Evaluation of a system for serial biopsy of cerebral cortical tissue in an awake goat

1984 ◽  
Vol 247 (3) ◽  
pp. R600-R609
Author(s):  
D. A. Pelligrino ◽  
D. J. Miletich ◽  
R. F. Albrecht ◽  
D. Visintine ◽  
R. Ripper ◽  
...  
Keyword(s):  
Cerebral Metabolism ◽  
Tricarboxylic Acid Cycle ◽  
Cortical Tissue ◽  
Tissue Samples ◽  
Co2 Partial Pressure ◽  
Cranial Window ◽  
Serial Sampling ◽  
Unanesthetized Animals ◽  
Cortical Regions ◽  
Design And Methods

No techniques to date have been developed that allow investigators to obtain serial, rapidly frozen brain tissue samples in unanesthetized animals. The design and methods for implantation of cranial windows in goats are described in detail. The cranial window allows one direct and repeated access to the cerebral cortical surface. With each window, a parietal cortical area of 7.9 cm2 (minus the dura) is available for biopsy. Serial tissue samples are obtained using a suction-freezing system. Samples (100-250 mg) are frozen in less than 1 s. Up to six samples can be taken from each site. Goats were studied over a period of 2-5 days. No signs of sampling or immobilization stress were present as evidenced by a relatively constant level of arterial catecholamines and CO2 partial pressure (PCO2). Local cerebral blood flow (CBF) in the tissue under the window was of the same magnitude as that in other cerebral cortical regions and was unaffected by serial sampling. Levels of labile phosphates and of some glycolytic and tricarboxylic acid cycle-associated intermediates were minimally influenced by serial sampling. Greater variability in metabolite levels was seen for biopsies taken 2-5 days apart than for biopsies taken at 1- to 2-min intervals. However, variations within animals were less than variations among animals. This was especially true for acutely biopsied samples. The described methods provide a model for studies of cerebral metabolism in unstressed goats where anesthetic influences are avoided and where each animal can be utilized as its own control.

scholarly journals Integrative Metabolomic and Transcriptomic Analysis for the Study of Bladder Cancer

Cancers ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 686 ◽  
Author(s):  
Alba Loras ◽  
Cristian Suárez-Cabrera ◽  
M. Carmen Martínez-Bisbal ◽  
Guillermo Quintás ◽  
Jesús M. Paramio ◽  
...  
Keyword(s):  
Amino Acids ◽  
Bladder Cancer ◽  
Tricarboxylic Acid Cycle ◽  
Tumor Biology ◽  
Magic Angle Spinning ◽  
Magic Angle ◽  
Tissue Samples ◽  
Invasive Approach ◽  
Non Invasive ◽  
Angle Spinning

Metabolism reprogramming is considered a hallmark of cancer. The study of bladder cancer (BC) metabolism could be the key to developing new strategies for diagnosis and therapy. This work aimed to identify tissue and urinary metabolic signatures as biomarkers of BC and get further insight into BC tumor biology through the study of gene-metabolite networks and the integration of metabolomics and transcriptomics data. BC and control tissue samples (n = 44) from the same patients were analyzed by High-Resolution Magic Angle Spinning Nuclear Magnetic Resonance and microarrays techniques. Besides, urinary profiling study (n = 35) was performed in the same patients to identify a metabolomic profile, linked with BC tissue hallmarks, as a potential non-invasive approach for BC diagnosis. The metabolic profile allowed for the classification of BC tissue samples with a sensitivity and specificity of 100%. The most discriminant metabolites for BC tissue samples reflected alterations in amino acids, glutathione, and taurine metabolic pathways. Transcriptomic data supported metabolomic results and revealed a predominant downregulation of metabolic genes belonging to phosphorylative oxidation, tricarboxylic acid cycle, and amino acid metabolism. The urinary profiling study showed a relation with taurine and other amino acids perturbed pathways observed in BC tissue samples, and classified BC from non-tumor urine samples with good sensitivities (91%) and specificities (77%). This urinary profile could be used as a non-invasive tool for BC diagnosis and follow-up.

