Biomedical subjects
Publications and source records attributed to K Kamata.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Simultaneous recordings of single-unit activity and oxidation current were obtained bilaterally from the neostriatum of rats in response to a unilateral infusion of D-amphetamine (2.0 microliters of 10 micrograms/microliter) into the substantia nigra. Whereas neuronal activity increases ipsilaterally and decreases contralaterally, the electrochemical signals, which reflect extracellular ascorbate, increase bilaterally. In each case, changes in unit activity precede the change in ascorbate release. Systemic administration of haloperidol (0.2 mg/kg) blocks the increase in oxidation current bilaterally, but reverses the neuronal activity response only on the ipsilateral side. These results lend further support to the view that intranigral amphetamine facilitates neostriatal ascorbate release, but this effect is not correlated with changes in single-unit activity.
We have identified a region (virG) on the 230 kb virulence plasmid of S. flexneri that is required for cell-to-cell spread of the bacterium. Tn5 insertions into this region result in avirulent mutants that can initially invade and multiply in epithelial cells, but tend to lose active movement and tend to localize within the cytoplasm, where they are gradually extinguished without infecting adjacent cells. The virG region was localized to within 4 kb and may contain a single cistron. Sequences hybridizing to this region were found in all intact virulence plasmids of Shigellae and enteroinvasive E. coli.
To investigate the influence of the striatonigral gamma-aminobutyric acid (GABA) system on the nigrostriatal dopamine (DA) system, the release of DA and/or 3,4-dihydroxyphenylacetic acid in the striatum ipsilateral to the injection side was examined by in vivo voltammetry following microinjection of GABA into the substantia nigra zona reticulata (SNR). The microinjection of GABA (100-300 micrograms/2 microliters) into the SNR produced a dose-dependent increase in the electrochemical signals recorded from the caudate nucleus ipsilateral to the injection side. Following chronic treatment with haloperidol, microinjection of GABA into the SNR produced only a slight (non-significant) increase in the electrochemical signals recorded from the caudate nucleus ipsilateral to the injection side. These results provide additional evidence to support the concept that DA cells in the substantia nigra zona compacta are regulated by the SNR non-DA neurons in an inhibitory manner. It appears, furthermore, that chronic treatment with haloperidol reduces the release of DA in the striatum ipsilateral to the injection side and that this effect may be due to a gradual development of depolarization block of DA cells by chronic administration of haloperidol.
Rats were trained to lever-press for intracranial self-stimulation (ICSS) with electrodes implanted in the ventral tegmental area (VTA). The effect of inescapable footshock on response rates to ICSS was examined in the present study. Markedly decreased response rates to ICSS were observed 15 min to 24 h following inescapable footshock. Naloxone (10.0 mg/kg) itself was without effect on response rates to ICSS, but completely antagonized the decreased response rates by the stressor treatment. A relatively low dose of methamphetamine (0.5 mg/kg), which showed no effect on ICSS rates in naive rats, also antagonized the decreased response rates to ICSS. The present results suggest that inescapable footshock may release endorphin in the mesolimbic or mesocortical area; the released endorphin may act on dopaminergic nerve endings and interrupt dopaminergic transmission. The decreased activity of dopaminergic neurons may cause the decreased response rates to ICSS.
An increase in the concentration of ascorbate in the extracellular fluid of the rat striatum following systemic amphetamine administration previously has been demonstrated with the use of in vivo electrochemistry, push-pull cannula and in vivo dialysis. In this report, the effect of infusions of amphetamine into the substantia nigra on extracellular ascorbate levels in the striatum is further investigated by in vivo electrochemistry. Electrolytic lesions in the crus cerebri of the striatonigral pathway abolish this effect. Furthermore, these lesions abolish the effect of systemic amphetamine in the striatum ipsilateral to the lesion but not on the contralateral side. This phenomenon is independent of neostriatal dopamine or gamma-aminobutyric acid since levels were shown to be unchanged relative to the intact side. These results lend further support to the hypothesis that ascorbate secretion in the striatum after amphetamine is mediated in the central nervous system, and indicate that a pathway that courses through the crus cerebri is necessary for this release.
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Making use of trinitrophenyl-Brucella abortus (TNP-Ba), a T-independent antigen, the mechanism of antibody production in vitro by human lymphocytes was studied, focusing on the accessory role played by macrophages (m phi). Human tonsillar cells and peripheral blood lymphocytes (PBL), and their fractions which were depleted of T cells, M phi, or both by rosetting with sheep erythrocytes and glass adherence plus passage through a Sephadex G-10 column, were stimulated in vitro with TNP-Ba under optimal culture conditions. Substantial antibody response against the antigen was induced in the whole tonsillar cells, while no appreciable level of response was induced in the whole PBL. The level of response observed after T-cell depletion was not different from that of the whole cells. In contrast, the response was significantly enhanced both in tonsillar cells and in PBL by depleting M phi to a low level, such as 1-2% of the cultured cells. It was further shown that a small amount of M phi added back to the M phi-depleted fraction activity suppressed the response again to the level seen in the whole cells. If allogenic M phi were substituted for autologous ones, the same degree of suppressor function was observed irrespective of the difference seen in the HLA types.
