The activities of noradrenergic and dopaminergic neuron systems in experimental hydrocephalus

1982 ◽  
Vol 57 (1) ◽  
pp. 67-73 ◽  
Author(s):  
Soichi Miwa ◽  
Chiyoko Inagaki ◽  
Motokazu Fujiwara ◽  
Shuji Takaori

✓ Experimental hydrocephalus was induced in rabbits by intracisternal injection of kaolin suspension, and the concentration of noradrenaline (NA), dopamine (DA), and their metabolites was determined in several brain regions. The NA concentration had decreased in the cerebellum, hypothalamus, and pons plus medulla oblongata, and increased in the caudate nucleus at 2 days after kaolin injection (the stage of early intracranial hypertension). At 1 week (the stage of progressive hydrocephalus), the NA content had returned to control levels in all brain regions studied, and it decreased again at 4 weeks (the stage of chronic hydrocephalus) in the pons plus medulla oblongata. The DA level was unchanged throughout the 4-week period after kaolin injection. The concentration of 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MOPEG-SO4), the major metabolite of NA, was elevated in all brain regions except the caudate nucleus at all stages after kaolin injection. An increase in MOPEG-SO4 in the caudate nucleus was also observed 1 week after kaolin injection. The content of homovanillic acid (HVA), the major metabolite of DA in the rabbit brain, was decreased in the cerebral cortex at 2 days and at 1 week after kaolin injection, and in the caudate nucleus at 2 days, 1 week, and 4 weeks. The level of HVA was increased in the hypothalamus at 2 days, in the cerebellum at 2 days and at 1 week, in the pons plus medulla oblongata at 2 days, 1 week, and 4 weeks, and in the midbrain at 4 weeks. These data suggest that, in experimental hydrocephalus in the rabbit, NA release is increased throughout the brain, while DA release is decreased in the cerebral cortex and caudate nucleus, and increased in the cerebellum, hypothalamus, midbrain, and pons plus medulla oblongata.

1988 ◽  
Vol 68 (6) ◽  
pp. 955-959 ◽  
Author(s):  
Toru Itakura ◽  
Ichiro Kamei ◽  
Kunio Nakai ◽  
Yutaka Naka ◽  
Kazuo Nakakita ◽  
...  

✓ The superior cervical ganglion (SCG) of rats was transplanted into their own parietal cortex. Four weeks after implantation, catecholamine histofluorescence revealed many transplanted catecholamine cells in the cortex. However, no fibers extended from the transplanted tissue to the cerebral cortex. In a second group of rats which had been pretreated with 6-hydroxydopamine (a specific neurotoxin to the catecholamine neuron), some showed extension of catecholamine fibers to the cerebral cortex. To simulate an animal model of Parkinson's disease, MPTP (1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine) was administered to five monkeys. Two weeks after MPTP administration, dopamine terminals in the caudate nucleus disappeared. After autotransplantation of the SCG into the caudate nucleus of these monkeys, many of the transplanted SCG cells extended axons beyond the graft into the caudate nucleus. These results show that transplanted SCG cells survived well in the brain. Under special circumstances, such as a shortage of catecholamine in the brain, implanted SCG cells extended their axons into the brain. It is suggested that autotransplantation of SCG grafts may be a new therapy for Parkinson's disease.


1997 ◽  
Vol 86 (2) ◽  
pp. 263-271 ◽  
Author(s):  
Yuzuru Tashiro ◽  
Shushovan Chakrabortty ◽  
James M. Drake ◽  
Toshiaki Hattori

