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-and K + -evoked stimulation) did not aect tyrosine hydroxylase activity in vivo. 6 These ®ndings suggest that striatal DOPA release is neurotransmitter-like and that, unlike the mechanisms of striatal dopaminergic transmission, this striatal DOPA transmission is at least partly regulated by voltage-sensitive Ca 2+ channels.

To clarify the effects of adenosine receptor subtypes (A1, A2, and A3) on hippocampal serotoninergic function, hippocampal extracellular serotonin (5‐HT) levels were determined by in vivo microdialysis in freely moving rats under various conditions. Both adenosine and an adenosine A1 receptor agonist, 2‐chloro‐N6‐cyclopentyladenosine, decreased extracellular 5‐HT levels, whereas an adenosine A1 receptor antagonist, 8‐cyclopentyl‐1,3‐dimethylxanthine (CPT), and caffeine increased these levels. A selective A2A receptor agonist (CGS‐21680), an adenosine A2 receptor agonist (PD‐125944), an adenosine A2 receptor antagonist, 3,7‐dimethyl‐1‐propargylxanthine (DMPX), and an adenosine A3 receptor agonist, N6‐2‐(4‐aminophenyl)ethyladenosine (APNEA), did not affect extracellular 5‐HT levels. When the adenosine A1 receptor was blocked by CPT, the hippocampal extracellular 5‐HT level was increased by adenosine, CGS‐21680, and PD‐125944, and decreased by caffeine, DMPX, and APNEA. When both adenosine A1 and A2 receptors were blocked by CPT and DMPX, the extracellular 5‐HT level was decreased by adenosine, caffeine, and APNEA. The hippocampal extracellular 5‐HT level was not affected by administration of APNEA alone, but was decreased by this agent when the adenosine A1 receptor was blocked, irrespective of whether the adenosine A2 receptor was functional. These inhibitory effects of adenosine, caffeine, and APNEA on extracellular 5‐HT levels, during both adenosine A1 and A2 receptor blockade, were inhibited by selective 5‐HT reuptake inhibitors. These results indicate that the stimulatory effects of the adenosine A2 receptor and the inhibitory effects of the A3 receptor on hippocampal extracellular 5‐HT levels are masked by the inhibitory effects of the adenosine A1 receptor.

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Key wordsO f the epileptic patients who were treated for 2 5 years until the end of 1990 and had more than four seizures in 1990, 63 patients had been treated without interruption until the end of 1995. W e analyzed their clinical courses from 1990 to 1995 prospectively. More than half the subjects were diagnosed with temporal lobe epilepsy. Twenty cases had presumed etiology, and 32 had neuropsychiatric complications. O f the subjects whose seizures were not controlled with conventional antiepileptic drugs (AED), 11 cases demonstrated significant improvement when new AED; that is, lamotrigine, vigabatrin, clobazam, topiramate, tiagabine or CGP33101 were added. However, 10 patients did not respond to new AED. Presumed etiology, neuropsychiatric complications, multiple epileptic foci in EEG and abnormalities on head CT or MRI were characteristics of the patients whose seizures were resistant to new AED. intractable epilepsy, neuropsychiatric complications, new antiepileptic drugs, presumed etiology, temporal lobe epilepsy.

