Microglial regulation of satiety and cognition

Microglia have been known for decades as key immune cells that shape the central nervous system (CNS) during development and respond to brain pathogens and injury in adult life. Recent findings now suggest that these cells also play a highly complex role in several other functions of the CNS. In this review, we provide a brief overview of the established microglial functions in development and disease. We also discuss emerging research suggesting that microglia are important for both cognitive function and the regulation of food intake. With respect to cognitive function, current data suggest microglia are not indispensable for neurogenesis, synaptogenesis or cognition in the healthy young adult, although they crucially modulate and support these functions. In doing so, they are likely important in supporting the balance between apoptosis and survival of newborn neurones and in orchestrating appropriate synaptic remodelling in response to a learning stimulus. We also explore the possibility of a role for microglia in feeding and satiety. Microglia have been implicated in both appetite suppression with sickness and obesity and in promoting feeding under some conditions and we discuss these findings here, highlighting the contribution of these cells to healthy brain function

The structures of the glia and of the synapses in the sympathetic chain of man

Del Rio Hortega teilte die Glia der sympathischen und spinalen Ganglien in 2 Gruppen ein: 1. die perisomatische Glia, welche das Perikaryon der Parenchymzellen mit 2 übereinandergelagerten Schichten umgibt und 2. periaxonale Glia (Spirocyten), welche die Fortsätze der Ganglienzellen versorgt.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47693/1/441_2004_Article_BF00325875.pd

Network-based analysis reveals differences in plant assembly between the native and the invaded ranges

Associated with the introduction of alien species in a new area, interactions with other native species within the recipient community occur, reshaping the original community and resulting in a unique assemblage. Yet, the differences in community assemblage between native and invaded ranges remain unclear. Mediterranean grasslands provide an excellent scenario to study community assembly following transcontinental naturalisation of plant species. Here, we compared the community resemblance of plant communities in Mediterranean grasslands from both the native (Spain) and invaded (Chile) ranges. We used a novel approach, based on network analysis applied to co-occurrence analysis in plant communities, allowing us to study the co-existence of native and alien species in central Chile. This useful methodology is presented as a step forward in invasion ecology studies and conservation strategies. We found that community structure differed between the native and the invaded range, with alien species displaying a higher number of connections and, therefore, acting as keystones to sustain the structure within the invaded community. Alien species acting like keystones within the Chilean grassland communities might exacerbate the threat posed by biological invasions for the native biodiversity assets. Controlling the spread of the alien species identified here as keystones should help managing potential invasion in surrounding areas. Network analyses is a free, easy-to-implement and straightforward visual tool that can be widely used to reveal shifts in native communities and elucidate the role of multiple invaders into communitie

Brain macrophages in human cortical contusions as indicator of survival period

The aim of this study was to establish a morphologic time scheme with which cases of cerebral contusion with unknown survival periods can be dated. Our study of 275 cases was limited to qualitative and quantitative changes in macrophages. The appearance of macrophages and their distribution as well as their content of neutral fat, esterified cholesterol, erythrocytes, siderin, hematoidin, and ceroid were correlated with the survival period. For each cytologic criterium, the observation period, distribution-free limits of tolerance, and relative frequency of identification in different survival periods were determined, and the limits of confidence calculated. The findings permit the dating of trauma in cases with unknown survival periods. Moreover, the probability of this dating was calculated

CNS Myelin Sheath Lengths Are an Intrinsic Property of Oligodendrocytes

SummarySince Río-Hortega’s description of oligodendrocyte morphologies nearly a century ago, many studies have observed myelin sheath-length diversity between CNS regions [1–3]. Myelin sheath length directly impacts axonal conduction velocity by influencing the spacing between nodes of Ranvier. Such differences likely affect neural signal coordination and synchronization [4]. What accounts for regional differences in myelin sheath lengths is unknown; are myelin sheath lengths determined solely by axons or do intrinsic properties of different oligodendrocyte precursor cell populations affect length? The prevailing view is that axons provide molecular cues necessary for oligodendrocyte myelination and appropriate sheath lengths. This view is based upon the observation that axon diameters correlate with myelin sheath length [1, 5, 6], as well as reports that PNS axonal neuregulin-1 type III regulates the initiation and properties of Schwann cell myelin sheaths [7, 8]. However, in the CNS, no such instructive molecules have been shown to be required, and increasing in vitro evidence supports an oligodendrocyte-driven, neuron-independent ability to differentiate and form initial sheaths [9–12]. We test this alternative signal-independent hypothesis—that variation in internode lengths reflects regional oligodendrocyte-intrinsic properties. Using microfibers, we find that oligodendrocytes have a remarkable ability to self-regulate the formation of compact, multilamellar myelin and generate sheaths of physiological length. Our results show that oligodendrocytes respond to fiber diameters and that spinal cord oligodendrocytes generate longer sheaths than cortical oligodendrocytes on fibers, co-cultures, and explants, revealing that oligodendrocytes have regional identity and generate different sheath lengths that mirror internodes in vivo

Targeted overexpression of a golli–myelin basic protein isoform to oligodendrocytes results in aberrant oligodendrocyte maturation and myelination

Recently, several in vitro studies have shown that the golli–myelin basic proteins regulate Ca2+ homoeostasis in OPCs (oligodendrocyte precursor cells) and immature OLs (oligodendrocytes), and that a number of the functions of these cells are affected by cellular levels of the golli proteins. To determine the influence of golli in vivo on OL development and myelination, a transgenic mouse was generated in which the golli isoform J37 was overexpressed specifically within OLs and OPCs. The mouse, called JOE (J37-overexpressing), is severely hypomyelinated between birth and postnatal day 50. During this time, it exhibits severe intention tremors that gradually abate at later ages. After postnatal day 50, ultrastructural studies and Northern and Western blot analyses indicate that myelin accumulates in the brain, but never reaches normal levels. Several factors appear to underlie the extensive hypomyelination. In vitro and in vivo experiments indicate that golli overexpression causes a significant delay in OL maturation, with accumulation of significantly greater numbers of pre-myelinating OLs that fail to myelinate axons during the normal myelinating period. Immunohistochemical studies with cell death and myelin markers indicate that JOE OLs undergo a heightened and extended period of cell death and are unable to effectively myelinate until 2 months after birth. The results indicate that increased levels of golli in OPC/OLs delays myelination, causing significant cell death of OLs particularly in white matter tracts. The results provide in vivo evidence for a significant role of the golli proteins in the regulation of maturation of OLs and normal myelination