✓ The authors investigated functional neuronal changes in experimental hydrocephalus using immunohistochemical techniques for glutamic acid decarboxylase (GAD) and two neuronal calcium-binding proteins: parvalbumin (PV) and calbindin D28K (CaBP). Hydrocephalus was induced in 16 adult Wistar rats by intracisternal injection of a kaolin solution, which was confirmed microscopically via atlantooccipital dural puncture. Four control rats received the same volume of sterile saline. Immunohistochemical staining for GAD, PV, and CaBP, and Nissl staining were performed at 1, 2, 3, and 4 weeks after the injection. Hydrocephalus occurred in 90% of kaolin-injected animals with various degrees of ventricular dilation. In the cerebral cortex, GAD-, PV-, and CaBP-immunoreactive (IR) interneurons initially lost their stained processes together with a concomitant loss of homogeneous neuropil staining, followed by the reduction of their total number. With progressive ventricular dilation, GAD- and PV-IR axon terminals on the cortical pyramidal cells disappeared, whereas the number of CaBP-IR pyramidal cells decreased, and ultimately in the most severe cases of hydrocephalus, GAD, PV, and CaBP immunoreactivity were almost entirely diminished. In the hippocampus, GAD-, PV-, and CaBP-IR interneurons demonstrated a reduction of their processes and terminals surrounding the pyramidal cells, with secondary reduction of CaBP-IR pyramidal and granular cells. On the other hand, Nissl staining revealed almost no morphological changes induced by ischemia or neuronal degeneration even in the most severe cases of hydrocephalus. Hydrocephalus results in the progressive functional impairment of GAD-, PV-, and CaBP-IR neuronal systems in the cerebral cortex and hippocampus, often before there is evidence of morphological injury. The initial injury of cortical and hippocampal interneurons suggests that the functional deafferentation from intrinsic projection fibers may be the initial neuronal event in hydrocephalic brain injury. Although the mechanism of this impairment is still speculative, these findings emphasize the importance of investigating the neuronal pathophysiology in hydrocephalus.


1979 ◽  
Vol 50 (1) ◽  
pp. 64-69 ◽  
Author(s):  
Fong Y. Tsai ◽  
James E. Huprich ◽  
Hervey D. Segall ◽  
James S. Teal

✓ The authors review 29 cases of surgically-proven isodense subdural hematomas examined by non-contrast and contrast-enhanced computerized tomography scans. Three types of isodense collections were noted: homogeneous isodense collections, mixed-density collections, and gravitational layering within subdural collections. Contrast enhancement within the cerebral cortex, cortical vessels, and subdural membranes led to the correct diagnosis in each case. Contrast-enhanced scans are essential for the evaluation of isodense subdural hematomas.


1998 ◽  
Vol 88 (6) ◽  
pp. 1058-1065 ◽  
Author(s):  
Kenneth R. Wagner ◽  
Guohua Xi ◽  
Ya Hua ◽  
Marla Kleinholz ◽  
Gabrielle M. de Courten-Myers ◽  
...  

Object. The authors previously demonstrated, in a large-animal intracerebral hemorrhage (ICH) model, that markedly edematous (“translucent”) white matter regions (> 10% increases in water contents) containing high levels of clotderived plasma proteins rapidly develop adjacent to hematomas. The goal of the present study was to determine the concentrations of high-energy phosphate, carbohydrate substrate, and lactate in these and other perihematomal white and gray matter regions during the early hours following experimental ICH. Methods. The authors infused autologous blood (1.7 ml) into frontal lobe white matter in a physiologically controlled model in pigs (weighing approximately 7 kg each) and froze their brains in situ at 1, 3, 5, or 8 hours postinfusion. Adenosine triphosphate (ATP), phosphocreatine (PCr), glycogen, glucose, lactate, and water contents were then measured in white and gray matter located ipsi- and contralateral to the hematomas, and metabolite concentrations in edematous brain regions were corrected for dilution. In markedly edematous white matter, glycogen and glucose concentrations increased two- to fivefold compared with control during 8 hours postinfusion. Similarly, PCr levels increased several-fold by 5 hours, whereas, except for a moderate decrease at 1 hour, ATP remained unchanged. Lactate was markedly increased (approximately 20 µmol/g) at all times. In gyral gray matter overlying the hematoma, water contents and glycogen levels were significantly increased at 5 and 8 hours, whereas lactate levels were increased two- to fourfold at all times. Conclusions. These results, which demonstrate normal to increased high-energy phosphate and carbohydrate substrate concentrations in edematous perihematomal regions during the early hours following ICH, are qualitatively similar to findings in other brain injury models in which a reduction in metabolic rate develops. Because an energy deficit is not present, lactate accumulation in edematous white matter is not caused by stimulated anaerobic glycolysis. Instead, because glutamate concentrations in the blood entering the brain's extracellular space during ICH are several-fold higher than normal levels, the authors speculate, on the basis of work reported by Pellerin and Magistretti, that glutamate uptake by astrocytes leads to enhanced aerobic glycolysis and lactate is generated at a rate that exceeds utilization.


