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Biomedical subjects

M Sasa

Publications and source records attributed to M Sasa.

At least 217 records · Page 12Linked to original sources
PubMed1984

Microiontophoretic studies of the dopaminergic inhibition from the ventral tegmental area to the nucleus accumbens neurons.

Microiontophoretic studies using chloral hydrate-anesthetized rats were performed to determine whether excitation of a dopaminergic pathway originating in the ventral tegmental area (VTA) inhibits neurons on the nucleus accumbens (Acc). In 13 of 17 Acc neurons which failed to respond to hippocampal stimulation, the spike generation produced by stimulation of the parafascicular nucleus of thalamus was inhibited by both VTA conditioning stimulation and iontophoretically applied dopamine. The inhibition induced by the VTA conditioning stimulation was antagonized by iontophoretic application of haloperidol in 10 of 13 Acc neurons tested. In contrast, spike generation induced by stimulation of the hippocampus was not affected by VTA conditioning stimulation in 14 of 15 Acc neurons, although iontophoretically applied dopamine produced an inhibition in 4 of those 15 Acc neurons. Spikes generated by stimulation of the VTA were obtained in 23 of 102 neurons and were not affected by iontophoretically applied haloperidol. These results strongly suggest that dopamine derived from VTA inhibits Acc neurons receiving input from the parafascicular nucleus of thalamus but not from the hippocampus.

Animals↗
PubMed1983

Effects of haloperidol and sulpiride on dopamine-induced inhibition of nucleus accumbens neurons.

Microiontophoretic study was performed to elucidate dopaminergic mechanism in the nucleus accumbens (Acc) of rats anesthetized with chloral hydrate. Iontophoretically applied dopamine produced an inhibition of glutamate-induced firing in 28 (62%) out of 45 Acc neurons tested. The dopamine-induced inhibition of 14 Acc neurons was clearly antagonized by simultaneous application of haloperidol, and a partial antagonism by sulpiride was observed in 3 out of 10 Acc neurons. These results indicate that dopamine produces an inhibition of the Acc neuron and that, compared to haloperidol, sulpiride is a less potent blocker of the postsynaptic dopamine receptor involved in the dopamine-induced inhibition.

Animals↗
PubMed1983

Vestibular efferent fibers to ampulla of anterior, lateral and posterior semicircular canals in cats.

Origins of vestibular efferent fibers to ampulla of semicircular canals in cats were examined using retrograde transport of horseradish peroxidase. The anterior canal was innervated from bilateral parvocellular reticular nucleus (PCRN), contralateral gigantocellular reticular nucleus and ipsilateral lateral reticular nucleus (LRN); the lateral canal, from ipsilateral PCRN and LRN as well as ipsilateral lateral vestibular nucleus; and the posterior canal, from bilateral PCRN and ipsilateral medial and lateral vestibular nuclei.

Animals↗
PubMed1983

Effects of diphenhydramine iontophoretically applied onto neurons in the medial and lateral vestibular nuclei.

Electrophysiological studies were carried out to elucidate the effects of diphenhydramine, an antihistamine (H1-receptor blocking) drug, on neuron activities in the medial vestibular nucleus (MVN) and lateral vestibular nucleus (LVN) of cats using a microiontophoretic method. According to the firing pattern and latency of the first spike with vestibular nerve stimulation, neurons in the MVN and LVN were classified into two groups: monosynaptic and polysynaptic neurons. In the MVN, the spike generation of polysynaptic neurons was dose-dependently inhibited with the iontophoretic application of diphenhydramine up to 200 nA, and that of the monosynaptic neurons was also suppressed by the maximum dose of 200 nA. In contrast to the MVN neurons, the spike generation of LVN monosynaptic neurons remained unaffected with diphenhydramine up to 200 nA, although an inhibition of the LVN polysynaptic neurons was obtained with 200 nA of the drug. These results suggest that small doses of diphenhydramine more selectively interfere with synaptic transmission in the MVN neuron than that in the LVN neuron.

Animals↗
PubMed1983

Studies on Japanese encephalitis virus infection of reptiles. I. Experimental infection of snakes and lizards.

