Neuron-specific γ-enolase derived from human glioma

Neuron-specific γ-enolase in human neurogenic tumors, including gliomas, transplanted gliomas, and permanent human glioma cell lines, was studied quantitatively, using newly established enzyme immunoassay methods, together with immunostaining of the tissue and cell preparations. A significantly high level of γ-enolase was found in some glioblastomas, astrocytomas and oligodendrogliomas as well as medulloblastomas. Glioblastomas transplanted into mice and cultured cell lines derived from the same origins, as well as the permanent human glioma cell lines, also contained γ-enolase, although the contents were low compared with findings in the original tumor tissues. Immunohistochemically, γ-enolase stained intensely in the glioblastomatous cells. Serum γ-enolase concentrations in some patients with gliomas and those of all the transplanted mice were enhanced. The serum γ-enolase levels in the mice correlated well with size of the transplanted tumor tissues. These results indicate that neuron-specific γ-enolase is produced in some neurogenic tumors of nonneuronal origin, therefore, serum γ-enolase may be a useful biomarker for monitoring the extent of disease in patients with gliomas.     

Calcium-dependent component of massive increase in extracellular potassium during cerebral ischemia as demonstrated by microdialysis in vivo

This study characterizes the physiological features and limitations of K(+)-free dialysis to detect changes in extracellular concentration of K+ ([K+]e) in the rat hippocampus in vivo. It also demonstrates the effects of Ca(2+)-free perfusate containing Co2+ or Mg2+, which blocks Ca2+ entry into the presynaptic nerve terminal, on the abrupt increase in [K+]e detected by this technique during cerebral ischemia. K(+)-free dialysis for 40 min caused no significant changes in the baseline [K+]e. In contrast, Ca(2+)-free dialysis for 40 min significantly reduced the extracellular Ca2+ concentration. Under this condition, together with addition of Co2+ or Mg2+ to the perfusate, the increase in [K+]e was delayed, and a delay in reaching the maximum level was observed in a dose-dependent manner. These results are consistent with the hypothesis that the initial increase in [K+]e during cerebral ischemia is related to the Ca(2+)-dependent exocytotic release of neurotransmitters from depolarized nerve terminals.     

The ventrolateral medulla of the cat mediates vestibulosympathetic reflexes

Extracellular recordings were made from 94 neurons located in the ventrolateral medulla (VLM) whose firing rate was affected by vestibular nerve (VN) stimulation; 50 of these units were in the subretrofacial (SRF) nucleus, which contains cells that make direct excitatory connections with sympathetic preganglionic neurons. The sample included 12 SRF cells which were antidromically driven from the upper thoracic spinal cord and had conduction velocities of 10 m/s or less; the effect of VN stimulation on all but one of these units was inhibition. The onset latency of the response to VN stimulation was long [20.3 +/- 3.7 (S.E.M.) ms, n = 9, for the antidromically activated neurons and 12.1 +/- 1.2 ms, n = 73, for the others], suggesting that the effects were predominantly polysynaptic. In addition, most of the spontaneously active units tested (33/36) received convergent inputs from the carotid sinus nerve (CSN), as would be expected for neurons which influence sympathetic outflow. Vestibular-elicited inhibition of SRF neurons with projections to the intermediolateral cell column could account for late, long duration inhibition of sympathetic discharges produced by labyrinth stimulation.     

A case of generalized komuragaeri disease (Satoyoshi disease) treated with glucocorticoid

