Increase In Glia Research Articles

Effect of prenatal loud music and noise on total number of neurons and glia, neuronal nuclear area and volume of chick brainstem auditory nuclei, field L and hippocampus: A stereological investigation

The present study explores whether prenatal patterned and unpatterned sound of high sound pressure level (110dB) has any differential effect on the morphology of brainstem auditory nuclei, field L (auditory cortex analog) and hippocampus in chicks (Gallus domesticus). The total number of neurons and glia, mean neuronal nuclear area and total volume of the brainstem auditory nuclei, field L and hippocampus of post-hatch day 1 chicks were determined in serial, cresyl violet-stained sections, using stereology software. All regions studied showed a significantly increased total volume with increase in total neuron number and mean neuronal nuclear area in the patterned music stimulated group as compared to control. Contrastingly the unpatterned noise stimulated group showed an attenuated volume with reduction in the total neuron number. The mean neuronal nuclear area was significantly reduced in the auditory nuclei and hippocampus but increased in the field L. Glial cell number was significantly increased in both experimental groups, being highest in the noise group. The brainstem auditory nuclei and field L showed an increase in glia to neuron ratio in the experimental groups as compared to control. In the hippocampus the ratio remained unaltered between control and music groups, but was higher in the noise group. It is thus evident that though the sound pressure level in both experimental groups was the same there were differential changes in the morphological parameters of the brain regions studied, indicating that the characteristics of the sound had a role in mediating these effects.

Evidence‐based electroconvulsive therapy

Evidence‐based electroconvulsive therapy

Neuronal Loss in the Rostral Ventromedial Medulla in a Rat Model of Neuropathic Pain

Cell death has been reported in the CNS in models of neuropathic pain (Sugimoto et al., 1990; Whiteside and Munglani, 2001; Scholz et al., 2005; Fuccio et al., 2009). In our present study, we examined the effects of spinal nerve ligation (SNL) on the number of neurons in the rostral ventromedial medulla (RVM), a brainstem region involved in modulation of nociception. In rats receiving SNL, we found that the number of RVM neurons decreased by 23% in the side ipsilateral to the surgery. The loss of RVM neurons was also associated with a bilateral increase in the number of glia as well as bilateral activation of both astrocytes and microglia. Administration of tauroursodeoxycholic acid (TUDCA), which reportedly inhibits apoptosis, significantly reduced the loss of neurons, the increase in glia, and the mechanical hypersensitivity induced by SNL. Among RVM neurons, we found that serotonergic (5-hydroxytryptamine, 5-HT) neurons decreased by 35% ipsilateral to SNL. Consistent with these findings, the density of 5-HT-immunoreactive varicosities in the superficial dorsal horn of the spinal cord was 15-30% lower, ipsilateral to SNL. To test the function of the remaining 5-HT neurons, we administered the 5-HT neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT). Interestingly, after 5,7-DHT, mechanical withdrawal thresholds increased significantly. We conclude that nerve injury induces death of antinociceptive RVM neurons that can be reduced or abolished by TUDCA. We propose that the loss of RVM neurons shifts the balance of descending control from pain inhibition to pain facilitation.

Homeodomain Interacting Protein Kinase 2 Regulates Postnatal Development of Enteric Dopaminergic Neurons and Glia via BMP Signaling

Trophic factor signaling is important for the migration, differentiation, and survival of enteric neurons during development. The mechanisms that regulate the maturation of enteric neurons in postnatal life, however, are poorly understood. Here, we show that transcriptional cofactor HIPK2 (homeodomain interacting protein kinase 2) is required for the maturation of enteric neurons and for regulating gliogenesis during postnatal development. Mice lacking HIPK2 display a spectrum of gastrointestinal (GI) phenotypes, including distention of colon and slowed GI transit time. Although loss of HIPK2 does not affect the enteric neurons in prenatal development, a progressive loss of enteric neurons occurs during postnatal life in Hipk2(-/-) mutant mice that preferentially affects the dopaminergic population of neurons in the caudal region of the intestine. The mechanism by which HIPK2 regulates postnatal enteric neuron development appears to involve the response of enteric neurons to bone morphogenetic proteins (BMPs). Specifically, compared to wild type mice, a larger proportion of enteric neurons in Hipk2(-/-) mutants have an abnormally high level of phosphorylated Smad1/5/8. Consistent with the ability of BMP signaling to promote gliogenesis, Hipk2(-/-) mutants show a significant increase in glia in the enteric nervous system. In addition, numbers of autophagosomes are increased in enteric neurons in Hipk2(-/-) mutants, and synaptic maturation is arrested. These results reveal a new role for HIPK2 as an important transcriptional cofactor that regulates the BMP signaling pathway in the maintenance of enteric neurons and glia, and further suggest that HIPK2 and its associated signaling mechanisms may be therapeutically altered to promote postnatal neuronal maturation.

