Search

Neopterin is produced by monocytes and is a useful biomarker of inflammatory responses. We found that neopterin enhances granulopoiesis, but suppresses B-lymphopoiesis triggered by the positive and negative regulations of cytokines produced by stromal cells in mice. In this study, neopterin was found to regulate mast cell development, which was confirmed in the mouse model of senescent stromal-cell impairment (SCI). In non-SCI mice (= less senescent stage of SCI mice), neopterin decreased the number of colonies of IL-3-dependent mast-cell progenitor cells (CFU-mast) from unfractionated bone-marrow cells, but not that from the lineage-negative bone-marrow cell population without stromal cells in a semisolid in vitro system. Neopterin increased the gene expression and protein production of TGF-β, a negative regulator of CFU-mast, in cultured stromal cells, indicating that neopterin suppressed CFU-mast colony formation by inducing TGF-β in stromal cells. In contrast to this in vitro study, in vivo treatment with neopterin did not significantly up-regulate TGF-β. The intravenous injection of neopterin into mice decreased the number of femoral CFU-mast and the expression level of the gene for stem cell factor (SCF), a positive regulator of CFU-mast, whereas the number of splenic CFU-mast and SCF gene expression level increased. In SCI mice, the in vivo and in vitro responses of mast cell development and cytokine gene expression level to neopterin treatment were less marked than those in non-SCI mice. These results suggest that, firstly, neopterin augments the splenic pool of CFU-mast by the production of SCF, and secondly, such neopterin function becomes impaired during senescence because of an impaired stromal-cell function, resulting in the down-modulation of host-defense mechanisms.

SummaryNeurotoxic effects of endogenous tissue plasminogen activator (tPA) have recently been reported. Employing a rat model of thromboembolic stroke, we evaluated the extent and degree of extravasation of exogenous tPA administered for the purpose of fibrinolysis. In a thromboembolic model using Sprague-Dawley rats, focal cerebral ischemia was induced at the territory of the middle cerebral artery (MCA). Early reperfusion was induced by administering tPA (10 mg/kg) intravenously at 30 minutes after the onset of ischemia. Extravasated tPA was evaluated by immunohistochemistry, and the concentration of tPA in the brain tissue was quantified by enzyme-linked immunosorbent assay methods. The integrity of the blood-brain barrier (BBB) was examined electronmicroscopically. In a thread model of transient ischemia, reperfusion was induced without tPA adminis-tration at 30 minutes or 2 hours after the onset of ischemia, and the tPA content of the brain was quantified. In the rats with thromboembolic stroke, extravasation of tPA was observed at the territory of the MCA. Both the endogenous and exogenous tPA contents were 3.5±1.6 ng/ml of homogenized brain in saline. Electronmicroscopically, mild ischemic changes were observed, although the integrity of the BBB was preserved. In the thread model rats, the endogenous tPA contents of the ischemic hemisphere were 0.9±0.1 and 1.0±0.2 ng/ml in the 30-minute and 2-hour ischemia groups, respectively, and were significantly lower than the tPA contents in the thromboembolic stroke rats (p < 0.01). The present findings indicate that significant extravasation of exogenous tPA occurs through the cerebral vessels even though early reperfusion is induced.

Homonymous hemianopia due to lateral geniculate body (LGB) lesion has rarely been reported. It is difficult to detect the LGB lesion by neuroimaging. We report two patients with characteristic homonymous hemianopia due to cerebral infarction of the LGB. In both patients, Goldmann perimetry showed incongruous and wedge-shaped homonymous hemianopia, and magnetic resonance imaging demonstrated infarction of the LGB. In addition, occlusion of the lateral posterior choroidal artery was confirmed by magnetic resonance angiography in one of these patients. To diagnose of a LGB lesion, we should carefully observe characteristic visual field defects, accompanying neurologic symptoms, and neuroimaging findings, including magnetic resonance angiography.

