Search PubMed⌕ Search

Biomedical subjects

Y Kudo

Publications and source records attributed to Y Kudo.

At least 343 records · Page 19Linked to original sources
PubMed1984

Intracellular Ca2+ elevation induced by a neurotransmitter in a glial cell clone.

By fluorometry using a Ca2+-indicator Quin 2, we found an elevation of intracellular Ca2+ concentration ([Ca2+]i) in response to an application of serotonin in a rat clonal glial cell (C6BU-1). The [Ca2+]i rise depended on the dose of applied serotonin and the level of environmental Ca2+. The possibility was suggested that neuron-glia interactions might be controlled by a receptor-coupled [Ca2+]i-regulation system.

Animals↗
PubMed1984

Ataxic hemiparesis from small capsular hemorrhage. Computed tomography and somatosensory evoked potentials.

We studied three cases that fit the clinical syndrome of ataxic hemiparesis. Computed tomography revealed small hemorrhages of the posterior limb of the internal capsule in all the cases, and somatosensory evoked potential studies predicted a disturbance of the lemniscal pathway from the thalamus to the parietal sensory cortex without demonstrable sensory loss. These results suggested that ataxia of the contralateral limbs following capsular lesion might result from a disruption of the thalamocortical sensory projection. The site of the lesion, the pathologic cause, and the underlying mechanism of ataxia are not necessarily homogeneous within the syndrome.

Aged↗
PubMed1984

Disappearance of sleep apnea by tracheal intubation in Creutzfeldt-Jakob disease.

We have described a patient with Creutzfeldt-Jakob disease who showed disappearance of sleep apnea by tracheal intubation. All night polygraphic study revealed a clear correlation between the cyclic EEG change and sleep apnea. The periodic synchronous discharge (PSD) phase in EEG corresponded to the breathing phase in respiration and non-PSD phase corresponded to the apneic phase. Intratracheal intubation has completely stopped both the apnea and the cyclic EEG change. Therefore, we assumed that the PSD-non-PSD cycle in EEG might causally relate with the peripheral obstruction of the airway during sleep.

Aged↗
PubMed1984

Actions of picrotoxinin and related compounds on the frog spinal cord: the role of a hydroxyl-group at the 6-position in antagonizing the actions of amino acids and presynaptic inhibition.

The frog spinal cord has been used to test the effects of naturally occurring picrotoxane compounds (picrotoxinin, picrotin, tutin and coriamyrtin) and semisynthetic ones (6-acetylpicrotoxinin and anhydropicrotin) on the electrical activities of dorsal and ventral roots and on amino acid-induced depolarizations of primary afferent terminals. Picrotoxinin, tutin and coriamyrtin (10(-5)-3 X 10(-5)M), which have a free hydroxyl group at the 6-position, caused a gradual depolarization in both ventral and dorsal roots. The depolarizations were accompanied by a reduction in the size of the dorsal root potential (DR-DRP), dorsal root reflex (DR-DRR) and ventral root potential (DR-VRP) and by an augmentation of the first spike potential and polysynaptic components in the ventral root reflex (DR-VRR). 6-Acetylpicrotoxinin (10(-5)-3 X 10(-5)M) caused a slight hyperpolarization in both roots, and this hyperpolarization was accompanied by the augmentation of DR-DRP, DR-VRP and DR-VRR. The DR-DRR was reduced or abolished by the compound. Picrotoxinin, tutin and coriamyrtin reduced gamma-aminobutyric acid (GABA)-, beta-alanine- and taurine-induced depolarizations of primary afferent terminals. 6-Acetylpicrotoxinin showed almost the same degree of inhibition of beta-alanine and taurine as did picrotoxinin, but the GABA- antagonizing action of the compound was significantly weaker than was that of picrotoxinin. Picrotoxinin, tutin, coriamyrtin and 6-acetylpicrotoxinin all blocked presynaptic inhibition of the first spike potential caused by antidromic conditioning stimulation. 6 The present results suggest that the hydroxyl group at the 6-position of picrotoxane compounds are important for antagonism of the effects of GABA, but not of beta-alanine and taurine and for the blocking action of the presynaptic inhibition in the frog spinal cord.

Action Potentials↗
PubMed1984

Effects of caroverine and diltiazem on synaptic responses, L-glutamate-induced depolarization and potassium efflux in the frog spinal cord.