Experimental infection of four species of snakes, Rhabdophis tigrinus tigrinus, Elaphe quadrivirgata, Elaphe climacophora and Agkistrodon halys, and five species of lizards, Takydromus tachydromoides, Eumeces latiscutatus, Eumeces barbouri, Eumeces marginatus oshimensis and Gekko japonicus, with Japanese encephalitis virus (JEV) was carried out. Evidence of JEV multiplication in snakes was not obtained at least under the conditions used in the present study. All lizards except G. japonicus were infected with JEV by ip injection of virus suspension. The minimum infectious dose for a lizard was around 10(3) MLD50/0.05 ml, and this dose was considered to be proportional to the virus dose which is injected into a host by a vector mosquito at a single bite. Temperature dependence of JE virus growth in the lizards was demonstrated. JEV multiplied slower at 20 degrees C than at 26 degrees C, though the peak titers of viremia were equivalent in both groups of lizards kept at 20 degrees C and 26 degrees C. E. latiscutatus developed viremia with ip injection of a partially attenuated strain, Nakayama NIH which could not infect adult mice by peripheral inoculation. T. tachydromoides and E. latiscutatus were also infected by oral feeding of JEV infected mosquitoes. E. latiscutatus was infected by oral feeding of only one infected mosquito.

Animals↗
PubMed1983

Studies on Japanese encephalitis virus infection of reptiles. II. Role of lizards on hibernation of Japanese encephalitis virus.

A series of experiments on the role of lizards as overwintering hosts of Japanese encephalitis virus (JEV) was carried out. Two species of lizards, T. tachydromoides and E. latiscutatus, 2 species of mosquitoes, Cx. p. fatigans and Cx. p. pallens, and 2 strains of JEV, JaGAr#01 and JaGAr 19461, were used in this study. Firstly transmission of JEV from infected mosquitoes to uninfected lizards and from infected lizards to normal mice by the bite of mosquitoes was demonstrated successfully. Cx. pipiens group mosquitoes were found to feed readily on lizards as compared to Cx. tritaeniorhynchus, the primary vector of JEV in Japan. Secondly simulated hibernation of JEV in lizards was carried out under indoor and outdoor conditions. In the outdoor hibernation, lizards were injected with JEV on October 14, 1968, entered in hibernation on October 19 and were recovered from hibernation on April 10, 1969. Viremias were demonstrated in the lizards for a few weeks in late April. Thirdly JEV isolation and HI antibody detection were attempted from blood samples of field-caught reptiles, 7 species of snakes and 3 species of lizards and among amphibians, 2 species of frogs. HI antibody against JEV was found at a rate of 14.3% from E. latiscutatus and 4.0% from T. tachydromoides, though JEV was not isolated from all the blood samples of these cold-blooded animals. The roles of lizards as overwintering hosts of JEV were discussed.

Animals↗
PubMed1982

Afferent projection from reticular nuclei, inferior olive and cerebellum to lateral vestibular nucleus of the cat as demonstrated by horseradish peroxidase.

Afferent connection to lateral vestibular nucleus (LVN) was examined using retrograde transport of horseradish peroxidase (HRP). When HRP was microiontophoretically applied to the immediate vicinity of the LVN neuron, which monosynaptically fired spike upon VIIIth cranial nerve stimulation, HRP-labelled cells were observed in the ipsilateral lateral reticular nucleus, bilateral gigantocellular nucleus, and contralateral dorsal cap and beta-nucleus of inferior olive in addition to various parts of cerebellum.

Afferent Pathways↗
PubMed1982

Inhibitory effect of betahistine on polysynaptic neurons in the lateral vestibular nucleus.

Effects of betahistine, an antivertigo drug, were examined on the lateral vestibular nucleus (LVN) neurons of cats anesthetized with alpha-chloralose. Spike generation of monosynaptic LVN neurons elicited by vestibular nerve stimulation remained unaffected with intravenous administration of betahistine up to 5 mg/kg and with iontophoretic application of the drug up to 200 nA. In contrast, the spike generation of polysynaptic I neurons in the LVN was dose-dependently inhibited by intravenous as well as iontophoretic application of betahistine. These results suggest that small doses of betahistine more selectively interfere with synaptic transmission in the polysynaptic I neurons than in the monosynaptic neurons.