✓ The authors report the case of a peripheral primitive neuroectodermal tumor (PNET) arising in the tentorium in a 5-year-old boy who presented with frequent vomiting and mild palsy of the left abducent nerve. Following complete surgical excision of the tumor via a transpetrosal approach, the patient has thus far been disease free for 7 years. The tumor tissue was composed of small cells with uniform round nuclei and minimal identifiable cytoplasm. Homer—Wright rosettes were frequently observed. Immunohistochemical studies demonstrated a positive reaction to HBA-71, which recognizes the cell surface glycoprotein p30/32, a product of the MIC2 gene. Both the clinical and immunohistochemical characteristics of this tumor are consistent with a diagnosis of peripheral PNET, which is genetically distinct from the more common intracranial PNET.

In contrast to previous reports denying the occurrence of axonal regeneration of the dorsal column (DC) projections, here we demonstrate for the first time that marked regeneration occurs spontaneously after transection in infant rats. Transection was made sharply so as to produce edema-free lesions without subsequent formation of either scars or cysts. Transganglionic labeling of axons revealed that regenerated axons ascended in the normal tract in a manner similar to normal projections as a tightly-packed fasciculus and terminated densely in the nucleus gracilis. The present study indicates that failure of regeneration of DC axons is due to neither intrinsic deficiency of regrowth potential nor globally-inhospitable axonal environment but rather the local conditions of the lesion site.

One major event taking place at the moment of traumatic brain injury in neuronal cells is the occurrence of massive ionic fluxes across the plasma membrane, which can be referred to as traumatic depolarization (TD). Unlike spreading depression, TD can occur over wide brain areas simultaneously. Furthermore, recovery from TD often takes far longer than recovery from ionic perturbation elicited by the passage of a single wave of spreading depression. Neuronal cell damage caused by ischemic brain injury is also initiated by massive ionic fluxes, termed anoxic depolarization. The occurrence of similar ionic events in these two forms of brain injury may account for the genesis of diffuse ischemia-like damage without actual episodes of hypoxia or ischemia in traumatic brain injury. We review the data indicating that excitatory amino acids (EAA) may play a vital role in producing TD, and that such EAA-mediated ionic perturbation is responsible for a number of posttraumatic events including subcellular metabolic dysfunction and cellular responses such as microglial activation and astrocytic transformation. TD may represent one of the most important mechanisms of diffuse neuronal cell dysfunction and damage associated with traumatic brain injury.

In normal spinal cord, acidic fibroblast growth factor (aFGF) immunoreactivity was localized in the cytoplasm of ventral motor neurons and sensory fibers in the dorsal columns. Basic FGF (bFGF) immunoreactivity was restricted to astrocyte nuclei and the cytoplasm of a few neurons in the intermediate gray matter. Spinal cord lesions resulted in complete destruction of the dorsal columns at T8. Two days postlesion, aFGF immunoreactivity was increased in ventral motor neurons and was now seen in intermediate gray matter neurons. Acidic FGF was not detected in the lesioned fasciculus gracilis at T4-5, but markedly increased in the fasciculus cuneatus. At L1-2, aFGF-immunoreactive fibers in the fasciculus gracilis also increased. This aFGF immunostaining was maintained 5 and 12 days postlesion. A lesion-induced loss of aFGF immunoreactivity in the nucleus gracilis suggests that aFGF is anterogradely transported in ascending sensory fibers. Two days postlesion, glial fibrillary acidic protein immunoreactivity increased at the lesion site, as well as at T4-5 and L1-2, with no change in bFGF staining. Five days postlesion, increased bFGF immunoreactivity appeared at the edge of the cystic cavity and the dorsal columns at T4-5 in both the nucleus and the cytoplasm of reactive astrocytes, and was increased at 12 days postlesion. The differential cellular, temporal, and spatial expression of aFGF and bFGF following spinal cord lesion suggest they subserve distinct roles in the response to CNS injury.

Cell suspensions obtained from the fetal hippocampus were transplanted into the adult rat hippocampus at 1 or 4 weeks after transient forebrain ischemia. Only when the ischemia induced death of most of the CA1 pyramidal cells of the host hippocampus and transplantation was performed at 1 week after the ischemia, did a large number of transplanted cells survive and the most extensive dendritic growth was demonstrated by microtubule-associated protein 2 immunohistochemistry. The dendrites of the cells located in the ventral part were oriented ventrally, lining up similarly to the parallel arrangements of apical dendrites of normal CA1 pyramidal cells. These findings suggest that certain forms of trophic factors, which appear to occur in association with the presence of free terminals of afferent fibers during the earlier period after ischemic insult, are involved in the survival of and dendritic growth from transplanted hippocampal cells.

