The incorporation of (1-3H)glucosamine into biochemical fractions of brain was studied in mice trained in a conditioned avoidance jump-up task, in mice yoked to the trained animals, and in undisturbed mice in their home cages. The (3H)glucosamine was injected subcutaneously 15 min before 15 min of training, and the mice killed after a total pulse time of one hour. There was a consistent and significant increase of about 21 percent of the incorporation of the 3H into the brain ganglioside fraction when trained mice were compared with quiet mice. This increase was not observed in any of the other chemical fractions studied, including the total chloroform-methanol-soluble compounds, the non-ganglioside lipids, and the chloroform-methanol-insoluble compounds (radioactivity principally in glycoprotein). Yoked mice showed an intermediate level of incorporation, exhibiting only a 12 percent increase in the ganglioside fraction. When the individual ganglioside species were analyzed by thin-layer chromatography the changed incorporation was not specific for any ganglioside species.

Animals↗

PubMedDate not supplied

Role of calpain in spinal cord injury: increased mcalpain immunoreactivity in spinal cord after compression injury in the rat.

Spinal cord injury was induced in rats by compression technique using 10 or 20 g compression for 5-10 min. Calpain immunoreactivity was examined in the lesion as well as in the adjacent areas of the cord at different times following injury. Elevated calpain immunoreactivity was found in the lesion compared to sham control. The increase in calpain immunoreactivity was dependent on the time and the degree of trauma. Areas adjacent posterior or caudal to the lesion also showed increased calpain immunoreactivity. Most of the cells in the dorsal and ventral funiculi with increased calpain staining were astrocytes and microglia. Proliferation of microglia and/or activation of astrocytes in the lesion, identified with lectin binding GSA and glial fibrillary acidic protein staining, was seen at 1 and 3 days after trauma, respectively. Eccentric nuclei and shrunken neurons with increased calpain staining were seen in the ventral horn. The extent of increase in calpain immunoreactivity in the lesion was also proportional to the degree of trauma. The elevated calpain immunoreactivity suggests increased calpain expression (mRNA), synthesis (protein level), and activity in the lesion of cord following injury as compared to sham control. This finding supports a pivotal role for calpain in tissue degeneration in spinal cord trauma.

Animals↗

PubMedDate not supplied

A model of focal ischemic stroke in the rat: reproducible extensive cortical infarction.

In the search for a more reproducible focal ischemic stroke model in the rat, we systematically interrupted blood flow to the right middle cerebral artery territory by ligating the right middle cerebral artery, and the right and left common carotid arteries in succession. Using a laser-Doppler flowmeter, we found that the relative surface blood flow in cerebral cortex supplied by the right middle cerebral artery decreased to 62, 48, and 18% of baseline respectively after successive ligation of the right middle cerebral artery, and the right and left common carotid arteries. A focal infarct in the cerebral cortex supplied by the right middle cerebral artery was consistently noted after ligation of the right middle cerebral and the right common carotid arteries and temporary clip occlusion of the left common carotid artery for 60 min. The surface areas of infarction measured 100 +/- 6 mm2 and the maximal cross-sectional area of infarction was 10.4 +/- 1.1 mm2 (N = 10). The mortality rate was 7% (N = 70). The characteristic changes of ischemic necrosis were limited to the cortex with sparing of subcortical structures. No motor deficits occurred. Occlusion of the right middle cerebral artery alone or together with the right common carotid artery did not consistently cause gross infarction and the maximal cross-sectional area of infarction was smaller (the right middle cerebral artery, 1.7 +/- 0.8 mm2, N = 10; the right middle cerebral artery plus the right common carotid artery, 4.8 +/- 1.9 mm2, N = 10). Permanent ligation of the right middle cerebral artery and both common carotid arteries had a high mortality (60% in 3 days, N = 10).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Intravenous prostacyclin in acute nonhemorrhagic stroke: a placebo-controlled double-blind trial.

The therapeutic efficacy of prostacyclin in nonhemorrhagic cerebral infarction was assessed in a placebo-controlled double-blind trial. A total of 80 patients with stroke onset within 24 hours were randomized into placebo (37 patients) and prostacyclin (43 patients) groups. Demographic data and risk factors were comparable. Patients in the prostacyclin group received a continuous i.v. infusion of prostacyclin at an average rate of 8.5 ng/kg/min for an average of 64 hours. The placebo group received vehicle only in a similar fashion. During treatment hemodynamic changes were more prominent in the patients receiving prostacyclin and included reduction of systolic and diastolic blood pressure and increase in pulse rate. In contrast there was only a slight (but significant) reduction of diastolic blood pressure in the placebo group. Neurologic deficit scores were determined on admission, at Day 3, and at Weeks 1, 2, and 4. Mean neurologic deficit scores upon entry were comparable in the placebo and prostacyclin groups, and a significant improvement in the score for neurologic deficit was noted in both. The placebo group tended to fare better throughout the study, with a significant difference in neurologic deficit score favoring the placebo group at Week 2 (p = 0.0048). Two patients in the placebo and one in the prostacyclin group died. The only difference in adverse reactions was flushing (6 patients in prostacyclin vs. 0 in placebo group, p less than 0.05). The results of this study suggest a lack of therapeutic efficacy of prostacyclin in a defined population of patients with nonhemorrhagic cerebral infarction.

Acute Disease↗

PubMedDate not supplied

Developmental and topographic expression of neutral glycosphingolipids in vertebrate brain.

We have examined neutral glycosphingolipid (Ngsl) expression in embryonic (E), post-natal (P) and adult rodent brain employing digoxigenin immunostaining (DIG-IS) and anti-Ngsl antisera (both monospecific polyclonal and monoclonal) directed toward specific carbohydrates. Several previously unknown long-chain (-CHO = or > 4) Ngsls have been identified. Four Ngsls have been purified and characterized as GgOse4Cer or GA1, Galactosyl beta 1-3globoside, Fuc alpha 1-3nLcOse4Cer or Lewis X (Le(x)) and a novel GalNAc beta 1-4GA1. A few transient bands appear at different developmental ages. Several fast migrating cerebrosides have also been identified during the early phase of active myelination and tentatively characterized as derivatives of galactosylceramide. Immunohistochemical localization of GA1, Le(x) and GalNAc-GA1 in adult rodent brain shows unique and specific cellular topographies of these carbohydrate antigens.

Animals↗