Circling behavior induced by dopamine (DA) agonists following microinjection of colchicine or 6-hydroxydopamine (6-OHDA) into the substantia nigra pars compacta (SNC) or electrolytic lesions of the SNC was investigated. Methamphetamine produced a contralateral circling behavior 3, 7 and 14 days following injection of colchicine into the SNC. Apomorphine produced an ipsilateral circling behavior followed by a contralateral rotation 3 and 7 days after the infusion of colchicine, whereas only an ipsilateral circling behavior was produced by apomorphine on day 14. 6-OHDA lesions of the SNC produced a contralateral circling behavior to apomorphine and an ipsilateral circling to methamphetamine, whereas both apomorphine and methamphetamine induced ipsilateral circling behaviors in rats with electrolytic lesions of the SNC. The possible mechanisms of action of colchicine are discussed in relation to the known effects of colchicine on axoplasmic transport.
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Voltammetric signals were recorded bilaterally with unmodified or electrochemically-modified carbon-fiber electrodes in the neostriatum of rats that sustained a unilateral depletion of dopamine by pretreatment with 6-hydroxydopamine. In both hemispheres, single daily injections of D-amphetamine (5.0 mg/kg or steadily increasing doses beginning with 6.0 mg/kg) for 6 consecutive days significantly reduced the rise in oxidation current produced by a challenge injection of 2.5 mg/kg D-amphetamine compared to the response obtained from saline-treated controls. Voltammetric scans indicated that the oxidized substance shared the electrochemical characteristics of ascorbic acid. It appears, therefore, that multiple amphetamine injections reduce the release of ascorbic acid in the neostriatum and that this effect does not depend on the integrity of dopaminergic neurons.
The effects of chronic administration of methamphetamine on the responsiveness of neurons of the substantia nigra zona reticulata (SNR) to gamma-aminobutyric acid (GABA) or to a GABA receptor agonist were examined. Neuronal activity was recorded from the SNR of rats that had been pretreated twice daily, for 6 consecutive days, with saline or with 5 mg/kg methamphetamine. Intravenous administration of the GABA receptor agonist, muscimol, caused a dose-dependent decrease in the unit activity of the SNR neurons and the SNR neurons became less sensitive to the depressant effects of the drug after chronic treatment with methamphetamine. Iontophoretic application, with increasing currents, of GABA produced a progressive inhibition of unit activity in control animals, an effect that was significantly reduced in rats pretreated with methamphetamine. These results support the hypothesis that long-term administration of methamphetamine increases the activity of the striatonigral GABA system and thereby reduces the sensitivity of postsynaptic GABA receptors in the SNR.
We studied 375 chronic hemodialysis patients for evidence of hepatitis B virus infection using first- and second-generation monoclonal radioimmunoassays. These assays employ high-affinity monoclonal antibodies produced against antigenic determinants that reside on hepatitis B surface antigen. Such assays have a lower limit of detection for hepatitis B surface antigen-associated determinants in serum of approximately 55 and 15 pg/ml, respectively. We found that 14 of 375 chronic hemodialysis patients were positive for hepatitis B surface antigen by both polyclonal and monoclonal radioimmunoassay. However, an additional 17, some of whom had chronic hepatitis and hepatocellular carcinoma, were identified as harboring hepatitis B virus infection only by the monoclonal radioimmunoassays. Thus the monoclonal radioimmunoassays improved the hepatitis B virus detection rate by 120% (3.7% vs. 8.3%). More importantly, 6 of the 17 monoclonal radioimmunoassay-reactive patients had no serologic evidence of recent or past hepatitis B virus exposure as shown by the absence of antibodies to the hepatitis B core and surface antigens in the blood. We conclude that there are hemodialysis patients with hepatitis B virus infection undetectable by conventional polyclonal radioimmunoassays.
The mode of action of mizoribine (MZR) as a B cell inhibitor was studied using DBA/2 mice. Its in vitro administration significantly delayed the primary response in hemagglutinin production against sheep erythrocytes by suppressing the IgM antibody formation. In vitro plaque-forming cell (PFC) response against both T-dependent and T-independent antigens, such as TNP-SRBC and TNP-Brucella abortus, was dose-dependently suppressed by MZR. Since PFC formation by the T-depleted fraction of splenocytes was likewise suppressed, MZR may inhibit humoral antibody response by directly affecting the B cells (and/or macrophages) as well as by modulating the regulatory T cells. MZR may only act on a certain stage of the cell cycle of B lymphocytes following antigenic stimulation. It may not interfere with the initial antigen recognition or with mature B cells.