Fibrous dysplasia, when it occurs in the craniofacial region, mostly involves the skull base and is rarely localized in the cranial vault. Although there have been several reports on magnetic resonance imaging (MRI) findings of fibrous dysplasia involving the skull base, cases occurring in the cranial vault have seldom been reported. We describe here a rare case of monostotic fibrous dysplasia that occurred in the parietal bone and discuss the characteristics of the MRI findings. A 47-year-old female was admitted to our hospital with a complaint of vertigo. A computed tomography (CT) scan did not reveal any intraparenchymal lesions in either the infra- or supratentorium, and her vertigo improved immediately without any treatments. However, a solitary osteolytic lesion was found incidentally in the left parietal bone. MRI showed that the lesion demonstrated hypointensity on T1-weighted images and hyperintensity on T2-weighted images, and was enhanced heterogeneously following injection of Gadolinium-DTPA. Removal of the parietal bone containing the lesion was performed according to the patient's wishes. The histopathological findings of the removed tissues corresponded to fibrous dysplasia. Although it is well known that craniofacial fibrous dysplasia demonstrates iso- or hypointensity on T1- as well as T2-weighted images, in the present case, the lesion showed apparent hyperintensity on T2-weighted images. These findings suggest that fibrous dysplasia can display various MR intensities depending on its origin.

It has been reported that high intensity on diffusion-weighted image (DWI) in magnetic reasonance imaging (MRI) accompanying a reduction of the apparent diffusion coefficient (ADC) can be detected at the ictal or postictal stage of epileptic seizure. However, it remains unclear whether such a change results from persisting systemic convulsive seizure or from certain physiological changes such as recurrent epileptic discharge prior to the occurrence of obvious convulsion. We report here a case of symptomatic epilepsy displaying a high intensity area on DWI in MRI before convulsive seizure was initiated. A 64-year-old man was admitted to our hospital due to complaints of dizziness and motor weakness. CT and conventional MRI scans failed to reveal any new lesions except for the scar of a ventricular tube in the right parietal lobe, which had been removed due to shunt infection. The DWI, however, demonstrated an apparent high intensity in the right parietal cortex, and the ADC was significantly reduced as compared to that on the contralateral side. Five days after admission, the patient showed convulsive seizures beginning from the right face and upper extremity which subsequently developed to status epilepticus. Following recovery from the convulsions with administration of anticonvulsants, the high intensity of the right parietal lobe on DWI appeared to be diminished. The present case indicates that the manifestation of a high intensity on DWI concomitant with ADC reduction at the epileptic focus can be readily induced by the occurrence of epileptic discharges before convulsive seizure is evident.

In this study, we examined the age-associated defect of stromal cells, which support B cell development, treated with 5-fluorouracil (5-FU) to induce severe perturbation of hematopoiesis, including B lymphocyte development, using SAMP1 mice exhibiting senescence-mimicking stromal-cell impairment after 30 weeks of age. Significant findings of this study are as follows: first, a marked and prolonged decrease in number of CFU-preB cells in non-SCI mice (58% of the steady-state level) associated with more markedly depressed number of CFU-preB cells in SCI mice (20% of the steady-state level), despite the absence of difference in the number of CFU-GMs during the period; second, in the non-SCI mice, a significant and prolonged up-regulation of GM-CSF and IL-6, positive regulators of myelopoiesis and suppressive factors of B lymphopoiesis, was observed. In SCI mice, greater and prolonged suppression of B lymphopoiesis was clearly demonstrated by the significant up-regulation of the negative regulator TNF-alpha associated with the concomitant marked down-regulation of the positive regulator SDF-1, although the increases of GM-CSF and IL-6 were limited. That is, 'negative complementation' makes preB recovery after 5-FU treatment impaired and prolonged. Principal component analysis clearly showed differences in the cytokine expression patterns in both early and later phases and the time course of the expression pattern of each cytokine between SCI and non-SCI mice without supervising information. An impaired regulation of the expressions of not only positive but also negative regulators after 5-FU treatment was, in part, the cause of the impaired regeneration of CFU-preB cells in SCI mice.