Purpose; Glutamate is the principal excitatory neurotransmitter in the central nervous system, and excessive release of glutamate may produce seizures in patients with epilepsy and in various animal models of epilepsy. Glutamatergic transmission also plays an important role in the development of neuronal damage after a variety of insults to the brain, including those caused by status epilepticus. Thus, to clarify the effects of the antiepileptic drugs (AEDs) carbamazepine (CBZ) and zonisamide (ZNS) on the multiple components of hippocampal glutamate release, this study was carried out to determine the Ca2+-and K+-evoked glutamate release in rat hippocampus with an in vivo microdialysis glutamate biosensor (MGB).Methods: The MGB was composed of a dialysis electrode (DE), a microdialysis probe, and a stainless steel recording electrode. The DE was filled with 100 U/ml of glutamate oxidase dissolved in a phosphate-modified Ringer's solution (PMRS) containing (in mM): 145 Na+, 2.7 KC, 1 .O Mg2+, 154.4 C1-and adjusted with 4.3 mM phosphate buffer to pH 7.4. The MGB was implanted into the rat hippocampus (A = -5.8 L = 4.8, and V = -4.0 mm from Bregma). The perfusion rate wdS maintained at 1.0 p,l/min, by using a modified Ringer's solution (MRS) composed of (in mM): 14.5 Na', 2.7 K+, 1.2 Ca2+, 1.0 Mg2+, 154.4 Cl-, 0.2 ascorbate, and adjusted to pH 7.4 with 2 mM phosphate buffer and 1.1 mM Tris buffer. To study the effects of an increase in extracellular Ca" or K' levels (Ca2+-or K+-evoked) on hippocampal glutamate release, MRS including either 3.4 m M Ca", SO mM K', 100 mM K', 3.4 mM Ca2+, and SO mM K', Ca2'-free, and 50 mM K+, or Caz'-free and 40 mM Mg2+ was infused for 60 min. To study the effects of CBZ and ZNS on basaMlippocampa1 extracellular glutamate levels, and on Ca2+-or K+-evoked hippocampal glutamate release, 100 mM CBZ or 1 mM ZNS was dissolved in each perfusate. The neuronal firing frequencies were recorded with a telemeter set at a bandpass of 0.1-3 kHz and were fed into the computer as discharge rates.Results: An increase in the extracellular K+ levels produced concentration-dependent increases in the extracellular glutamate levels in the hippocampus. This K+-evoked glutamate release consisted of three components: an initial transient rise (ITR), a late gentle rise (LGR), and multiple phasic transient rises (MPTR). An increase in the extracellular Ca2+ levels did not affect hippocampal extracellular glutamate levels; however, it did enhance the K'-evoked hippocampal glutamate release. ).Purpose: Excitatory amino acids are one of the factors related to epileptogenesis. We studied the excitatory amino acid receptors, Nmethyl-D-aspartate receptor (NMDAR) and a-amino-3-hydroxy-5methyl-4-isoxazol propionate receptor (AMPAR), with in vitro auto-

66 PLATFORM AND POSTER SESSIONSwas seen in all cases. Motor deficits were seen only in one case whose age at seizurem onset was 2 years, the youngest case in our series. Five died during the chronic stage: four sudden deaths (due to seizures?) and one suicide, Pleocytosis in the cerebrospinal fluid (CSF) was negative or minimal in most cases. Thorough viral and metabolic studies, including the polymerase chain reaction (PCR) method have failed as yet to reveal the etiology. Interictal EEG showed generalized high-voltage slow waves without spikes during the acute phase and multifocal spikes during the convalescent phase. Computed tomography (CT) and magnetic resonance imaging (MRI) scans revealed diffuse cerebral atrophy during the convalescent phase.Conclusions: It is difficult to discriminate between the seizures during the acute phase of AEs and the sequelae of AEs. The critical point is "when did epileptogenesis develop? " One possibility is that intractable seizures continued because of AEs with strong epileptogenesis followed by seizures due to AEs sequelae. These patients were similar to those reported by Brett (1967) in terms of both status epilepticus and encephalitis. However, the frequency, seizure mode, and severity of the sequelae were much greater in our group. We can also exclude Rasmussen syndrome, as none of our patients showed progressive paresis and epilepsia partialis continua. In Japan, this type of PEE has received attention, and similar case reports have been published. However, there have as yet been no reports in the international literature. This group might be categorized as AEs of unknown origin. In fact, the unknown group had a higher frequency of secondary epilepsies, than other groups of AEs (Gibbs and Gibbs, 1964). The etiology might be viral encephalitis with strong epileptogenesis and poor CSF pleocytosis, except in the case of herpes simplex virus. We recommend that such patients be started on barbiturate therapy under intensive care unit (ICU) management as promptly as possible. This intractable epilepsy group merits close attention. Rehabilitation, Quality of LifeReliability and Validity of the Japanese Versions of SEALS and QOLIE-31. Toshiaki Kugoh (Department of Neuropsychiatry, Faculty of Medicine, Kagawa Medical University, Kagawa, Japan). Purpose:The growing evidence that factors other than epileptic seizures affect the quality of life (QOL) of people with epilepsy has led to the development of a number of tools for assessing QOL. These tools were originally published in English. It has been considered that a patient's perception of QOL may be influenced significantly by cultural differences. Many cultural differences exist between the West and Japan, and one of the major problems is linguistic differences. The translation process for creating valid Japanese versions of tests made in foreign languages must involve many problems that would affect the reliability and validity of the test results. In this study, we investigated the reliability and validity of the Japanese v...