1982 ◽  
Vol 56 (2) ◽  
pp. 235-240 ◽  
Author(s):  
Hideo Hiratsuka ◽  
Hitoshi Tabata ◽  
Shin Tsuruoka ◽  
Masaru Aoyagi ◽  
Kodai Okada ◽  
...  

✓ Hydrocephalus was induced in 13 dogs by injecting kaolin into the cisterna magna and was evaluated by computerized tomography (CT) scans. Modification of periventricular hypodensity was observed by metrizamide-enhanced CT ventriculography. Periventricular hypodensity was seen as early as 12 hours after kaolin injection. On CT ventriculography, metrizamide stayed longer in the ventricles of hydrocephalic dogs than in those of normal dogs, and migrated into the areas of periventricular hypodensity; the changes became significant within 12 to 24 hours. Four of the dogs were killed immediately after CT ventriculography, and the iodine concentration was measured. Iodine concentration was highest in the periventricular white matter, followed by the basal ganglia, and it was low in the cerebral and cerebellar cortex. When the change in Hounsfield units found by CT ventriculography at the regions of interest was compared to the actual iodine concentrations, the figures were quite compatible. Similarly, the specific gravity was measured in tissue from various parts of the brain of two hydrocephalic dogs, and compared against the value of that from five normal dogs. The specific gravity values were particularly low in the periventricular white matter of the hydrocephalic brains, suggesting a higher water content in that region. Since the increased migration of metrizamide occurred at the same region, it is suggested that development of periventricular hypodensity is due to increased transit of cerebrospinal fluid from the ventricles to the white matter.


1972 ◽  
Vol 37 (5) ◽  
pp. 538-542 ◽  
Author(s):  
George J. Dohrmann

✓ Adult dogs were rendered hydrocephalic by the injection of kaolin into the cisterna magna. One group of dogs was sacrificed 1 month after kaolin administration, and ventriculojugular shunts were performed on the other group. Hydrocephalic dogs with shunts were sacrificed 1 day or 1 week after the shunting procedure. All dogs were perfused with formalin at physiological pressure, and the brain stem and cervical spinal cord were examined by light microscopy. Subarachnoid granulomata encompassed the superior cervical spinal cord and dependent surface of the brain stem. Rarefaction of the posterior white columns and clefts or cavities involving the gray matter posterior to the central canal and/or posterior white columns were present in the spinal cords of both hydrocephalic and shunted hydrocephalic dogs. Predominantly in the dogs with shunts, hemorrhages were noted in the spinal cord in association with the clefts or cavities. A mechanism of ischemia followed by reflow of blood is postulated to explain the hemorrhages in the spinal cords of hydrocephalic dogs with shunts.