Both microglia and astrocytes respond immediately to traumatic brain injury (TBI). The present study was undertaken to examine whether or not excitatory amino acid (EAA) antagonists could attenuate such glial responses.EAA antagonists, including the broad spectrum EAA antagonist, kynurenic acid (KYN), specific N-methyl-D-aspartate (NMDA) receptor blocker, 2-amino-5-phosphonovalerate (AP-5), and AMPA-KA receptor blocker, 6,7-dinitroquinoxaline-2,3-dione (DNQX), as well as the voltage-dependent ion channel blocker, tetrodotoxin (TTX), were administered into the unilateral hippocampus of rats through a dialysis probe for 30 minutes before the induction of unilateral controlled cortical impact injury. The rats were killed 10 minutes after injury and their brains were processed immunohistochemically for OX42 (marker for microglia) and glial fibrillary acidic protein (GFAP; marker for astrocytes).Ten minutes after injury, microglial activation with increased OX42 immuno-reactivity was evident in the entire hemisphere including the hippocampus ipsilateral to the injury side. Similarly, swollen astrocytes with increased GFAP expression could be detected exclusively on the injury side. When KYN was administered in situ before injury, both the rapid microglial and astroglial responses in the hippocampus were significantly attenuated. However, AP-5, DNQX and TTX, the voltage-dependent ion channel blocker, at doses which can inhibit each channel activation, failed to attenuate these glial reactions.These findings indicate that massive ionic fluxes and/or concomitantly occurring EAA release may be closely related to the initiation of microglial and astroglial responses following TBI.

Nasal dermal sinus-cyst (NDSC) is a rare abnormality consisting of a dermal sinus opening at the nasal skin and dermoid cyst localized in the frontobasal area. A 2-year-old boy was admitted to our hospital due to swelling of the fronto-nasal regions with pus running from an orifice situated in the nasal skin. Bone-image CT and 3D-CT revealed bone defects within the frontal skull base. MRI demonstrated that a dermoid cyst centered in a bone defect was in contact with the dura of the frontobasal area, and a dermal sinus extending to the frontonasal skin could also be detected. Surgical resection was performed by frontobasal craniotomy. The dermal sinus was followed subcutaneously into the orifice of the nasal skin. A small skin incision was made and the sinus was then totally removed. The authors describe in detail this case of NDSC which extended to the intracranium, and review the literature regarding this abnormality.

Neopterin is produced by monocytes and is a useful biomarker of inflammatory activation. We found that neopterin enhanced in vivo and in vitro granulopoiesis triggered by the stromal-cell production of cytokines in mice. The effects of neopterin on B lymphopoiesis during the enhancement of granulopoiesis were determined using the mouse model of senescent stromal-cell impairment (SCI), a subline of senescence-accelerated mice (SAM). In non-SCI mice (a less senescent stage of SCI mice), treatment with neopterin decreased the number of colonies, on a semisolid medium, of colony-forming units of pre-B-cell progenitors (CFU-preB) from unfractionated bone marrow (BM) cells, but not that from a population rich in pro-B and pre-B cells without stromal cells. Neopterin upregulated the expression of genes for the negative regulators of B lymphopoiesis such as tumor necrosis factor-alpha (TNF-alpha ), interleukin-6 (IL-6), and transforming growth factor-beta (TGF-beta) in cultured stromal cells, implying that neopterin suppressed the CFU-preB colony formation by inducing negative regulators from stromal cells. The intraperitoneal injection of neopterin into non-SCI mice resulted in a marked decrease in the number of femoral CFU-preB within 1 day, along with increases in TNF-alpha and IL-6 expression levels. However, in SCI mice, in vivo and in vitro responses to B lymphopoiesis and the upregulation of cytokines after neopterin treatment were less marked than those in non-SCI mice. These results suggest that neopterin predominantly suppressed lymphopoiesis by inducing the production of negative regulators of B lymphopoiesis by stromal cells, resulting in the selective suppression of in vivo B lymphopoiesis. These results also suggest that neopterin facilitated granulopoiesis in BM by suppressing B lymphopoiesis, thereby contributing to the potentiation of the inflammatory process; interestingly, such neopterin function became impaired during senescence because of attenuated stromal-cell function, resulting in the downmodulation of the host-defense mechanism in the aged.

