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Biomedical subjects

M Sasa

Publications and source records attributed to M Sasa.

At least 181 records · Page 10Linked to original sources
PubMed1988

Different sensitivity to hypoxia in neuronal activities of lateral vestibular and spinal trigeminal nuclei.

Electrophysiologic studies were performed to examine the effects of hypoxia on neuronal activities of the lateral vestibular and spinal trigeminal nuclei using rats anesthetized with chloral hydrate. The rats inhaled a gas mixture of 5% oxygen and 95% nitrogen for 3.5 minutes to induce hypoxia, followed by room air. Under these conditions, mean PaO2 was decreased from 85 to 22 mm Hg 3 minutes after the start of the inhalation concomitant with a decrease in blood pressure from 108 to 55 mm Hg. There were no significant differences in these variables between rats used for vestibular nucleus experiments and rats used for trigeminal nucleus experiments. In the lateral vestibular nucleus, hypoxia inhibited postsynaptic components of the evoked field potential, spike generation of monosynaptic neurons on vestibular nerve stimulation, and firing induced by iontophoretic application of glutamate. In the spinal trigeminal nucleus, however, there were no alterations of the field potential or spike generation of the neurons on trigeminal nerve stimulation. These results indicate that the lateral vestibular nucleus neurons are much more sensitive to hypoxia than the spinal trigeminal nucleus neurons. The failure of transmission in the monosynaptic neurons of the lateral vestibular nucleus is suggested to be due to the inhibition of excitability of the postsynaptic membrane.

Acetylcholine↗
PubMed1988

Muscarinic receptor-mediated inhibition of dopaminergic excitatory input to caudate neurons from the substantia nigra.

Microiontophoretic studies using rats anesthetized with chloral hydrate were performed to elucidate the relationship between the striatal cholinergic system and nigrostriatal dopaminergic system. Iontophoretic application of carbachol inhibited the spikes elicited by substantia nigra (SN) stimulation in 21 of 24 caudate neurons in which the spikes induced by SN stimulation were inhibited by microiontophoretically applied domperidone, a dopamine D-2 receptor antagonist. This inhibitory effect was completely blocked by atropine, although the spike generation induced by SN stimulation remained unaffected by the drug. However, carbachol did not affect the glutamate-induced firing of the caudate neurons of which the spikes induced by SN stimulation were inhibited by application of both domperidone and carbachol. Furthermore, carbachol had inhibitory effects on the spikes induced by SN stimulation even after the systemic application of bicuculline. In contrast, in 17 of 24 caudate neurons in which the spikes induced by SN stimulation were not affected by domperidone, carbachol did not inhibit the spikes induced by SN stimulation. These results suggest that the muscarinic receptors located on the SN-derived dopaminergic nerve terminals mainly play a role in inhibiting inputs from the SN to the caudate neurons, probably by reducing the release of dopamine from the nerve terminals.

Animals↗
PubMed1988

Inhibitory effects of L-threo-DOPS, an L-noradrenaline precursor, on locus coeruleus-originating neurons in the caudate nucleus.

Electrophysiological studies using reserpine-treated cats were carried out to elucidate the effects of L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS) on the noradrenergic pathway from the locus coeruleus (LC) to the caudate nucleus (CN) neurons, which were activated by iontophoretically applied bromocriptine, a dopamine D-2 receptor agonist. In the CN neurons, glutamate-induced firing was inhibited by iontophoretic application of noradrenaline, but not by repetitive stimulation of the LC or iontophoretically applied L-threo-DOPS. After intraventricular administration of L-threo-DOPS, however, LC stimulation inhibited the glutamate-induced firing. These results suggest that L-noradrenaline that was produced from the conversion of L-threo-DOPS inhibited the CN neurons which possess dopamine D-2 receptors.

Animals↗
PubMed1988

Muscarinic inhibition as a dominant role in cholinergic regulation of transmission in the caudate nucleus.

