name suggests, microglia are tiny glial cells. They act as the brain's own dedicated immune system, which is necessary since the BBB isolates the brain from the rest of your body.
Microglia are alert to signs of injury and disease. When they detect it, they charge in and take care of the problem—whether it means clearing away dead cells or getting rid of a toxin or pathogen. When they respond to an injury, microglia cause inflammation as part of the healing process. In some cases, such as Alzheimer's disease , they may become hyper-activated and cause too much inflammation. Along with Alzheimer's, illnesses that may be linked to microglial dysfunction include:.
Microglia are believed to have many jobs beyond that, including roles in learning-associated plasticity and guiding the development of the brain, in which they have an important housekeeping function. Our brains create a lot of connections between neurons that allow them to pass information back and forth. In fact, the brain creates a lot more of them than we need, which isn't efficient.
Microglia detect unnecessary synapses and "prune" them, just as a gardener prunes a rose bush to keep it healthy. Microglial research has really taken off in recent years, leading to an ever-increasing understanding of their roles in both health and disease in the central nervous system.
Ependymal cells are primarily known for making up a membrane called the ependyma, which is a thin membrane lining the central canal of the spinal cord and the ventricles passageways of the brain. They also create cerebrospinal fluid and are involved in the BBB. Ependymal cells are extremely small and line up tightly together to form the membrane. Inside the ventricles, they have cilia, which look like little hairs, that wave back and forth to get the cerebrospinal fluid circulating. Cerebrospinal fluid delivers nutrients to and eliminates waste products from the brain and spinal column.
It also serves as a cushion and shock absorber between your brain and skull. It's also important for homeostasis of your brain, which means regulating its temperature and other features that keep it operating as well as possible.
Radial glia are believed to be a type of stem cell , meaning that they create other cells. In the developing brain, they're the "parents" of neurons, astrocytes, and oligodendrocytes. When you were an embryo, they also provided scaffolding for developing neurons, thanks to long fibers that guide young brain cells into place as your brain forms. Their role as stem cells, especially as creators of neurons, makes them the focus of research on how to repair brain damage from illness or injury.
Later in life, they play roles in neuroplasticity as well. Schwann cells are named for physiologist Theodor Schwann, who discovered them.
They function a lot like oligodendrocytes in that they provide myelin sheaths for axons, but they exist in the peripheral nervous system PNS rather than the CNS. However, instead of being a central cell with membrane-tipped arms, Schwann cells form spirals directly around the axon. The nodes of Ranvier lie between them, just as they do between the membranes of oligodendrocytes, and they assist in nerve transmission in the same way. Schwann cells are also part of the PNS's immune system.
When a nerve cell is damaged, they have the ability to, essentially, eat the nerve's axons and provide a protected path for a new axon to form. Diseases involving Schwann cells include:. We've had some promising research on transplanting Schwann cells for spinal cord injury and other types of peripheral nerve damage. Schwann cells are also implicated in some forms of chronic pain. Their activation after nerve damage may contribute to dysfunction in a type of nerve fibers called nociceptors , which sense environmental factors such as heat and cold.
Satellite cells get their name from the way they surround certain neurons, with several satellites forming a sheath around the cellular surface. Satellite cells are found in the peripheral nervous system, however, as opposed to astrocytes, which are found in the central nervous system. Satellite cells' main purpose appears to be regulation the environment around the neurons, keeping chemicals in balance.
The neurons that have satellite cells make up gangila, which are clusters of nerve cells in the autonomic nervous system and sensory system.
The autonomic nervous system regulates your internal organs, while your sensory system is what allows you to see, hear, smell, touch, feel, and taste.
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