1. To investigate postsynaptic potentials (PSPs), we made intracellular recordings from neurons of the amygdaloid central nucleus in slices from the guinea pig and rat brains maintained in vitro. The results from guinea pigs and rats were very similar. 2. In the presence of bicuculline (20 microM), focal electrical stimulation of the amygdaloid basal nucleus with low intensities elicited short-latency excitatory PSPs (EPSPs) followed by long-latency EPSPs. The short-latency EPSP was selectively blocked by 6-cyano-7-nitroquinoxaline-2,3-dion (CNQX; 10-20 microM). The long-latency EPSP was preferentially abolished by D,L-2-amino-5-phosphonovaleric acid (D,L-APV; 40 microM) and was augmented by removal of extracellular Mg2+. The compound EPSP reversed at -4 mV, which was close to -1 mV, the reversal potential for pressure-ejected glutamate (Glu). 3. When the intensity of the focal stimulation was increased in the presence of bicuculline (20 microM), CNQX (20 microM), and D,L-APV (50 microM), a second EPSP with a short latency and a prolonged duration could be evoked in approximately 65% of the neurons. The EPSPs were reversibly blocked by d-tubocurarine (50 microM) or hexamethonium (200 microM) but were unaffected by atropine (1 microM) or a 5-hydroxytryptamine type 3 receptor antagonist, ICS-205930 (5-10 microM). In these neurons, acetylcholine (ACh; 1-3 mM) caused a depolarization, associated with a decreased input resistance. 4. In the presence of CNQX (20 microM) and D,L-APV (50 microM), single focal stimulation of the dorsolateral subdivision in the central nucleus with low intensities elicited a depolarizing inhibitory PSP (IPSP). The IPSP was reversibly abolished by bicuculline (20-40 microM). The reversal potential (-63 mV) for the IPSP was similar to the reversal potential (-61 mV) for the response to gamma-aminobutyric acid (GABA) applied by pressure ejection. 5. In the presence of bicuculline (20-40 microM) and CNQX (20 microM), a repetitive focal stimulus with high intensities delivered to the dorsolateral subdivision produced a hyperpolarizing PSP followed by a slow depolarization in most neurons. Of putative inhibitory amino acid transmitters, glycine (Gly; 3 mM) produced only a hyperpolarization, associated with a decrease in input resistance. Strychnine (1-2 microM) reversibly blocked both the Gly hyperpolarization and the synaptically evoked hyperpolarization. The reversal potential of -81 mV for the hyperpolarizing PSP was close to -82 mV for the Gly hyperpolarization. The reversal potential for the Gly response was shifted to less negative values by increasing the external K+ concentration or decreasing the extracellular Cl- concentration.(ABSTRACT TRUNCATED AT 400 WORDS)

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A 24-year-old male with recurrent hypersomnia associated with decreased blood flow in the thalamus on single photon emission computed tomography (SPECT) is reported. In the hypersomnolent period, the decrease of blood flow in the left thalamus was revealed in the SPECT and slow waves appeared sporadically or sometimes as a burst on the electroencephalogram (EEG).In a phase of insomnia in the convalescent period there were almost no slow waves in the resting EEG but many slow waves appeared on hyperventilation EEG and the power spectrum at this hyperventilation resembled the power spectrum at the resting EEG in the hypersomnolent period. In the remission period there was no abnormal data in these testings.

Summary: We experienced a case of chronic hepatitis type C accompanied with hallucination and delusion induced by interferon (IFN) therapy positive. The case was a 47-year-old male, whose laboratory data showed positive for antiHepatitis C Virus (HCV) and elevated transa ninase level. He was treated with 6 MU/day of natural-type IFN-a (HLBI). Sleeplessness and delusions of persecution developed about 2 months after the start of IFN therapy. The interview of the psychiatrist disclosed that the patient had a history of addiction to drugs, and these psychiatric symptoms were diagnosed as being of "the flashback phenomenon." These side effects were improved after the administration of psychotropics and it was suggested that we had to take care of the development of flashback phenomenon during the treatment of IFN in cases of chronic hepatitis with a history of addiction to drugs.

The aim of this study was to assess the substantial impact of obstructive sleep apnea (OSA) on emotional states and quality of life (QOL) along with the effect of treatment with continuous positive airway pressure (CPAP). Patients with any psychiatric disorders and serious physical diseases were excluded from the study. Thirty-one OSA patients and 63 healthy controls were asked to complete Profile of Mood States (POMS) and QOL-26 questionnaires at the commencement of the study, and then again after 3 months of CPAP treatment. The OSA group scored significantly higher (worse) in five mood factors and significantly lower (worse) in four QOL domains than the control group. Continuous positive airway pressure treatment produced significant improvement in the majority of emotional states and QOL after 3 months. These findings suggest that sleep apnea is at least partially responsible for emotional changes and reducing QOL. Furthermore, we found significant correlations between the apnea-hypopnea index (AHI) and tension-anxiety as well as fatigue-inertia and the physical QOL domain after 3 months of CPAP treatment. Some OSA patients had residual sleep apnea in spite of CPAP treatment due to severe obesity and tonsillar hypertrophy, and their mood states and QOL did not improve. Thus residual sleep apnea may impede improvement in emotional states and QOL in OSA patients. We believe that the frequency of apnea and hypopnea during sleep needs to be brought as close as possible to zero with intensive and combined therapy to improve emotional states and QOL in OSA patients.