1978 ◽  
Vol 48 (4) ◽  
pp. 587-593 ◽  
Author(s):  
Victor A. Levin ◽  
Pokar M. Kabra ◽  
Mary A. Freeman-Dove

✓ A comparison of intravenous to intracarotid artery (ICA) administration of 14C-BCNU (1,3-bis(2-chloroethyl)-1-nitrosourea) was made in squirrel monkeys. Radioactivity was measured as soluble drug products and as RNA-, DNA-, and protein-bound radioactivity. The ICA administration of BCNU achieved 190% to 280% higher brain nucleic acid-bound drug levels than use of the intravenous route in the infused hemisphere and 130% to 280% higher levels than in the noninfused hemisphere. In addition, some brain regions directly subserved by the middle cerebral artery had bound drug levels four- to fivefold greater than those found in regions of noninfused brain. The data suggest that a need for BCNU dose reduction due to myelotoxicity may be an indication for ICA therapy in selected brain-tumor cases.


1986 ◽  
Vol 65 (2) ◽  
pp. 135-153 ◽  
Author(s):  
Edward G. Jones

✓ This article surveys the conventional neurotransmitters and modulatory neuropeptides that are found in the cerebral cortex and attempts to place them into the perspective of both intracortical circuitry and cortical disease. The distribution of these substances is related, where possible, to particular types of cortical neuron or to afferent or efferent fibers. Their physiological actions, where known, on cortical neurons are surveyed, and their potential roles in disease states such as the dementias, epilepsy, and stroke are assessed. Conventional transmitters that occur in afferent fibers to the cortex from brain-stem and basal forebrain sites are: serotonin, noradrenaline, dopamine, and acetylcholine. All of these except dopamine are distributed to all cortical areas: dopamine is distributed to frontal and cingulate areas only. The transmitter in thalamic afferent systems is unknown. Gamma aminobutyric acid (GABA) is the transmitter used by the majority of cortical interneurons and has a profound effect upon the shaping of receptive field properties. The vast majority of the known cortical peptides are found in GABAergic neurons, and the possibility exists that they may act as trophic substances for other neurons. Levels of certain neuropeptides decline in cases of dementia of cortical origin. Acetylcholine is the only other known transmitter of cortical neurons. It, too, is contained in neurons that also contain a neuropeptide. The transmitter(s) used by excitatory cortical interneurons and by the efferent pyramidal cells is unknown, but it may be glutamate or aspartate. It is possible that excitotoxins released in anoxic disease of the cortex may produce damage by acting on receptors for these or related transmitter agents.


1988 ◽  
Vol 68 (3) ◽  
pp. 487-490 ◽  
Author(s):  
Douglas B. Moreland ◽  
Franz E. Glasauer ◽  
James G. Egnatchik ◽  
Reid R. Heffner ◽  
George J. Alker

✓ A histologically confirmed case of focal dysplasia of the cerebral cortex is presented. The computerized tomographic, electroencephalographic, pathological, and angiographic findings are discussed with respect to this rare developmental disorder. A review of the literature is presented with a possible etiology for this condition.


2000 ◽  
Vol 92 (3) ◽  
pp. 442-447 ◽  
Author(s):  
Eric M. Massicotte ◽  
Richard Buist ◽  
Marc R. Del Bigio

Object. It can be inferred from data published in the literature that brain compression occurs in the early stages of acute hydrocephalus and that drainage of extracellular waste products is impaired. The authors hypothesized that compression of the cortex would alter water distribution and retard the diffusion of fluid in the hydrocephalic brain.Methods. Proton diffusion, blood perfusion, and T1 and T2 relaxation times were determined in adult rat brain by using magnetic resonance imaging prior to, and 1 and 8 days after induction of hydrocephalus by kaolin injection. Five anatomical regions of interest were studied. The striatum, dorsal cortex, and lateral cortex exhibited decreased T2 and apparent diffusion coefficient (ADC) values but no change in perfusion. Examination of white matter revealed an initial decrease in ADC followed by a significant increase. The T2 relaxation times increased and perfusion decreased progressively between 1 and 8 days after induction of hydrocephalus.Conclusions. Acute experimental hydrocephalus causes compression of gray matter, perhaps associated with reduction in total water, which impairs diffusion of water in the tissue. White matter compression and hypoperfusion precede the development of edema. These findings have importance for understanding the neurochemical changes that occur in hydrocephalic brains.


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