Combined estradiol and lithium increase ER-alpha mRNA in embryonic C57BL/6J primary hippocampal cultures.

Estrogen replacement therapy (ERT) is commonly prescribed during menopause. Post-menopausal women also tend to suffer from bipolar disorders and as a result are prescribed mood stabilizers - in addition to ERT. There is a paucity of data on how combined hormones and mood stabilizers interact in regulating gene expression that led us to hypothesize that in primary cultures of mixed brain cells predominated by glia, combined 17beta-estradiol (E2) and lithium chloride (LiCl) (E2÷LiCl) will alter estrogen receptor-alpha (ER-alpha) mRNA expression. We quantified mRNA expression of ER-alpha using the cDNA of treated primary cultures of mixed brain cells from a previous study. Our results indicate that hippocampal cultures predominated by glia increase in ER-alpha mRNA expression when treated for 48 h with combined E2÷LiCl. Our findings may encourage further investigation on the molecular mechanisms involved in combined estrogen and lithium treatment.

VENTRAL NERVE CORD TRANSECTION IN CRAYFISH: A STUDY OF FUNCTIONAL ANATOMY

ABSTRACT In crayfish, neural degeneration and regeneration in the ventral nerve cord occur in one of two ways, depending on the injured fiber. Most fibers degenerate in 1 or 2 weeks, while giant fibers degenerate slowly. Although degenerative changes are similar in both cases, they do not seem to correlate with motor behavioral alterations. The aim of this work was to characterize the time course of behavioral and anatomical changes following ventral nerve cord (VNC) transection in crayfish. The behavioral analysis was focused on the righting reflex whose changes were correlated with morphological studies performed on longitudinal sections and analyzed with transmission (TEM) and scanning electron microscope (SEM). Latency for the righting reflex increased after VNC transection and then slowly decreased toward control values. Anatomically, degenerative changes began to appear 10 days after VNC transection. Disruption in membrane arrangement, subcellular organelles, and a strong increase in glia appeared in small fibers. To a lesser degree, similar changes could be detected in medial and lateral giant fibers. Glial growth reconnected the transected VNC where regeneration signs were detected in small fibers. Both stumps were reconnected at least by glial tissue 90 days after transection, while giant axons were still degenerating; at this time, the righting reflex returned to control values.

Repetitive stimulation in the central nervous system.

There has been a considerable change in ideas about the effect of a lesion in the central nervous system (CNS) and the view of a fixed neurological deficit following a lesion in the CNS is no longer tenable. The clinical picture seen after a partial lesion in the CNS depends in part on the destruction or partial destruction of nerve pathways and cells, but is also the result of changes which occur in synaptic zones following degeneration and the triggering off of the sequence of events which includes sprouting of intact terminals and the 'unmasking' of pre-existing, but relatively insignificant, neural pathways. The effect of this is to produce an altered connectivity within the intact CNS. Destruction of a major input would not only have a negative effect but would also have a positive effect of making previously minor inputs relatively more important. This not only provides a theoretical basis for attempting to improve function in patients with a partial lesion of the CNS, but also suggests that the problem of rehabilitation of such patients should be aimed at the intact but poorly functioning central nervous system, since not only is there evidence of adaptation and reorganisation, even in the adult animal, but there is also evidence of stimulation. Environmental stimulation produces changes which include expansion of visual cortex, increase in dendritic branching, increase in glia and increase in cholinester-ase. In addition to structural changes, environmental stimulation produces behavioural changes. Experimental electrical stimulation produces changes in synapse size, synaptic vesicle change, dendritic branching and changes in synaptic transmission. Experimental spinal cord stimulation (in cat and monkey) has been shown to alter evoked responses, to produce postsynaptic inhibition, primary afferent depolarisation, increase in Renshaw cell activity and inhibition of monosynaptic activity. In man, spinal cord stimultion produces improvement in cervical and brain stem evoked responses, changes in plasma and CSF catecholamines, changes in H-reflex, and decrease in tonic stretch reflex. The major changes in man, however, are in bladder function where there has been repeated demonstration of improved residual urine, bladder capacity, sphincter EMG, urethral pressure and flow rate. The best controlled studies have been in multiple sclerosis, where spinal cord stimulation has been used to treat the deficit produced by multiple sclerosis and these changes are given in more detail.