The frog spinal cord was used to determine the characteristics of the actions of caroverine and diltiazem, two organic Ca2+-antagonists, on synaptic responses and L-glutamate-induced depolarization. Caroverine and diltiazem (10(-4)M) depressed the dorsal root potential (DR-DRP) induced by electrical stimulation of an adjacent dorsal root. Diltiazem also depressed the ventral root potential (DR-VRP), whereas caroverine augmented both the polysynaptic component in the ventral root reflex and the size of the DR-VRP. The root potentials induced by high frequency stimulation (20 Hz, for 1 s) were markedly depressed by these Ca2+-antagonists at a concentration of 10(-4)M. When the preparation was perfused with normal medium, the compounds depressed L-glutamate-induced depolarizations in ventral and dorsal roots. In preparations treated with tetrodotoxin (TTX) (2 X 10(-7)M), the antagonizing actions of the drugs against L-glutamate-induced depolarizations in the ventral root were markedly reduced or abolished, while significant antagonizing actions on the depolarization in the dorsal root were still observed. The increase in extracellular K+ activity induced by L-glutamate in the TTX-treated preparation was significantly reduced by the compounds. Caroverine and diltiazem had no effect on the presynaptic nerve spike and on the focal synaptic potential induced by a single stimulation of a dorsal root; however, the focal synaptic potential induced by high frequency stimulation (20 Hz, 1 s) was attenuated. Motoneuronal action potentials were abolished by the drugs, while the excitatory postsynaptic potential remained unaffected. 9 The present results suggest that caroverine and diltiazem are not specific L-glutamate antagonists in the frog spinal cord, but that they block the initiation of an action potential without affecting presynaptic nerve conduction, transmitter release or transmitter-receptor interactions. The inhibitory effects of these compounds on L-glutamate-induced K+-efflux are discussed with reference to their Ca2+-antagonizing actions.

Animals↗
PubMed1984

Mechanisms of depressant action of muscle relaxants on spinal reflexes: participation of membrane stabilizing action.

The participation of local anesthetic action in spinal reflex inhibition produced by mephenesin-type muscle relaxants was examined by comparing the local anesthetic effects (in vitro), the depressant effects on muscle afferent discharges (in situ) and the depressant effects on spinal reflexes (in situ) of the drugs in rats. At doses producing depression of spinal reflexes, mephenesin, tolperisone (mephenesin-type) and lidocaine (local anesthetic) reduced the frequency of afferent discharges from the muscle. The order of reducing afferent discharges by these drugs corresponded to that of their conduction blocking activities in the isolated sciatic nerve of rats. These results suggest the participation of a membrane stabilizing action in spinal reflex inhibition produced by mephenesin-type muscle relaxants. Baclofen (non-mephenesin-type) did not show any local anesthetic action.

Action Potentials↗
PubMed1983

Electrical activities of the frog spinal cord are resistant to perfusion with hypoxic medium.

Synaptic functions of the isolated and intra-arterially perfused frog spinal cord were investigated in terms of dorsal root-dorsal root potential (DR-DRP) and dorsal root-ventral root reflexes (DR-VRR), and under the influences of hypoxic Ringer solution, replacement of medium glucose with 2-deoxyglucose ('hypoglycemic Ringer'), and suspension of perfusion. The synaptic functions were markedly degraded during the suspension of perfusion, but they were remarkably resistant to hypoxic or hypoglycemic Ringer for more than 6 h, if the preparation was continuously perfused. The presynaptic inhibition of the first spike potential of the DR-VRR induced by a conditioning antidromic stimulation, however, was markedly reduced during prolonged exposure to hypoxic conditions. In contrast to earlier concepts that the spinal cord is vulnerable to hypoxia, the present results demonstrate that the frog spinal cord is resistant to prolonged perfusion with hypoxic and hypoglycemic media, although they suggest a latent deterioration of some processes which are believed to be more energy dependent.

Animals↗
PubMed1983

Supersensitivity of the GABA receptor in the frog spinal cord, as induced by kainic acid.

In the isolated frog spinal cord perfused with kainic acid (KA, 5 X 10(-4) M) containing Ringer's solution, within 2 hr there were increases in the amplitude of the dorsal root depolarization, as induced by the GABA-agonists. KA perfusion produced increases in the specific binding of [3H]muscimol to crude synaptic membranes and incubation with KA for 3 hr did not increase [3H]muscimol binding. [3H]GABA was released from KA-treated spinal cord slices in the presence of high K+. KA-induced supersensitivity of the dorsal root to GABA may relate to direct actions on primary afferent terminals and not to denervation of GABAergic neurons.