The effects of cholinergic agonists and antagonists were investigated using slice preparations of the rat caudate nucleus (CN) to elucidate the role of the cholinergic system in the CN. Either carbachol (10(-7) to 10(-5) M) or muscarine (10(-7) to 10(-5) M) dose-dependently inhibited extracellular action potentials orthodromically elicited by local stimulation in the CN. A combination of acetylcholine (10(-6) to 10(-4) M) with physostigmine (10(-6) M) also inhibited the orthodromic response of CN neuron, but nicotine (10(-6) to 10(-3) M) had no effects on the neuronal activity. Atropine (10(-8) to 10(-6) M) antagonized the carbachol-induced inhibition of CN neuron with pA2 of 7.58. Carbachol (10(-5) M) or muscarine (10(-5) M) decreased the amplitude of excitatory postsynaptic potential (EPSP) without altering the resting membrane potential or input impedance of the CN neuron, whereas nicotine (10(-5) M) did not affect either the resting membrane potential or amplitude of EPSP. When carbachol (10(-5) M) was added to the bath, the number of action potentials elicited by applying a depolarizing current into the cell was increased, whereas action potentials transsynaptically elicited by local stimulation were inhibited conversely. The excitatory effects of carbachol on the postsynaptic site of the neuron were also blocked by atropine (3 x 10(-7) M). Carbachol (10(-5) M) did not affect the time courses of the rise and decay phases of EPSP induced by the local stimulation, but did reduce the amplitude of the EPSP.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1987

Effects of L-threo-DOPS, an L-noradrenaline precursor, on locus coeruleus-originating neurons in spinal trigeminal nucleus.

Electrophysiological studies using reserpinized cats were performed to examine the effects of L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS) on the noradrenergic pathway from the locus coeruleus (LC) to the spinal trigeminal nucleus (STN). The spike generation of STN relay neurons induced by trigeminal nerve stimulation was not affected by LC conditioning stimulation nor iontophoretic application of L-threo-DOPS. After intraventricular administration of L-threo-DOPS, the inhibition of the spike generation was seen with LC conditioning stimulation and blocked by iontophoretically applied sotalol, suggesting that L-noradrenaline converted from L-threo-DOPS inhibits transmission of STN relay neurons.

Action Potentials↗
PubMed1987

Excitatory and inhibitory effects of dopamine on neuronal activity of the caudate nucleus neurons in vitro.

Effects of dopamine on the rat caudate nucleus neurons were examined in a slice preparation using an intracellular recording technique. Perfusion of the bath with a low concentration (1 microM) of dopamine produced a depolarization concomitant with an increase in the spontaneous firing and the number of action potentials evoked by a depolarizing pulse applied into the cells. In contrast, higher concentrations (100-500 microM) of dopamine inhibited the spontaneous and current-induced firings without apparent effects on the resting membrane potential. In addition, during application of a high concentration (100 microM) of dopamine there was a marked elevation of the threshold potential of the action potential elicited by a higher depolarizing current. Simultaneous application of haloperidol (0.5-5 microM) antagonized both excitatory and inhibitory effects induced by the low and high concentrations of dopamine, respectively. In addition, the excitatory effect induced by a low concentration (1 microM) of dopamine was antagonized by domperidone (0.5 microM), a selective D2 receptor antagonist, while the inhibitory effect by a high concentration (100 microM) was blocked by SCH 23390, a selective D1 receptor antagonist. These results strongly suggest that the postsynaptic sites of caudate nucleus neurons have at least two subtypes of dopamine receptors (D1 and D2 receptors) that mediate inhibitory and excitatory responses of the neuron to dopamine, respectively.

Action Potentials↗
PubMed1987

Opioid-mediated inhibition from the subnucleus caudalis of spinal trigeminal nucleus to the neurons in the subnucleus oralis.

The influence of enkephalin-containing neurons in the subnucleus caudalis of the spinal trigeminal nucleus (STN caudalis) on the subnucleus oralis of the STN (STN oralis) was examined using chloral hydrate-anesthetized rats. In the STN oralis, conditioning stimuli applied to the STN caudalis 10-50 ms preceding the test stimulus inhibited spikes produced by tooth pulp stimulation in type B interneuron, which was activated by orthodromic stimulation but not by thalamic stimulation, without affecting those of the relay neuron. When the type B interneurons were further classified into type B1 and type B2 neurons, which were characterized by the occurrence of the STN caudalis-induced inhibition with long and short latencies, respectively, microiontophoretically applied naloxone reduced the STN caudalis-induced inhibition of th orthodromic spikes of type B1 interneurons with little effects on type B2 interneuron. Furthermore, naloxone-reversible inhibition of tooth pulp-induced spikes of the type B1 interneurons were also observed during iontophoretic application of enkephalin. These results suggest that the type B1 interneurons in the STN oralis are inhibited by opioid peptides-containing neurons in the STN caudalis.

