Characteristics of 3HGABA release evoked by oxygen-glucose deprivation in rat cerebral cortex slices

In present study, the mechanism for oxygen-glucose deprivation -induced [3H]gamma-aminobutyric acid (GABA) from cerebral cortex slices of the rat was examined. Deprivation of oxygen and glucose(OGD) from Mg2+-free artificial cerebrospinal fluid, induced significant release of [3H]GABA (7.4+/-0.6% of total tissue content) from cerebral cortex slices. OGD-induced release of [3H]GABA was significantly attenuated by tetrodotoxin(TTX)(1 micrometer), Mg2+(1.2 mM), MK-801(10 micrometer), ketamine(10 micrometer), N-methyl-D-aspartate(NMDA) receptor antagonists, (DNQX)(30 micrometer), and 6-cyano-7-nitroquinoxaline-2,3-dione(CNQX)(30 micrometer), kainate/AMPA receptor antagonists, or 6-nitro-7-sulphamoyl-benzo[f]quinoxaline-2, 3-dione(NBQX)(10 micrometer), a selective AMPA receptor blocker. OGD-evoked [3H]GABA release was attenuated by (NG-nitro-L-arginine methyl ester(L-NAME) and 7-nitronidazole, nitric oxide synthase inhibitors, and methylene blue, potentiated by zaprinast, a cGMP phosphodiesterase inhibitor. OGD-induced release of [3H]GABA was inhibited by nipecotic acid, a selective neuronal GABA transporter blocker, and potentiated by DL-2.4-diamino-n-butyric acid(DABA), a neuronal and glial GABA transporter blocker. Dantrolene (30 micrometer) and 1,2-bis (2-aminophenoxy)-ethane-N, N, N', N'-tetraacetic acid tetrakis (acetoxymethyl) ester(BAPTA-AM)(30 micrometer), inhibitors of intracellular Ca2+ release, verapamil(5 micrometer), omega-conotoxinGVIA(100 nM) and omega-agatoxinIVA(100 nM), inhibitors of voltage-dependent Ca2+ channels, significantly attenuated the OGD-induced release of [3H]GABA. These results suggest that glutamate is involved in OGD-evoked [3H]GABA release, and this release is achieved by Ca2+-dependent exocytosis and reversal of transporters, and can be modulated by various neuronal mechanisms.

Mechanisms of release of 3H Hydroxytryptamine evoked by hypoxia and hypoglycemia in rat cerebral cortex slices

Pathophysiology of brain ischemia is characterixed by a complex cascade of hemodynamic, electrophysiological and biochemical processes. It has been generally accepted that glutamate mediates the ischemic brain damage, excitotoxicity, and induce neurotramsmitter release from various brain tissues in ischemic milieu. In presen study, the mechanism for ischemia-induced [3HT]5-hydroxytryptamine(5-HT) from cerebral cortex slices of the rat was examined. Ischemia, deprivation of oxygen and glucose from Mg2+-free artificl cerebrospinal fluid, induced significiant release of [3H]5-HT(7.2+0.6% of total tissue content) from the tissues. This ischemia-induced release of [3H]5-HT from the slices was significiantly attenuated by TTX(1 yM), Mg2+(102mM). MK-801(10yM), ketamine(10yM), NMDA receptor antagonists, DNQX(30yM), a kainate/AMPA receptor antagonist, or carbetapentane(31yM), an inhibitor of glutamate release. Fluoxetine, a selective blocker for 5-HT transporter, inhibited the ischemia-induced release of [3H]5-HT. Omission of Ca2+ from incubation media potentiated ischemia-evoked [3H]5-HT release and the inhibitory effect of blockers for transporter. Dantrolene (30yM) and ryanodine(100 nM) and -conotoxinGVIA(100 nM), inhibitors of N-type Ca2+ channels, sifnificiantly attenuated the ischemia-induced release of [3H]5-HT, but verapamil(5 yM), an inhibitor of L-type Ca2+ channels, did not. Fluoxetine(100 nM), a relatively selective 5-HT transporter blocker, significiantly inhibited the ischemia-induced release of [3H]5-HT. Theses results suggest that glutamate is involned in ischemia-evoked [3H]5-HT release, and this release is achieved by Ca2+=dependent exocytosis and reverdsal of transporters, and can be modulated by various neuronal mechanisms.