Animals↗
PubMed1982

Effects of 7-ethoxycarbonyl-6,8-dimethyl-4-hydroxymethyl-1(2H)-phthalazinone (EG626) on the spinal trigeminal nucleus, ventral posteromedial nucleus, and sensory cortex.

Effects of 7-ethoxycarbonyl-6,8-dimethyl-4-hydroxymethyl-1 (2H)-phthalazinone (EG626) on the spinal trigeminal nucleus (STN), ventral posteromedial nucleus (VPM), and sensory cortex were examined in cats anesthetized with alpha-chloralose in comparison with the effects of morphine. EG626 produced a dose-dependent inhibition of the polysynaptic components of the cortical field potentials upon VPM stimulation and either facilitatory or inhibitory effects on the polysynaptic components of the VPM field potential upon stimulation of the medial lemniscus, while the drug failed to affect the STN field potential with trigeminal nerve stimulation. Morphine inhibited the postsynaptic components of the STN field potentials and to a lesser extent, the polysynaptic components of the cortical field potential; and the effects of morphine on the VPM field potential were similar to those seen with EG626. Pretreatment of the animal with naloxone antagonized the facilitatory effect on the VPM field potentials produced by morphine, but not those by EG626. Morphine and EG626 induced either a prolonged increase in the blood flow or transient increase followed by a decrease in the blood flow in the VPM. These results suggest that EG626 may impair the polysynaptic transmission and/or neuron excitability in the sensory cortex and the VPM at least partly due to the change in blood flow there as does morphine. Unlike morphine, however, EG626 did not produce any obvious effect on the STN.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1981

Inhibition from ventral tegmental area of nucleus accumbens neurons in the rat.

The role of the ventral tegmental area (VTA), which is rich in dopamine-containing cell bodies, on nucleus accumbens (Acc) neurons was examined. In Acc neurons receiving input from parafascicular nucleus (Pf) of thalamus, VTA conditioning stimulation produced an inhibition of spike generation with Pf stimulation. In contrast, VTA conditioning stimulation did not affect Acc neurons receiving input from limbic structures such as the amygdala nucleus and hippocampus.

Amygdala↗
PubMed1981

Peripheral and central vestibular disorders in alcoholics. A three-year follow-up study.

Vestibular disorders were found in all 33 Japanese men who had been drinking alcohol for over 20 years and who had abstained from alcohol for over 3 months before the tests were done. Six, 12, and 15 patients showed peripheral, central, and combined types of vestibular disorders, respectively. The peripheral disorder occurred in younger alcoholics (under 50 years old) with a drinking history of 20-30 years, and the combined disorder in older patients with a longer drinking history. The vestibular disorders, however, were not observed in any of 16 control non-alcoholics. A follow-up study on seven alcoholics with a 3-year abstinence from alcohol revealed an improvement of vestibular dysfunctions, in particular of peripheral disorders, with an abstinence of over 2 years.

Adult↗
PubMed1981

Inhibition from locus coeruleus of caudate neurons activated by nigral stimulation.

Electrophysiological studies were performed to determine if the locus coeruleus (LC) plays a role in regulating activity of caudate nucleus (CN) neurons. Cats were anesthetized with alpha-chloralose and when conditioning stimuli were applied to the LC, preceding the test stimulus, there was a significant inhibition of spike generation in 33 out of 93 CN neurons transsynaptically activated by test stimulus to the pars compacta of the substantia nigra (SN). An inhibition of spike generation with LC conditioning stimulation and iontophoretic application of noradrenaline was obtained in 9 out of the same 23 CN neurons and 8 neurons remained unaffected with either treatment. In contrast to these neurons, LC conditioning stimulation did not affect the spontaneous firing and spike generation of CN neurons antidromically excited by SN stimulation. Spike firing of CN neurons transsynaptically activated by motor cortex stimulation remained unaffected with LC conditioning stimulation. These results suggest that noradrenaline derived from the LC produced an inhibition of spike generation in about one-third of CN neurons tested and transsynaptically activated by SN stimulation.