64 CRYOPRESERVATION OF CAT OVARIAN TISSUE BY VITRIFICATION

2013 ◽  
Vol 25 (1) ◽  
pp. 179 ◽  
Author(s):  
J. Galiguis ◽  
C. E. Pope ◽  
M. C. Gómez ◽  
C. Dumas ◽  
S. P. Leibo
Keyword(s):  
Ethylene Glycol ◽  
Dimethyl Sulfoxide ◽  
Ovarian Tissue ◽  
Genetic Material ◽  
Cortical Tissue ◽  
Rock Inhibitor ◽  
Tissue Samples ◽  
Preantral Follicles ◽  
Wide Range ◽  
Chi Square Analysis

The cryopreservation of ovarian tissue is linked to a wide range of possible applications, from oocyte harvesting to allo- and xenotransplantation. These procedures have significant potential for the preservation of valuable genetic material and endangered-species conservation. The objectives of the present study were to (1) compare viability of preantral follicles obtained from fresh v. vitrified feline ovarian cortex, (2) evaluate the effect of apoptotic inhibitors (ROCK inhibitor v. glutathione) on viability of follicles from vitrified samples, and (3) determine the optimal inhibitor concentration for follicle viability. In Experiment 1, 5 × 5 × 1 mm cortical tissue samples were obtained from excised cat ovaries and assigned to either the fresh control or vitrification group. Fresh samples were processed through a 230-micron-pore dissection strainer to collect preantral follicles. Follicles were then stained in Trypan blue to determine membrane integrity and survival rates. Vitrification samples were first equilibrated in 7.5% dimethyl sulfoxide and 7.5% ethylene glycol at ~22°C and then in vitrification solution consisting of 20% dimethyl sulfoxide, 20% ethylene glycol, and 0.5 M sucrose. They were then vitrified on a thin, perforated, metal strip (Cryotissue, Kitazato Biopharma, Fujinomiya, Japan). Samples were later warmed in 1.0 M sucrose at 38°C. Follicles were then collected and assessed for survival. In Experiment 2, follicles were collected from samples vitrified/warmed in cryo-media supplemented with either 3 × 104 nM ROCK inhibitor or 6 nM glutathione. Follicles from samples vitrified/warmed without inhibitor treatment were used as controls. In Experiment 3, tissue samples were vitrified/warmed in cryo-media supplemented with 0, 2, 6, or 10 nM glutathione before follicle viability was determined. Data were evaluated by chi square analysis. In Experiment 1, 637 and 340 follicles were collected from fresh and vitrified samples, respectively. Overall, survival was higher in freshly collected follicles when compared to those from the vitrified group (67 v. 18%, respectively; P < 0.05). Evaluation of apoptotic inhibitors was determined through collection of 314, 354, and 506 follicles from inhibitor-free, ROCK inhibitor, and glutathione-treated media, respectively. Follicles from samples vitrified in inhibitor-free media and in ROCK inhibitor survived at a lower rate than those from glutathione-treated samples (10 and 13% v. 18%, respectively; P < 0.05). In Experiment 3, a total of 539, 641, 625, and 632 follicles were collected from samples treated in 0, 2, 6, and 10 nM glutathione, respectively. There were no statistical differences in follicle survival among the 0, 2, and 6 nM groups. However, follicles treated in 10 nM glutathione survived at a higher rate than those vitrified/warmed in the absence of glutathione (20 v. 14%; P < 0.05). In summary, viability of preantral follicles from ovarian cortical tissue was significantly reduced by vitrification. Despite this, tolerance of such follicles to cryopreservation was improved by vitrifying and warming in cryo-media containing 10 nM glutathione. Partially funded by the LSU/ACRES Collaborative Project.

scholarly journals Effect of Glucose on Recovery of Energy Metabolism following Hypoxia—Oligemia in Mouse Brain: Dose-Dependence and Carbohydrate Specificity

1983 ◽  
Vol 3 (4) ◽  
pp. 486-492 ◽  
Author(s):  
Frank A. Welsh ◽  
Renee E. Sims ◽  
Ann E. McKee
Keyword(s):  
Blood Glucose ◽  
Energy Metabolism ◽  
Cerebral Metabolism ◽  
Dose Dependence ◽  
Poor Correlation ◽  
Dependent Manner ◽  
Tissue Samples ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Effect Of Glucose