A comparative quantitative and morphological study of ageing in the mouse neostriatum, indusium griseum and anterior commissure.

The glia:neuron ratio increased between 5 and 9 months in the neostriatum and indusium griseum and thereafter remained constant until 18 months-of-age. Between 18 and 22 months the glia:neuron ratio did not change in the neostriatum, but increased significantly in the indusium griseum due to a combination of a loss of neurons and an increase in glia. The 6--9 months rise was mainly due to an increase in the number of astrocytes in both regions although there was some increase in oligodendrocytes at this time. The increase in glia in the indusium griseum between 18 and 22 months was due to an increase in both astrocytes and microglia. In the anterior commissure, the pattern of glial change was almost identical in both limbs with oligodendrocytes increasing between 6 and 9 months then decreasing between 9 and 18 months. Astrocytes decreased between 6 and 18 months. Between 18 and 22 months oligodendrocytes and microglia both increased in number. There was a decrease in glioblasts in both limbs with age. The age at which lipofuscin appeared was different in each type of glial cell and in each region studied. Microglia contained lipofuscin at 6 months in all regions. Astrocytes first contained lipofuscin at 6 months in the neostriatum, at 9 months in the indusium griseum and at 15 months in the anterior commissure. Oligodendrocytes first contained lipofuscin at 12 months in the anterior commissure, at 18 months in the indusium griseum and at 18 months in the neostriatum. Ependymal cells adjacent to the neostriatum contained lipofuscin and osmiophilic lipid at 6 months but by 12 months the latter had become much less osmiophilic. Foamy pericytes were found in all regions: from 6 months in the neostriatum; from 9 months in the indusium griseum and from 15 months in the anterior commissure. These contained lipid droplets, were only found adjacent to arterioles or venules, and were likely Ibrahim's neurolipomastocytes. The response of glia to ageing varies in different regions of grey matter, but is similar in two different regions of white matter. These age changes may be related to different levels of metabolic activity of glia in different parts of the brain.

Increases in cortical depth and glia numbers in rats subjected to enriched environment.

AbstractWe have previously reported anatomical and chemical changes in the cerebral cortex of rats living in an enriched, stimulating environment. The present study includes additional histological measures such as more extensive depth measures, differential cell counts, and cell size measurements.Celloidin‐embedded, thionin‐stained sections of the visual cortex from environmentally enriched rats and their impoverished littermates were measured. Two methods for calculating cortical depths were used: one, with an ocular micrometer taking eight measures lateral to the elevation in the corpus callosum on each hemisphere; two, on enlarged photographs taking 51 measurements 2 mm apart on each hemisphere. With the ocular micrometer method the cortical depth of the enriched brains was 6.4% greater than the depth of the impoverished cortex. On the enlarged photographs the more medial depths in the enriched rats showed greater increases than the lateral depths.Overlapping photomicrographs were made of a medial cortical area 1.00 mm by 0.75 mm on each transverse section and were combined into one composite picture for each animal. Differential cell counts from the composite pictures were determined independently by two technicians. Results indicate a 14% (p<0.01) increase in glia among the enriched rats. No significant differences between enriched and impoverished groups were found in the perikarya and nuclear circumferences as measured with a planimeter from camera lucida drawings.

MULTIPLE SCLEROSIS AND AMYOTROPHIES

Multiple sclerosis is well defined clinically by signs and symptoms referable to almost any part of the central nervous system. Pathologically, it is characterized by numerous plaques scattered throughout the neural axis and involving essentially the white matter. The main feature of the plaque is the destruction of the myelin sheaths, with some sparing of the axis-cylinders and ganglion cells, and a replacement of the destroyed parenchyma by an excessive increase in glia. Occasionally cases of this protean disease are encountered which do not conform to the classic description and which offer diagnostic difficulties, such as those marked by the atrophy of muscles. Of a series of 20 cases of multiple sclerosis which came to necropsy, 12 showed atrophy of one or more groups of muscles or of a whole extremity; atrophies of this nature also occurred in 17 of 110 other cases of multiple sclerosis observed clinically at Montefiore