A case of superior sagittal sinus thrombosis which was complicated with ulcerative colitis is reported. A 16-year-old male patient had a 2-year history of ulcerative colitis. He was admitted to our hospital complaining of abdominal pain, bloody bowel discharge and appetite loss, and was then treated conservatively. Two days after admission, he demonstrated generalized convulsions which were followed by right hemiplegia. MRI showed a low intensity lesion on T1 and an irregular high intensity in the subcortical area of the left frontal lobe on T2 and T2 FLAIR-weighted images. The MRI findings resembled either invasive brain tumor or local inflammation. Cerebral angiography appeared to demonstrate complete obstruction of the superior sagittal sinus with congestion of venous flow in the cortical veins. Ulcerative colitis has been reported to show hypercoagulation, leading to deep vein thrombosis within the body which sometimes causes pulmonary infarction; however, occurrence of venous thrombosis in the intracranial veins and sinus is rare. This report underscores the fact that cerebral venous thrombosis should be suspected in the case of patients with ulceritive colitis who suffer sudden onset of neurological deficits.

Background We present here the first report of a jugular bulb venous thrombosis after mild head injury, which lacked either a skull fracture or abnormal findings on CT scan. Case Description An 8-year-old boy was hit on the back of the head and experienced headache and vomiting beginning the next morning. A CT scan and cranial x-ray examination failed to reveal any abnormal findings. The patient was treated conservatively; however, his headache and vomiting persisted. At 13 days after the injury, he began to show double vision due to left VIth nerve palsy and bilateral papilloedemas, suggesting an increased ICP. Although repeated CT scan failed to detect abnormal findings in both the supra- and infra-tentorial regions, MRI clearly visualized a thrombus which was situated within the right jugular bulb. Furthermore, MRV demonstrated disruption of venous flow at the jugular bulb. The patient was administered heparin continuously. His symptoms improved and the CSF pressure on lumbar puncture returned to a normal level at 20 days after admission. Magnetic resonance imaging showed resolution of the clot, and MRV appeared to demonstrate partial recanalization simultaneously. The patient was discharged without any neurologic deficits. The clot in the jugular bulb disappeared completely after 4 months, and he could be followed up for 1 year. Conclusion This case underscores the fact that MRI may represent the exclusive screening examination in cases of sinus thrombosis when it occurs within the jugular bulb, as CT scan fails to reveal any findings suggestive of venous thrombosis.

The pteridine neopterin (NP) is produced by monocytes and is known to be a useful marker of immunological activation, although, it remains elusive whether neopterin itself exhibits biological functions. Recently, we found that NP stimulates hematopoietic cell proliferation and differentiation by activating bone marrow stromal cell function. In order to elucidate the biological effect of NP on stromal cells, its effects on hematopoiesis was determined in the mouse model of age-related stromal impairment, senescence-accelerated mice (SAMs). An intraperitoneal administration of NP increased the number of peripheral leukocytes and CFU-GM in the bone marrow and spleen of young SAMs, however, no increase of CFU-GM in old SAMs (stromal impairment) was observed when compared with young SAMs. NP also increased the CFU-GM colony formation of bone marrow and spleen cells from young SAMs in a soft agar culture system, but it did not enhance CFU-GM colony formation of cells from old SAMs cultured in this system. Treatment with NP induced the production of hematopoietic stimulating factors, including IL-6 and GM-CSF, by bone marrow stromal cells from young SAMs but stromal cells from old SAMs did not respond to NP stimulation. Further studies will be required to clarify the mechanism by which NP stimulates the production of hematopoietic growth factors from stromal cells, the results of this study indicate that NP is a potent hematopoietic regulatory factor by activating stromal cell function(s).