Unilateral cerebral hypoxia–oligemia was produced in anesthetized mice using carotid artery occlusion combined with systemic hypoxia (10% O2). In the cerebral cortex ipsilateral to the carotid occlusion, ATP levels were depleted during a 30-min insult, but were restored to 64% of control during 60 min of recovery. Pretreatment of animals with glucose diminished the restoration of ATP in a dose-dependent manner. Thus, when blood glucose levels exceeded 12–13 m M (225 mg/dl), ATP recovery was greatly impaired. Neither galactose nor 3- O-methylglucose mimicked the detrimental effect of glucose. However, pretreatment with mannose, which is readily metabolized by brain, impaired restoration of ATP. The impairment, therefore, appears to be specific for substrates of cerebral metabolism. The ischemic accumulation of lactate in the ipsilateral cortex was augmented by only 30% at blood glucose levels well above the threshold for ATP recovery. Thus, unless recovery of energy metabolism is sensitive to small increments in brain lactate, it is difficult to explain the glucose-induced energy failure on the basis of enhanced lactic acidosis. Ipsilateral cerebral blood flow (CBF), measured with [14C]iodoantipyrine during hypoxia and recovery, was lower in glucose-pretreated than in saline-pretreated animals. However, the poor correlation between CBF and ATP, measured in the same tissue samples at 15 min recovery, failed to substantiate that regeneration of ATP was flow-limited early in recovery.

Cerebral Metabolism during Propofol Anesthesia in Humans Studied with Positron Emission Tomography 

1995 ◽  
Vol 82 (2) ◽  
pp. 393-403 ◽  
Author(s):  
Michael T. Alkire ◽  
Richard J. Haier ◽  
Steven J. Barker ◽  
Nitin K. Shah ◽  
Joseph C. Wu ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Animal Studies ◽  
Cerebral Metabolism ◽  
Anterior Cingulate ◽  
Emission Tomography ◽  
Whole Brain ◽  
Metabolic Pattern ◽  
Positron Emission ◽  
Cortical Regions

Background Although the effects of propofol on cerebral metabolism have been studied in animals, these effects have yet to be directly examined in humans. Consequently, we used positron emission tomography (PET) to demonstrate in vivo the regional cerebral metabolic changes that occur in humans during propofol anesthesia. Methods Six volunteers each underwent two PET scans; one scan assessed awake-baseline metabolism, and the other assessed metabolism during anesthesia with a propofol infusion titrated to the point of unresponsiveness (mean rate +/- SD = 7.8 +/- 1.5 mg.kg-1.h-1). Scans were obtained using the 18fluorodeoxyglucose technique. Results Awake whole-brain glucose metabolic rates (GMR) averaged 29 +/- 8 mumoles.100 g-1.min-1 (mean +/- SD). Anesthetized whole-brain GMR averaged 13 +/- 4 mumoles.100 g-1.min-1 (paired t test, P &lt; or = 0.007). GMR decreased in all measured areas during anesthesia. However, the decrease in GMR was not uniform. Cortical metabolism was depressed 58%, whereas subcortical metabolism was depressed 48% (P &lt; or = 0.001). Marked differences within cortical regions also occurred. In the medial and subcortical regions, the largest percent decreases occurred in the left anterior cingulate and the inferior colliculus. Conclusion Propofol produced a global metabolic depression on the human central nervous system. The metabolic pattern evident during anesthesia was reproducible and differed from that seen in the awake condition. These findings are consistent with those from previous animal studies and suggest PET may be useful for investigating the mechanisms of anesthesia in humans.

scholarly journals Focally administered succinate improves cerebral metabolism in traumatic brain injury patients with mitochondrial dysfunction

2021 ◽  
pp. 0271678X2110421
Author(s):  
Abdelhakim Khellaf ◽  
Nuria Marco Garcia ◽  
Tamara Tajsic ◽  
Aftab Alam ◽  
Matthew G Stovell ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Energy Metabolism ◽  
Mitochondrial Dysfunction ◽  
Cerebral Metabolism ◽  
Tricarboxylic Acid Cycle ◽  
Resonance Spectroscopy ◽  
Brain Tissue Oxygenation ◽  
Clinical Algorithm ◽  
Management Protocol