Animals↗
PubMed1983

Metabolism of D-phenylalanine and its effects on concentrations of brain monoamines and amino acids in rats--a basic study on possibility of clinical use of D-phenylalanine as an antidepressant.

The effect of D-phenylalanine on the concentrations of brain catecholamines, serotonin, beta-phenylethylamine and amino acids was examined using rats injected intraperitoneally with 200 mg/kg of D-phenylalanine. The contents of these monoamines in the rat brain were not affected by the administration of D-phenylalanine. No spectacular change was observed in the concentrations of brain amino acids except phenylalanine, which increased about four times during 30-60 minutes after the injection. This increase was attributed to the administered D-phenylalanine. To confirm the finding that D-phenylalanine did not affect the content of beta-phenylethylamine, the metabolism of D-phenylalanine was examined using D-[14C]-phenylalanine. It was proven that D-phenylalanine did not convert to beta-phenylethylamine. On the basis of these findings the antidepressant effect of D-phenylalanine was critically discussed.

Amino Acids↗
PubMed1983

Dendrobine, an antagonist of beta-alanine, taurine and of presynaptic inhibition in the frog spinal cord.

1 The effects of dendrobine and nobiline, alkaloids isolated from Dendrobium nobile, on the electrical activity and on amino acid-induced depolarizations of primary afferent terminals were tested on the frog isolated spinal cord and were compared with those of picrotoxinin and strychnine. 2 Dendrobine (3 X 10(-5) M) caused a slight hyperpolarization in both dorsal and ventral roots and this hyperpolarization was accompanied by the augmentation of the dorsal root potential (DR-DRP) and the ventral root potential and reflex (DR-VRP and DR-VRR). The amplitude of the dorsal root reflex (DR-DRR) however, was reduced significantly. Nobiline (3 X 10(-5) M) had no significant effect on either the root potentials or the reflexes. 3 Dendrobine (3 X 10(-5) M) reduced the dorsal root potential induced by repetitive antidromic stimulation of ventral root (VR-DRP) as well as diminishing the maximum rate of rise of the dorsal root potential induced by the stimulation of adjacent dorsal roots (DR-DRP), during which time the amplitude of the DR-DRP was seen to be augmented. 4 Dendrobine (3 X 10(-5) M) reduced the beta-alanine- and taurine-induced depolarizations of primary afferent terminals, while having little effect upon GABA- and glycine-induced depolarizations. 5 Dendrobine (10(-5) M) reversibly blocked the presynaptic inhibition caused by antidromic conditioning stimulation of the ventral root. 6 These effects of dendrobine were qualitatively similar to those of strychnine but were somewhat different from those of picrotoxinin, a molecule having the same picrotoxane skeleton. 7 The present results are discussed with reference to the likely neurotransmitters involved in presynaptic inhibition in the frog spinal cord, and with respect to the structure-activity relationship of picrotoxane compounds as amino acid antagonists.

Action Potentials↗
PubMed1983

Effects of acute and chronic treatments with atenolol and propranolol on cardiovascular responses to handling stress in spontaneously hypertensive rats.

Although the mechanism of antihypertensive action of beta-adrenergic blocking drugs (beta-blockers) is not known, a theoretical advantage of cardioselective beta-blockers over nonselective ones has been proposed in the treatment of hypertension. To study this hypothesis, we examined cardiovascular responses to handling stress in spontaneously hypertensive (SHR) rats after a single (100 mg/kg) and multiple oral treatments (100 mg/kg per day for 17 d) with either atenolol or propranolol. Atenolol and propranolol markedly suppressed the tachycardia induced by handling stress after acute and chronic administration. Resting mean arterial pressure (MAP) was reduced by acute and chronic atenolol treatment, but not by propranolol. Stress-induced increase in MAP was significantly reduced by chronic treatment with propranolol, whereas no consistent effects were observed with atenolol. Acute treatment with guanethidine (30 mg/kg) markedly reduced the rise in MAP induced by stress. These results suggest that suppression of cardiac function by beta-blockers does not always attenuate the rise in MAP induced by stress, thus cardioselective beta-blockers might not confer any further reduction of the blood pressure increase due to sympatho-adrenal excitation. Inhibition of stress-induced MAP rise by propranolol could be mediated by a modulation of the catecholamine release.

Adrenergic beta-Antagonists↗