A novel supramolecular oligomer, cyclic polylactate (CPL) that was originally discovered in the culture medium of HeLa-S tumor cells, reportedly inhibits the growth of FM3A ascites tumor cells by inhibiting enzymes involved in the glycolytic pathway. We synthesized CPL containing 3- to 13-mers by prolonged heating and rapidly mixing a carbohydrate compound of the L-lactic acid monomer (C(3)H(6)O(3)) under decreased pressure, and studied its effects on the growth of the cloned leukemic cell, TF-1. CPL inhibited the growth of TF-1 cells and induced 7A6 antigen, which is expressed by cells undergoing apoptosis, on the surface of TF-1 cells. In addition, caspase 3, 8 and 9 activities of TF-1 cells were increased after exposure to CPL, indicating that CPL induces apoptotic changes in TF-1. Among the 6 glycolytic enzymes examined in this study, the activities of PFK and HK, induced by CPL, decreased. Interestingly, CPL was detected in conditioned medium of the stromal cell line, LS801, obtained from human bone marrow. This conditioned medium inhibited the growth of TF-1 cells, and induced the expression of 7A6 antigen. These findings suggest that CPL will be a useful chemotherapeutic agent against leukemia.

In order to assess the role of circulating blood in early microglial activation after traumatic brain injury (TBI), controlled cortical impact injury was applied to adult rat brain slices (400 microm in thickness) and the microglial response was examined. The complement receptor (CR3) expression and morphological transformation of the microglia were evaluated by OX42 immunohistochemistry. At 5 min following injury, activated microglia with intense CR3 expression appeared throughout the hemisphere on the injured side. In contrast, the morphology and CR3 expression of the microglia on the contralateral side were indistinguishable from those of the resident ramified microglia seen in normal brains. At 30 min following injury, microglial activation was more pronounced on the injured side, while the microglia on the contralateral side still retained a ramified morphology. These results are consistent with our previous observations made in in vivo experiments, which indicate that, as the brain slice paradigm excludes variables arising from the circulating blood, the rapid and widespread microglial activation observed following TBI can not be attributed exclusively to the infiltration of blood-borne macrophages or molecules. Rather this activation is most likely caused by intrinsic mechanisms within the brain tissue, such as traumatic depolarization.

The jugular bulb oxygen saturation (SjO 2 ) and end-tidal carbon dioxide (ETCO 2 ) were monitored continuously during surgery in six cases of Moyamoya disease who had demonstrated multiple episodes of transient ischemic attacks (TIAs) and/or fluctuating neurological deficits preoperatively. The arterial carbon dioxide tension (PaCO 2 ) levels were also measured repeatedly at predetermined interval. In two cases (group H), the ETCO 2 was controlled at hypercapnic levels during surgery (45.5±1.5 mmHg) and the remaining four (group N) were operated on in a normocapnic state (39.0±2.0 mmHg). The group H patients demonstrated high levels of SjO 2 ranging from 72 to 85%, indicative of excessive hyperemia. One of the group H patients demonstrated mild and transient motor weakness postoperatively. The group N patients demonstrated normal levels of SjO 2 ranging from 66 to 78%. All the patients in both groups demonstrated fluctuations in SjO 2 levels in clear positive correlation with spontaneous changes in PaCO 2 levels. The present findings indicated that: (1) Global carbon dioxide reactivity of cerebral perfusion is well preserved in patients with Moyamoya disease; and (2) hypercapnia in these patients often causes excessive hyperemia. The occurrence of postoperative neurological deficits in association with such an excessive hyperemia suggests that hyperapnia during surgery is not always beneficial. Intraoperative monitoring of SjO 2 is useful for maintaining cerebral perfusion within the optimum range.

In a previous study we demonstrated that fetal hippocampal cells, when transplanted into ischemic lesions of the adult rat hippocampus, can survive in large numbers in the host brain and show the innervation of the transplants by cholinergic fibers originated from the host brain. The present study was undertaken in an attempt to elucidate the hypothesis that the fiber connections forming synapses between the transplanted fetal neurons and the host brain play an important role in the survival of the transplanted cells. We transplanted the polymer-encapsulated fetal hippocampal cells prepared from E17–18 rat fetuses into the ischemic lesions in the adult rat hippocampus at which the CA1 pyramidal cells selectively died, and examined both histochemically or immunohistochemically for their survival and the expression of the synaptic vesicle protein, synaptophysin, and dendritic cytoskeltal protein, microtubule-associated protein 2 (MAP 2) within them. In addition, the cholinergic fibers originated from the host brain were examined by acetylcholine esterase (AChE) histochemistry. The results demonstrated that the polymerencapsulated hippocampal cells could survive in the brain; however, the number of surviving cells markedly decreased following the transplantation, whereas no host-derived cholinergic fibers penetrated the polymer membrane of the capsules following the transplantation. In the cluster of surviving cells, only slight synaptophysin expression and no extensive growth of the dendrites were detected. The present results indicate that the direct contact between the host brain tissue and the transplant play an important role in the survival of such allografted neurons.