Following traumatic brain injury (TBI), raised cerebral lactate/pyruvate ratio (LPR) reflects impaired energy metabolism. Raised LPR correlates with poor outcome and mortality following TBI. We prospectively recruited patients with TBI requiring neurocritical care and multimodal monitoring, and utilised a tiered management protocol targeting LPR. We identified patients with persistent raised LPR despite adequate cerebral glucose and oxygen provision, which we clinically classified as cerebral ‘mitochondrial dysfunction’ (MD). In patients with TBI and MD, we administered disodium 2,3-13C2 succinate (12 mmol/L) by retrodialysis into the monitored region of the brain. We recovered 13C-labelled metabolites by microdialysis and utilised nuclear magnetic resonance spectroscopy (NMR) for identification and quantification. Of 33 patients with complete monitoring, 73% had MD at some point during monitoring. In 5 patients with multimodality-defined MD, succinate administration resulted in reduced LPR(−12%) and raised brain glucose(+17%). NMR of microdialysates demonstrated that the exogenous 13C-labelled succinate was metabolised intracellularly via the tricarboxylic acid cycle. By targeting LPR using a tiered clinical algorithm incorporating intracranial pressure, brain tissue oxygenation and microdialysis parameters, we identified MD in TBI patients requiring neurointensive care. In these, focal succinate administration improved energy metabolism, evidenced by reduction in LPR. Succinate merits further investigation for TBI therapy.

Permissive role of prostacyclin in cerebral vasodilation to hypercapnia in newborn pigs

1994 ◽  
Vol 267 (1) ◽  
pp. H285-H291 ◽  
Author(s):  
C. W. Leffler ◽  
R. Mirro ◽  
L. J. Pharris ◽  
M. Shibata
Keyword(s):  
Sodium Nitroprusside ◽  
Co2 Partial Pressure ◽  
Cranial Window ◽  
Prostacyclin Receptor ◽  
Artificial Cerebrospinal Fluid ◽  
Before And After ◽  
Newborn Pigs ◽  
Cerebral Vasodilation ◽  
Prostanoid Synthesis

Hypercapnic cerebral vasodilation in piglets is accompanied by increased cerebral prostanoid synthesis. Interventions that prevent the increased prostanoids also interfere with the vasodilation. However, the increased prostanoids may not produce vasodilation directly; instead, they may allow or enhance function of another mechanism. The present experiments examined the hypothesis that prostacyclin can allow, but may not directly produce, cerebral vasodilation to hypercapnia. Chloralose-anesthetized piglets were equipped with closed cranial windows for measurements of pial arteriolar diameters. Hypercapnia (arterial CO2 partial pressure approximately 70 mmHg) was administered before and after indomethacin (5 mg/kg iv) in all animals. Then artificial cerebrospinal fluid (aCSF) under the cranial window was replaced for the remainder of the experiment with aCSF containing vehicle, carbaprostacyclin (60 pM), iloprost (1 pM), prostaglandin E2 (PGE2; 1.7 and 3.3 nM), isoproterenol (10 and 100 nM), or sodium nitroprusside (1 microM), and hypercapnia was repeated. The two prostacyclin receptor agonists restored cerebral vasodilation to hypercapnia that had been blocked by indomethacin (to 92 +/- 31% and 76 +/- 11% of the before-indomethacin dilation for carbaprostacyclin and iloprost, respectively.) The highest dose of PGE2 partially restored the dilation (43 +/- 7% of the pre-indomethacin response). In contrast, neither isoproterenol nor sodium nitroprusside permitted significant dilation to hypercapnia following indomethacin treatment. These data indicate that prostacyclin can allow hypercapnic vasodilation to occur, but increasing levels do not appear to be necessary to cause the dilation directly. The short half-life of prostacyclin may explain why active prostanoid synthesis appears to be necessary for hypercapnia-induced cerebral vasodilation in newborn pigs.

Cerebral metabolism in hypoglycemic and hyperglycemic fetal lambs

1983 ◽  
Vol 245 (5) ◽  
pp. R730-R736 ◽  
Author(s):  
B. S. Richardson ◽  
A. R. Hohimer ◽  
J. M. Bissonnette ◽  
C. M. Machida
Keyword(s):  
Blood Glucose ◽  
Cerebral Metabolism ◽  
Blood Gases ◽  
Glucose Consumption ◽  
Ph Measurements ◽  
Co2 Partial Pressure ◽  
Sagittal Sinus ◽  
Cerebral O2 Consumption ◽  
Central Chemoreceptors ◽  
Fetal Breathing Movements

