Sulfated glycoprotein-2 mRNA in the rat brain following transient forebrain ischemia.

Expression of sulfated glycoprotein-2 (SGP-2) mRNA was studied by in situ hybridization in rat brains submitted to transient forebrain ischemia of 30 min. Induction of this multifunctional protein has been previously observed following diverse types of brain lesions, and an involvement in programmed cell death and synaptic remodelling has been proposed. Ischemia was produced by four-vessel occlusion and followed by various recirculation times ranging from 15 min to 7 days.

Temperature effect on immunostaining of microtubule-associated protein 2 and synaptophysin after 30 minutes of forebrain ischemia in rat.

The regional distribution of the postsynaptic microtubule-associated protein 2 (MAP2) and the presynaptic marker protein synaptophysin was investigated by immunohistochemistry in brains of rats submitted to 30-min forebrain ischemia by four-vessel occlusion. The following brain temperature profiles during ischemia were compared: (1) constant brain temperature of 36 degrees C (normothermia; n = 5); (2) spontaneous temperature decline from 36 degrees to 31 degrees C (spontaneous hypothermia; n = 5) and (3) constant temperature of 30 degrees C (induced hypothermia; n = 5). Normothermia was produced by exposing the ischemic head to an external heat source, and induced hypothermia by cooling the head with liquid nitrogen vapours.

Heating of the brain to maintain normothermia during ischemia aggravates brain injury in the rat.

During brain ischemia temperature spontaneously declines. In animal experiments this decline is frequently prevented by stabilizing the temperature at the pre-ischemic level, using an external heat source. The present study examines whether this procedure influences the severity of ischemic injury.

In vivo relaxometry of three brain tumors in the rat: effect of Mn-TPPS, a tumor-selective contrast agent.

T1 and T2 were determined simultaneously in vivo at 4.7 T in implanted rat brain tumors. Three different tumor cell lines were implanted in the right caudate nucleus: the F98 glioma, the E367 neuroblastoma, and the RN6 schwannoma.

Microglial reaction in the rat cerebral cortex induced by cortical spreading depression.

The response of microglial cells to cortical spreading depression (CSD) was studied in rat brain by immunocytochemistry. CSD was elicited for one hour by the topical application of 4M potassium chloride solution and the microglial reaction examined immunocytochemically after 4, 16, 24 and 72 hours. CSD was sufficient to induce a microglial reaction throughout the cortex at 24 hours.

Barbiturate promotes post-ischemic reaggregation of polyribosomes in gerbil hippocampus.

A brief period of cerebral ischemia is followed by severe inhibition of protein synthesis which is slowly reversed in the resistant but not in the selectively vulnerable regions of the brain. Inhibition occurs at the translational level, as evidenced by the disaggregation of ribosomes into monosomes. In order to evaluate the importance of this disturbance for the evolution of ischemic injury, the effect of the neuroprotective drug, pentobarbital, on ribosomal aggregation was studied in gerbils subjected to 5 min bilateral carotid artery occlusion.

T1 snapshot FLASH measurement of rat brain glioma: kinetics of the tumor-enhancing contrast agent manganese (III) tetraphenylporphine sulfonate.

The ultrafast inversion recovery snapshot FLASH technique was used to determine the kinetics of the contrast agent manganese (III) tetraphenylporphine sulfonate (MnTPPS) in experimental brain tumors in rats. In the first part of the investigation this technique was validated with the conventional inversion recovery spin-echo method by comparing in vivo T1 data of a normal rat brain. Agreement between T1 values obtained from both techniques was complete, as tested for a large number of pixels in identical coronal slices.

Laser doppler flowmetry in CA1 sector of hippocampus and cortex after transient forebrain ischemia in gerbils.

Background And Purpose: Local differences in the hemodynamic response to transient ischemia could be involved in the development of selective vulnerability. These differences were studied in vulnerable and nonvulnerable regions of the brain.

Methods: Five gerbils were subjected to 10 minutes of bilateral forebrain ischemia, and cerebral blood flow was measured continuously in the frontal cortex and CA1 sector of the hippocampus using laser Doppler flowmetry.

Neuronal damage after repeated 5 minutes of ischemia in the gerbil is preceded by prolonged impairment of protein metabolism.

The effect of single or repeated episodes of cerebral ischemia on protein biosynthesis and neuronal injury was studied in halothane-anesthetized gerbils by autoradiography of [14C]leucine incorporation into brain proteins and light microscopy. For quantification of the protein synthesis rate, the steady-state precursor pool distribution space for labeled and unlabeled free leucine was determined by clamping the specific activity of [14C]leucine in plasma, and by measuring free tissue leucine in samples taken from various parts of the brain. Control values of protein synthesis were 14.

Immunocytochemical study of an early microglial activation in ischemia.

Transient arrest of the cerebral blood circulation results in neuronal cell death in selectively vulnerable regions of the rat brain. To elucidate further the involvement of glial cells in this pathology, we have studied the temporal and spatial distribution pattern of activated microglial cells in several regions of the ischemic rat brain. Transient global ischemia was produced in rats by 30 min of a four-vessel occlusion.

The microglial reaction in the rat hippocampus following global ischemia: immuno-electron microscopy.

Transient arrest of the cerebral circulation leads to neuronal cell death in selectively vulnerable regions of the central nervous system. It has recently been shown at the light microscopical level that neuronal necrosis is accompanied by a rapid microglial reaction in ischemia (Gehrmann et al. (1992) J.

Time profile of calcium accumulation in hippocampus, striatum and frontoparietal cortex after transient forebrain ischemia in the gerbil.