Action Potentials↗
PubMed1987

Coexistence of inhibitory dopamine D-1 and excitatory D-2 receptors on the same caudate nucleus neurons.

Microiontophoretic studies using cats anesthetized with alpha-chloralose were performed to determine whether or not dopamine D-1 and D-2 receptors co-exist in the same caudate nucleus (CN) neurons that receive inputs from the substantia nigra (SN), and in which spikes elicited by SN stimulation were blocked by domperidone, a selective D-2 antagonist. Iontophoretic application of dopamine produced a dose-dependent inhibition of spontaneous firing in 2 of 4 spontaneously active CN neurons and an increase in firing in the remaining 2 neurons. However, dopamine inhibited the glutamate-induced firing in 31 of 32 CN neurons that were not spontaneously active. Similar inhibition with iontophoretically applied SKF 38393, a selective D-1 agonist, was observed in 33 of 34 spontaneously inactive neurons tested. When the effects of dopamine, SKF 38393 and bromocriptine (D-2 agonist) were examined on the same CN neurons, the inhibitory effects of both dopamine and SKF 38393 were seen in 14 of 15 neurons, and both an inhibition by SKF 38393 and an excitation by bromocriptine were observed in 15 of 17 neurons. The inhibitory effects of dopamine and SKF 38393 were antagonized by haloperidol and SCH 23390 (D-1 antagonist) without being affected by domperidone. Furthermore, the dopamine-induced inhibition was converted to an excitation during simultaneous application of SCH 23390 in 6 of 10 CN neurons, and this excitation was antagonized by domperidone. These results strongly suggest that the inhibitory D-1 and excitatory D-2 receptors co-exist on the same CN neurons receiving inputs from the SN.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1987

Inhibitory effects of thyrotropin-releasing hormone on neuronal activity in the nucleus accumbens.

The effects of thyrotropin-releasing hormone (TRH) were examined on neuronal activity in the nucleus accumbens, receiving an input from the parafascicular nucleus of the thalamus or the hippocampus, in chloral hydrate-anesthetized rats, using a microiontophoretic technique. The spikes produced by stimulation of the parafascicular nucleus were predominantly and dose-dependently inhibited during iontophoretic application of TRH. When the effects of TRH and dopamine were tested on the same neurons of the nucleus accumbens, inhibition of the generation of spikes by both drugs was observed in most neurons. In contrast, spikes elicited by stimulation of the hippocampus in most neurons of the nucleus accumbens were not affected by TRH or dopamine. Both TRH- and dopamine-induced inhibition of the spikes induced by stimulation of the parafascicular nucleus was antagonized by simultaneous application of haloperidol. In animals treated with reserpine, inhibition of the generation of spikes upon stimulation of the parafascicular nucleus did not occur in any neurons in the nucleus accumbens during application of TRH, whereas the dopamine-induced inhibition was still observed. These results suggest that inhibitory effects of TRH on the neurons of the nucleus accumbens receiving an input from the parafascicular nucleus are mediated by dopamine released from the dopaminergic nerve terminals located in the nucleus accumbens.

Action Potentials↗
PubMed1987

Acute effects of methamphetamine applied microiontophoretically to nucleus accumbens neurons in rats.

Microiontophoretic studies were performed to elucidate the acute effects of methamphetamine on the nucleus accumbens (Acc) neurons receiving input from the parafascicular nucleus (Pf) of the thalamus using rats anesthetized with chloral hydrate. Spike generation upon Pf stimulation was inhibited by conditioning stimuli applied to the ventral tegmental area (VTA), which is rich in dopamine-containing neurons, and by iontophoretic application of methamphetamine as well as dopamine. The VTA-, methamphetamine- and dopamine-induced inhibition of the spikes elicited by Pf stimulation was antagonized during simultaneous application of haloperidol. Glutamate-induced firing was also inhibited during iontophoretic application of methamphetamine and dopamine in neurons receiving input from the Pf, and the inhibition was blocked by simultaneously applied haloperidol. In the reserpine-treated animals, however, the Pf-induced spikes were not affected by methamphetamine, but inhibited by dopamine. These results indicate that methamphetamine inhibits the Acc neurons receiving input from the Pf, probably by releasing dopamine from dopaminergic nerve terminals from the VTA.