Animals↗
PubMed1981

[Effects of ifenprodil on lateral vestibular nucleus neurons in the cat (author's transl)].

Electrophysiological studies were performed to elucidate effects of ifenprodil, an antivertigo drug, on neuron activity in the lateral vestibular nucleus (LVN) of cats anesthetized with alpha-chloralose. LVN neurons were classified into three types, according to the response pattern upon vestibular nerve stimulation: monosynaptic, polysynaptic I and polysynaptic II neurons, which fired spikes with the mean latencies of 1.07 +/- 0.12 (n = 6), 2.20 +/- 0.19 (n = 8) and 16.37 +/- 2.11 msec (n = 7), respectively. Intravenous administration of ifenprodil up to 5 mg/kg did not affect spike generation of monosynaptic neurons. Spike generation of polysynaptic I and II neurons was dose-dependently inhibited by ifenprodil up to 1 mg/kg. However, increasing doses of the drug up to 5 and 10 mg/kg produced complex effects such as an enhancement of the inhibitory effect in some neurons or a facilitation of responses in others. These results indicate that ifenprodil acts on the polysynaptic I and II neurons without affecting the monosynaptic neurons. It is likely that a small dose of ifenprodil may directly inhibit polysynaptic neurons and higher doses may indirectly enhance the responsiveness of the neurons, probably as a result of an increase in blood flow in the vertebral artery.

Adrenergic alpha-Antagonists↗
PubMed1981

Dopaminergic inhibition from substantia nigra of caudate neurons activated by cortical stimulation.

Studies were performed to elucidate the role of dopamine originating in the pars compacta of the substantia nigra (SN) on caudate nucleus (CN) neurons receiving input from the motor cortex using cats anesthetized with alpha-chloralose. Activation with cortical stimulation was observed in 50 CN neurons, five out of which also excited by SN stimulation. Conditioning stimuli applied to the SN, 30 msec preceding the test stimulus to the cortex, produced a significant inhibition of spike generation upon cortical stimulation in 28 out of 45 neurons tested and did not affect the remaining 17 neurons. The mean spike number of the 45 neurons was significantly reduced with SN conditioning stimulation. When dopamine up to 200 nA was iontophoretically applied to CN neurons, there was a significant inhibition of the spike generation with cortical stimulation in 9 out of 16 neurons. The mean spike number of the 16 neurons upon cortical stimulation was significantly reduced during dopamine application. In addition, a close correlation was observed between the effects of SN conditioning stimulation and iontophoretic dopamine. These results suggest that dopamine derived from the SN produces an inhibition of CN neurons receiving input from the motor cortex.

Animals↗
PubMed1981

Effects of harmaline on membrane excitability and ATPase activity of the crayfish giant axon.

Effects of harmaline on excitability of crayfish giant axon in relation to effects on Na,K-ATP activity were investigated and the findings were compared with relative data on ouabain. Exposure of the axon to harmaline in doses over 0.5 mM resulted in a dose-dependent reduction of the action potential. Harmaline of 2.5 mM produced a complete blockade of the action potential with a slight decrease in the resting membrane potential (5.7 mV), but no alterations of Na,K-ATPase activity. In contrast, ouabain (5 mM) produced a more pronounced decrease in the resting membrane potential (10.6 mV) and also a partial reduction in the action potential, while a significant decrease in Na,K-ATPase activity was obtained. Increasing the membrane potential to the initial level resulted in a partial recovery (46%) of the rising rate (dV/dt) of action potential. The dV/dt was exponentially decreased when the resting potential was reduced with application of KCl solution over 8 mV. These results suggest that harmaline externally applied produces a decrease in sodium conductance without affecting Na,K-ATPase activity, while ouabain inhibits Na,K-ATPase activity and, to lesser extent, decreases in sodium conductance.

Action Potentials↗