To investigate the mechanism whereby glucose affects fetal breathing movements (FBM), cerebral metabolism was studied in 12 unanesthetized fetal lambs, during fasting-induced hypoglycemia and after a subsequent fetal infusion of glucose. Preductal arterial and sagittal sinus blood samples were analyzed for glucose and oxygen concentrations and for blood gases and pH. Measurements of regional brain blood flow were made with radioactive microspheres. Maternal fasting of 24- to 36-h duration resulted in a decrease in fetal blood glucose from 1.061 +/- 0.085 mmol X l-1 to 0.664 +/- 0.053 (P less than 0.001). Although cerebral glucose and O2 uptake remained unchanged, sagittal sinus CO2 partial pressure (Pco2) and [H+] were significantly decreased and may have contributed to the observed decrease in FBM. A 2-h infusion of glucose to the fetuses of fasted animals resulted in an increase in blood glucose to 2.452 +/- 0.173 mmol X l-1. Cerebral O2 consumption was again unchanged; however, cerebral glucose consumption was significantly increased as were sagittal sinus Pco2 and [H+], which may have contributed to the observed increase in FBM. These findings are consistent with the hypothesis that glucose affects the incidence of FBM in part by altering the environment of central chemoreceptors.

scholarly journals Focally perfused succinate potentiates brain metabolism in head injury patients

2016 ◽  
Vol 37 (7) ◽  
pp. 2626-2638 ◽  
Author(s):  
Ibrahim Jalloh ◽  
Adel Helmy ◽  
Duncan J Howe ◽  
Richard J Shannon ◽  
Peter Grice ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Lactate Dehydrogenase ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Cerebral Metabolism ◽  
Tricarboxylic Acid Cycle ◽  
Redox Status ◽  
Tricarboxylic Acid ◽  
Acid Cycle ◽  
Pyruvate Ratio

Following traumatic brain injury, complex cerebral energy perturbations occur. Correlating with unfavourable outcome, high brain extracellular lactate/pyruvate ratio suggests hypoxic metabolism and/or mitochondrial dysfunction. We investigated whether focal administration of succinate, a tricarboxylic acid cycle intermediate interacting directly with the mitochondrial electron transport chain, could improve cerebral metabolism. Microdialysis perfused disodium 2,3-13C2 succinate (12 mmol/L) for 24 h into nine sedated traumatic brain injury patients' brains, with simultaneous microdialysate collection for ISCUS analysis of energy metabolism biomarkers (nine patients) and nuclear magnetic resonance of 13C-labelled metabolites (six patients). Metabolites 2,3-13C2 malate and 2,3-13C2 glutamine indicated tricarboxylic acid cycle metabolism, and 2,3-13C2 lactate suggested tricarboxylic acid cycle spinout of pyruvate (by malic enzyme or phosphoenolpyruvate carboxykinase and pyruvate kinase), then lactate dehydrogenase-mediated conversion to lactate. Versus baseline, succinate perfusion significantly decreased lactate/pyruvate ratio (p = 0.015), mean difference −12%, due to increased pyruvate concentration (+17%); lactate changed little (−3%); concentrations decreased for glutamate (−43%) (p = 0.018) and glucose (−15%) (p = 0.038). Lower lactate/pyruvate ratio suggests better redox status: cytosolic NADH recycled to NAD+ by mitochondrial shuttles (malate-aspartate and/or glycerol 3-phosphate), diminishing lactate dehydrogenase-mediated pyruvate-to-lactate conversion, and lowering glutamate. Glucose decrease suggests improved utilisation. Direct tricarboxylic acid cycle supplementation with 2,3-13C2 succinate improved human traumatic brain injury brain chemistry, indicated by biomarkers and 13C-labelling patterns in metabolites.

scholarly journals In vivo Monitoring of Cerebral Hemodynamics in the Immature Rat: Effects of Hypoxia-Ischemia and Hypothermia

2015 ◽  
Vol 37 (4-5) ◽  
pp. 407-416 ◽  
Author(s):  
Erin M. Buckley ◽  
Shyama D. Patel ◽  
Benjamin F. Miller ◽  
Maria Angela Franceschini ◽  
Susan J. Vannucci
Keyword(s):  
Cerebral Metabolism ◽  
Correlation Spectroscopy ◽  
Ordinal Scale ◽  
Cerebral Damage ◽  
Artery Ligation ◽  
Rat Pups ◽  
Baseline Levels ◽  
Term Births ◽  
Unanesthetized Animals