Action Potentials↗
PubMed1987

A new model of petit mal epilepsy: spontaneous spike and wave discharges in tremor rats.

A mutant rat, which was found in a colony of Kyoto:Wistar rats and genetically defined as a tremor rat (tm/tm), developed tremor of the whole body at 2 weeks of age but the tremor gradually disappeared between 6 and 8 weeks of age. The electroencephalogram (EEG) recorded using chronically implanted electrodes showed a 5-7 Hz (mostly 6 Hz) spike and wave complex synchronously in the cerebral cortex and hippocampus accompanied by absence-like seizure in all six tremor rats examined. The spike and wave complex appeared 0.8-1.9 times per minute and lasted for 1-17 s. However, normal EEG activity was observed in the intervening periods, free of absence-like seizure. Thus the tremor rat is considered to be a possible model for studying the pathogenesis and therapy of petit mal epilepsy in humans.

Animals↗
PubMed1987

Effects of ethanol on vestibular nucleus neurons responding to sinusoidal rotation.

Effects of ethanol applied by electro-osmosis were examined on the rat vestibular nucleus neurons responding to vestibular nerve stimulation and horizontal sinusoidal rotation. Ethanol (50-150 nA) inhibited the neurons monosynaptically activated by vestibular nerve stimulation and also suppressed the activity of the type I neuron, which responded with an increase in firing on ipsilateral rotation and a decrease on contralateral rotation. However, the drug did not affect the type II neuron, which showed the opposite response to the ipsi- and contralateral rotation compared with the type I neuron. Iontophoretic application of atropine (25-50 nA) inhibited spontaneous and rotation-induced firing in both type I and II neurons. These results suggest that ethanol inhibits the type I neuron projecting to the abducens nucleus, thereby impairing the vestibulo-ocular reflex.

Action Potentials↗
PubMed1987

Common occurrence in Toyama of bronchial asthma induced by chironomid midges.

A total of 119 asthmatic children were investigated by prick tests for the hypersensitivity against chironomid antigens. The percentages of cases who showed positive prick tests to the antigens of the adults of Polypedilum kyotoense, Chironomus yoshimatsui and Tokunagayusurika akamusi, that of the larvae of Tokunagayusurika akamusi and of Dermatophagoides farinae were 23.5%, 17.6%, 7.6%, 16.0% and 94.2%, respectively. The correlations among the wheal size in prick test, the threshold dilution in the intradermal test, the RAST score, and the result of the provocation test were significant. The specific IgE antibodies against two additional midge species were measured with the Phadezyme RAST test in a total of 27 asthmatic cases who were positive to either of the 3 adult midge antigens previously tested. RAST was positive in 59.3% with Chironomus plumosus and 100% with Tanytarusus oyamai. In the RAST inhibition tests, the Polypedilum kyotoense antigen causing allergic reaction was shown to be quite independent from Dermatophagoides farinae. These results suggest that the extracts of chironomid midges have strong allergenicity, and are one of the important inhalant antigens causing asthma in Toyama.

Adolescent↗
PubMed1987

IgG and IgE antibodies to Chironomidae in asthmatic patients.

IgG antibodies to Chironomidae and its correlations to radioallergosorbent and skin reactions were examined with the aim of clarifying the relationship between asthma and Chironomidae. The level of specific IgG antibody in asthmatic patients (0.698 +/- 0.034, n = 104) was significantly greater than that in normal subjects (0.367 +/- 0.032, n = 52) (P less than 0.01). The specific IgG level was not correlated to skin reaction, nor to IgE RAST scores. Specific IgG1 and IgG4 levels in asthmatic patients were significantly greater than in control subjects (n = 14) (P less than 0.01).

Animals↗