Acute encephalitis following rubella virus infection

Two patients(17-year-old and 23-year-old men) with rubella infection had maculopapular rash, lymphadenopathy and lower grade fever. Several days after the onset of rash, they showed convulsions and fell in confused states. The CSF examinaion showed lymphocytic pleocytosis, increased protein and normal glucose level. Rubella infection and its CNS complications in both cases were diagnosed by detection of IgG and IgM in serum and CSF employing radioimmunoassay. Imaging study was done. A brain magnetic resonance imaging(MRI) findings were normal but brain single photon emmission computed bomography(SPECT) sjhowed slightly decreased uptake of left frontal and temporal lobe in one case. Both patients were recovered without any sequelae.

A Familial Case of Choreoacanthocytosis

We have experienced a family case of 3 sisters in whom the proband showed a complete form of the choreo-acanthosytosis. 439-year-old female proband was admitted because of frequent seizures. She was alert, well-oriented, and had no gross memory defects. She had slurred speech, choreic movements of chin. Deep tendon reflexes on the both lower extremities were decreased. Laboratory examination showed acanthocytes in her peripheral red blood cells, normal serum lipid values, increased creatine-phosphokinase levels and bilateral caudate atrophy on her brain CT scan. Electrophysiological data were consistent with lower motor neuron dysfunction. Another 33-year-old sister with frequent seizures and psychic problems also showed acanthocytosis. The other 36-year-old sister has been treated under the diagnosis of schizophrenia for 10 years, not showing acanthocytosis.

The Mechanism on the Glutamate-evoked Release of 3H) norepinephrine in Rat Cortex Slices

Glutamate Is the predominant excitatory neurotransmitter in the mammalian CNS. To elucidate the influence of glutamate on the noradrenergic neurotransmission in rat cortex, we examined the effects of agents that act in several steps of neurotransmission on [3H]norepinephrine ([3H])NE) release evoked by glutamate. Glutamate (1 mM) evoked significant release of [3H]NE from rat cortex slices in the absence of Mg2+in the incubation media. This effect was attenuated by cromakalime (10 nM) and lemakalime (10 nM), and the inhibitory effect of cromakalime was abolished by glipizide. Inhibitory effect of muscimol (30 uM) and baclofen (3 uM, 30 uM) was antagonized by biccuculine (3 uM), respectively. Nipecotic acid(10 uM), DABA(300 uM), and beta-alanine(100 uM) attenuated the glutamate-induced release of [3H]NE. Dihydrokinate (300 uM) PDC (100 nM) increased the glutamate-induced release of [3H]NE. Ifenprodile (10 nM) and arcaine (1 uN), blockers of polyamine site, attenuated the release of ("H)NE. The stimulatory effect of spermine was abolished by arcaine. CPA(100 nM) and CPCA(100 nM), EHNA(30 uN) and NBTI(1 uN) attenuated the release of ("H)NE. Verapamil(S uN), nitredipine(10 uN), u- conotoxin (100 nM) and flunarizine (5 uM) attenuated the release of (3H)NE. Dantrolene(30 uM), KT-362(3 uM), and ryanodine(10 nM), attenuated the glutamate-induced release of [3H]NE. Glycine (10 uM) increased the release of [3H]NE. DCQX (30 uN) attenuated the release of [3H]NE. These results suggest that glutamate-evoked release of norepinephrine can be modulated by GABAergic, adenosinergic neurotransmitters, and by various drugs which modulate ion channel activities in rat cortex.

Henoch-schonlein Purpura Involving Cerebral Hemisphere

Henoch-Schonlein Purfrura is a generalized small vessel vasculitis of hypersensitivity type characterized primarily by a purpuric skin lesion, renal involvementwith hematuria and proteinuria, arthralgia, and colicky abdominal pain. A possible neurologic involvement was recognized in 1914 by Osler. A case of a 7 1/2-year-old male patient with Henoch-Schonlein purpura developed neurologic manifestations including seizure and mental status change. The cranial CT demonstrated a occipital hemorrhage of right side and cerebral edema with contrast enhancing scattered dilated vessels. The EEGchanges were slow wave activities in acute stage. The follow-up EEG shows that the slow wave activities were more improved than previous and that multiple spike waves were recorded at bothfronto-temporo-parietal areas with phase reversals. The vasculitis of HenochSch6nlein purpura can involve the nervous system.