Generalized komuragaeri disease (Satoyoshi disease) is a rare disorder of unknown etiology, characterized by painful muscle spasms, alopecia, diarrhea and various endocrine disorders. We administered glucocorticoid to a girl with this disease, resulting in a marked improvement of all clinical features. The patient was a 15-year-old girl. Since the age of 13 years, she had had intermittent painful muscle spasms, which affected any skeletal muscles 5 to 15 times a day at exercise and at rest and lasted for a few minutes. At the age of 14 years, she had idiopathic thrombocytopenic purpura which responded to the glucocorticoid treatment. Amenorrhea and orthostatic hypotension developed at the age of 14 years. Then the loss of body and head hair was noticed and progressed slowly. She had not experienced severe diarrhea. On admission, her physical and neurological examinations showed no abnormalities except for the thin hair and frequent muscle spasms. Laboratory examinations showed elevated levels of serum creatine kinase and aldolase, positive antinuclear antibody of speckled pattern and a mild disturbance in carbohydrate absorption. Endocrinological tests suggested the dysfunction of hypothalamus as a cause of amenorrhea. Electromyogram showed large action potentials on spasms. She was treated with glucocorticoid, 2 mg/kg on alternate days. The muscle spasms decreased gradually in frequency and duration in 1 month of treatment, and disappeared in 4 months. The growth of her hair was noticed and orthostatic hypotension disappeared in 4 months. Menstruation became regular in 7 months. The muscle spasms worsened when the dosage of glucocorticoid was reduced, and they improved on the increased dosage. She was free of symptoms at 6 months after the successful diminution of glucocorticoid. The etiology of this disease has not been revealed. The association of autoimmune disorders and the responsiveness of all clinical features to glucocorticoid suggest that an autoimmune process is involved in the pathogenesis of generalized komuragaeri disease.     

Effect of endothelin on gastric mucosal lesion in rats

Gastric mucosal blood flow and gastric mucosal prostaglandin E2 (PGE2) and prostacyclin (PGI2) were investigated in male Wistar rats intraarterially injected with endothelin (ET), an endothelium-derived vasoconstrictor peptide. Immediately following ET (4 nmol/kg) administration, gastric mucosal blood flow decreased. Then 30 min later, the blood flow reached the minimum, but PGE2 and PGI2 showed the highest value. PGE2 showed a tendency to decrease 90 min later, while PGI2 continued to show high value. There were redness and hemorrhagic damage in the gastric mucosa. Endogenous PGs were presumed to be relate to the regulation of the development of the mucosal damage owing to decrease in the blood flow after ET administration.     

Effects of chronic treatment with trihexyphenidyl and carbamazepine alone or in combination with haloperidol on substance P content in rat brain: a possible implication of substance P in affective disorders

To assess the roles of substance P in neurologic or psychiatric illnesses, effects of acute or chronic (40- or 80-day dietary) treatment with trihexyphenidyl and carbamazepine alone or in combination with haloperidol on substance P content were investigated in the rat brain. Either acute or chronic trihexyphenidyl administration did not alter substance P content when administered alone and did not prevent the haloperidol-induced substance P decrease in the striatum and substantia nigra when coadministered with haloperidol. Chronic dietary carbamazepine administration dose-dependently increased substance P content in the striatum and substantia nigra, but not in the raphe area, in a haloperidol-reversible manner. Carbamazepine also dose-dependently increased gamma-aminobutyric acid levels in the substantia nigra without altering the striatal dopamine turnover rate. The lack of effect of trihexyphenidyl, an anticholinergic drug used to treat antipsychotic drug-induced extrapyramidal (Parkinson) syndromes, suggests that antipsychotic drug-induced reduction in substance P content is not involved in the extrapyramidal side effects. Since the effects of carbamazepine on substance P content are identical with previously described effects of lithium, an alteration in substance P neurotransmission may be one of the neurochemical bases of common clinical and behavioral effects of carbamazepine and lithium on affective disorders.     

Patulous Eustachian tube in spontaneous intracranial hypotension syndrome

A 48-year-old slender woman presented with a rare case of spontaneous intracranial hypotension syndrome manifesting as patulous Eustachian tube. The patient complained of sudden onset of ear fullness and nasal voice as well as typical orthostatic headache. Patulous Eustachian tube was identified by observation of synchronous movement of the tympanic membrane with respiration and swallowing. The diagnosis of spontaneous intracranial hypotension was confirmed by negative cerebrospinal fluid pressure, and typical magnetic resonance imaging and radioisotope cisternography findings. All symptoms completely resolved within a few days after epidural blood patch treatment. Changes in the venous blood distribution led by collapse of the dural sac of the cervical spine in the standing position presumably caused decreased size of the pterygoid venous plexus around the Eustachian tube.