The role of microglia in the response to CNS injury is not fully understood. We characterized the temporal activation of microglia in the adult spinal cord following a lesion that severed the axons of the dorsal columns and corticospinal tract at T8. Two days after lesion, microglia in the severed T4-T5 fasciculus (f.) gracilis were ameboid and expressed intense OX42 and increased class I major histocompatibility complex (MHC) antigen (OX18) immunoreactivities. No activated microglia were seen in the intact f. cuneatus or the corticospinal tract. Five days postlesion, OX42 immunoreactivity was slightly decreased in the f. gracilis, and OX18 expression was slightly enhanced. By 12 days postlesion, OX42 and OX18 immunoreactivities were near control levels. At L1-L2, activated microglia with increased OX18 expression were restricted to the corticospinal tract and were maximal 5 days postlesion, returning to near control levels by 12 days postlesion. In the medulla, enhanced OX42 and OX18 immunoreactivities were seen in the nucleus (n.) gracilis, but not the n. cuneatus, at 2 days postlesion. At 5 days postlesion, OX42 immunoreactivity was markedly decreased, but class I MHC antigen expression was still enhanced. GFAP immunoreactivity increased only in the n. gracilis and remained elevated 2-12 days postlesion. Microglial activation is an early lesion-induced event in the CNS, and activated microglia may play a role in mediating the regenerative capacity of injured CNS axons.

A case of meningioma with extensive xanthomatous metaplasia occurring in the left frontal convexity of a 37-year-old woman is reported. The tumour was demonstrated as a hypodense mass with minimal enhancement on CT. Our findings suggest that magnetic resonance imaging may provide a clue to the diagnosis of meningiomas with extensive xanthomatous metaplasia when CT is less specific.

The long-term potentiation (LTP) of the Schaffer collateral/CA1 pyramidal cell system of the rat hippocampus was investigated at various periods after induction of hydrocephalus by cisternal kaolin injection. There was a progressive decrease in LTP during the initial 3 weeks, and LTP remained decreased thereafter following the induction of hydrocephalus. Since the intraventricular pressure reached its maximum level within 2 weeks after kaolin injection, the continuous presence of hydrocephalus appeared to be necessary for producing the deficit in LTP induction. Dendritic dysfunction was apparently important for this functional change, since in a previous study by electron microscopy, we revealed a number of swollen dendrites in the CA1 region, while the changes in the axons, synaptic structures, and soma were far less pronounced. In agreement with this interpretation, a swelling of the dendrites of the CA1 pyramidal cells and irregularity of their arrangement was demonstrated by microtubule-associated protein 2-immunohistochemistry to be associated with the decreased LTP. Since LTP is likely to reflect the hippocampal function related to memory retention, functional changes underlying the impaired LTP might be responsible for memory deficit in hydrocephalus.

The influence of interstitial oedema on the survival of fetal raphe cells transplanted into serotonin (5-HT)-denervated rats and the fibre outgrowth from these cells was investigated. Fetal raphe cells were transplanted into the corpus callosum in which long-lasting interstitial oedema had been induced by intracisternal kaolin injection. The 5-HT and 5HIAA levels in the corpus callosum were restored to their maximum within 5–6 weeks post-transplantation regardless of whether interstitial oedema was induced or not. Furthermore, it was appeared that the presence of interstitial oedema even facilitated fibre growth as demonstrated by the 5-HT immunohistochemistry and the restoration of the 5-HT and 5-HIAA levels in brain areas distant from the transplantation sites. These results imply favourable effects of interstitial oedema on the survival of transplanted raphe cells and their fibre outgrowth.