The topical and temporal relationship between neuronal injury and calcium loading was investigated in gerbils following bilateral carotid artery occlusion for 5 or 10 min and recirculation times from 15 min to 7 days. The association of histochemically visible calcium deposits with neuronal death was assessed by combining two calcium stains, alizarin red and arsenazo III, with conventional histological techniques. Neuronal calcium accumulation was evaluated morphometrically in the striatum, the frontoparietal cortex and the CA1 and CA4 sectors of the hippocampus.

Therapeutic window of halothane anesthesia for reversal of delayed neuronal injury in gerbils: relationship to postischemic motor hyperactivity.

The effect of postischemic halothane anesthesia on locomotor activity and delayed neuronal injury in the hippocampal CA1 sector was examined in gerbils subjected to 5-min forebrain ischemia. Locomotor activity was assessed for 48 h after ischemia using an animal activity monitor, and CA1 injury was evaluated by counting the number of surviving neurons following 7 days of recirculation. Sham-treated animals exhibited a slight decrease of motor activity for about 1 day after surgery.

Cerebral polyamine metabolism in reversible hypoglycemia of rat: relationship to energy metabolites and calcium.

Thirty minutes of insulin-induced reversible hypoglycemic coma (defined in terms of cessation of EEG activity) was produced in anesthetized rats. At the end of the hypoglycemic coma or after recovery for 3, 24, or 72 h induced by glucose infusion, the animals were reanesthetized and their brains frozen in situ. Two control groups were used: untreated controls without prior manipulations, and insulin controls, which received injections of insulin followed by glucose infusion to maintain blood glucose within the physiological range.

[14C]leucine incorporation into brain proteins in gerbils after transient ischemia: relationship to selective vulnerability of hippocampus.

Regional [14C]leucine incorporation into brain proteins was studied in gerbils after global ischemia for 5 min and recirculation times of 45 min to 7 days, using a combination of quantitative autoradiography and biochemical analysis. After recirculation for 45 min, incorporated radioactivity was reduced to approximately 20-40% of control values in all ischemic brain regions. Specific activity of the tracer, in contrast, was increased, a finding indicating that the reduced incorporation of radioactivity was not due to reduced tracer influx from plasma or a dilution of the tracer by increased proteolysis.

Locomotor hyperactivity and hippocampal CA1 injury after transient forebrain ischemia of gerbils.

The influence of a repeated transient forebrain ischemia on the development of post-ischemic locomotor hyperactivity was determined in the gerbil. Animals were subjected to two episodes of 5 min bilateral carotid artery occlusion in halothane anesthesia separated by one week. By using an animal activity monitor for counting spontaneous movements, the locomotor activity was assessed before and after each ischemic period.

Ornithine decarboxylase in reversible cerebral ischemia: an immunohistochemical study.

Anesthetized Mongolian gerbils were subjected to 5-min ischemia and 8 h of recirculation. Vibratom sections were taken for studying changes in ornithine decarboxylase (ODC) immunoreactivity using an antiserum to ODC, and tissue samples were taken for measuring ODC activity. After 5-min ischemia and 8-h recirculation ODC activity increased 11.

Therapeutic window of CA1 neuronal damage defined by an ultrashort-acting barbiturate after brain ischemia in gerbils.

Previous therapeutic studies on the prevention of selective vulnerability of neurons in the hippocampus have suggested that the critical period for induction of delayed neuronal injury occurs early during recirculation. To determine the onset and duration of this period, an ultrashort-acting barbiturate (methohexital) was infused into the left carotid artery of 47 gerbils after various times of recirculation following 10 minutes of bilateral forebrain ischemia. Neuronal density in the left CA1 sector was determined 7 days later by counting the number of surviving neurons per millimeter of pyramidal cell layer.

Threshold of carotid artery back pressure for delayed neuronal injury in the hippocampus after bilateral common carotid artery occlusion in gerbils.

The threshold of carotid artery back pressure for the development of neuronal injury in the hippocampus was determined in gerbils following bilateral carotid artery occlusion of 5 or 10 min. Arterial back pressure was measured during ischemia at the left carotid bifurcation distal to the vascular occlusion, and neuronal injury evaluated one week after ischemia by counting the number of surviving neurons in the left hippocampal CA1 sector. With an arterial back pressure below 5 mm Hg, the mean density of surviving neurons decreased from 199 +/- 16/mm (mean +/- SD) to less than 21/mm both after 5 and 10 min ischemia (P less than 0.

Prevention of postischemic hyperthermia prevents ischemic injury of CA1 neurons in gerbils.

Halothane-anesthetized Mongolian gerbils were submitted to 5-min bilateral carotid artery occlusion. After ischemia, halothane anesthesia was continued for various periods of up to 85 min, and the degree of CA1 neuronal injury was estimated 7 days later by counting the number of surviving pyramidal cells. During ischemia and postischemic halothane anesthesia, rectal and cranial temperature was kept at control level (37.

Selective vulnerability in the gerbil hippocampus: morphological changes after 5-min ischemia and long survival times.

The morphology of the hippocampus of Mongolian gerbils was investigated by light and electron microscopy after 5-min forebrain ischemia and survival times of up to 10 months. After 3 weeks recirculation only 5.8% of pyramidal neurons of the CA1 (cornu ammonis 1) sector had survived but the thickness of the inner and outer hippocampal layers did not change.

Myelin phagocytosis by peritoneal macrophages in organ cultures of mouse peripheral nerve. A new model for studying myelin phagocytosis in vitro.

Organ cultures of degenerating nerve fascicles were exposed to cultured macrophages obtained by peritoneal lavage. Invasion of the nerve fascicle by phagocytes was shown by prelabeling with carbon and with electron microscopy. There was massive active phagocytosis of degenerating myelin sheaths.