Background: Neonatal hypoxic-ischemic (HI) encephalopathy occurs in 1-4 per 1,000 live term births and can cause devastating neurodevelopmental disabilities. Currently, therapeutic hypothermia (TH) is the only treatment with proven efficacy. Since TH is associated with decreased cerebral metabolism and cerebral blood flow (CBF), it is important to assess CBF at the bedside. Diffuse correlation spectroscopy (DCS) has emerged as a promising optical modality to noninvasively assess an index of CBF (CBFi) in both humans and animals. In this initial descriptive study, we employ DCS to monitor the evolution of CBFi following HI with or without TH in immature rats. We investigate potential relationships between CBF and subsequent cerebral damage. Methods: HI was induced on postnatal day 10 or 11 rat pups by right common carotid artery ligation followed by 60-70 min hypoxia (8% oxygen). After HI, the pups recovered for 4 h under hypothermia (HI-TH group, n = 23) or normothermia (HI-N group, n = 23). Bilateral measurements of hemispheric CBFi were made with DCS in unanesthetized animals at baseline, before HI, and 0, 1, 2, 3, 4, 5, and 24 h after HI. The animals were sacrificed at either 1 or 4 weeks, and brain injury was scored on an ordinal scale of 0-5 (0 = no injury). Results: Carotid ligation caused moderate bilateral decreases in CBFi. Following HI, an initial hyperemia was observed that was more prominent in the contralateral hemisphere. After initiation of TH, CBFi dropped significantly below baseline levels and remained reduced for the duration of TH. In contrast, CBFi in the HI-N group was not significantly decreased from baseline levels. Reductions in CBFi after 4 h of TH were not associated with reduced damage at 1 or 4 weeks. However, elevated ipsilateral CBFi and ipsilateral-to-contralateral CBFi ratios at 24 h were associated with worse outcome at 1 week after HI. Conclusions: Both HI and TH alter CBFi, with significant differences in CBFi between hypothermic and normothermic groups after HI. CBFi may be a useful biomarker of subsequent cerebral damage.

Decreased c-fos expression in experimental neonatal hydrocephalus: evidence for reduced neuronal activation

1999 ◽  
Vol 7 (4) ◽  
pp. E14 ◽  
Author(s):  
James P. McAllister ◽  
Arcangela S. Wood ◽  
Martha J. Johnson ◽  
Robert W. Connelly ◽  
David J. Skarupa ◽  
...  
Keyword(s):  
Immunohistochemical Analysis ◽  
Cellular Level ◽  
Early Gene ◽  
Neuronal Activation ◽  
Cellular Mechanisms ◽  
Tissue Samples ◽  
Functional Changes ◽  
Fos Expression ◽  
Regulate Protein ◽  
Cortical Regions

Although neonatal hydrocephalus often results in residual neurological impairments, little is known about the cellular mechanisms responsible for these deficits. The immediate early gene, fos (c-fos), functions as a “third messenger” to regulate protein synthesis and is a good marker for neuronal activation. To identify functional changes in neurons at the cellular level, the authors quantified fos RNA expression and localized fos protein in the H-Tx rat model of congenital hydrocephalus. Tissue samples from sensorimotor and auditory regions were obtained from hydrocephalic rats and age-matched, normal litter mates at 1, 6, 12, and 21 days of age (four-six animals in each group) and processed for immunohistochemical analysis of fos and Northern blot analysis of RNA. At 12 days of age, hydrocephalic animals exhibited significant decreases in the ratio of fos immunoreactive cells to Nissl-stained neurons from both cortical regions, but no statistical differences were noted in fos expression. At 21 days of age, both the ratio of fos immunoreactive cells to Nissl-stained neurons and fos expression decreased significantly. The number of fos-positive neurons decreased in all cortical layers but was most prominent in layers V through VI. This decrease did not appear to be caused by neuronal death because examination of Nissl-stained sections revealed many viable neurons within the areas where fos immunoreactivity was absent. These results suggest that progressive neonatal hydrocephalus reduces the capacity for neuronal activation in the cerebral cortex, primarily in those neurons that provide corticofugal projections, and that this impairment may begin during relatively early stages of ventriculomegaly.

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