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Biomedical subjects

C Yamamoto

Publications and source records attributed to C Yamamoto.

At least 235 records · Page 13Linked to original sources
PubMed1986

A revised method for generation of unitary postsynaptic potentials for quantal analysis in the hippocampus.

For quantal analysis of excitatory postsynaptic potentials (EPSPs) in hippocampal CA3 neurons, a method was devised to evoke trains of unitary EPSPs at intended intervals and to control the number of unitary EPSPs composing each train at will. The amplitudes of the first EPSPs in EPSP trains evoked with this method were measured. From the mean and variance of the EPSP amplitudes, the mean number of quanta (m) released by a single impulse and the mean amplitude of EPSPs induced by individual quanta (q) were estimated in a standard solution and in a high calcium solution.

Animals↗
PubMed1986

The magnitude of long-term potentiation of field potentials induced monosynaptically in region CA3 of guinea pig hippocampus.

The magnitude of long-term potentiation (LTP) was re-examined for monosynaptic transmission between mossy fibers and CA3 neurons in thin sections of the hippocampus of the guinea pig. Although an initial negative deflection in the field potential showed apparent short-term potentiation, this deflection was concluded to reflect non-synaptic activation of CA3 neurons. Accordingly, the magnitude of LTP of monosynaptic transmission was re-calculated at 3.4 +/- 0.9.

Animals↗
PubMed1986

Improved insulin sensitivity in carbohydrate and lipid metabolism after physical training.

To estimate physical training effects quantitatively, the relationship between tissue sensitivity to exogenous insulin (glucose metabolism determined by euglycemic insulin-clamp technique) and maximal oxygen uptake (VO2 max) was defined in 9 well-trained athletes and 14 untrained subjects with normal glucose tolerance. Tissue sensitivity to exogenous insulin in the athletes was significantly higher than in the controls (P less than 0.001). Seven untrained subjects continued the physical exercise program. After physical training for 1 month, glucose metabolism increased from 40.3 +/- 3.9 mumol/kg/min to 42.2 +/- 4.4 mumol/kg/min (P less than 0.05) and VO2 max also increased significantly (P less than 0.05). During euglycemic hyperinsulinemia, both plasma FFA (P less than 0.001) and glycerol (P less than 0.05) decreased rapidly after physical training. Glucose metabolism directly correlated with VO2 max (P less than 0.001). These results suggest that the euglycemic insulin-clamp technique provides a reliable estimate of training effects, tissue sensitivity to physiologic hyperinsulinemia is 46% higher in trained athletes, and physical training improves insulin sensitivity not only in glucose metabolism but also in lipid metabolism.

Adolescent↗
PubMed1985

Blocking action of pentobarbital on receptors for excitatory amino acids in the guinea pig hippocampus.

The actions of pentobarbital sodium (Pent) on receptors for glutamate (Glu) and related compounds were studied in thin sections of the guinea pig hippocampus. Depolarizations induced by Glu and quisqualate (Quis) in CA3 neurons were reduced in amplitude during iontophoretic administration of Pent. This action of Pent was not accompanied by any noticeable changes in membrane potential or neuron input resistance. Depolarizations induced by N-methyl-D-aspartate were less sensitive to Pent. The fast kainate (KA) response was as susceptible as the Glu response, whereas the slow KA response was unaffected by Pent in three quarters of the neurons examined. Pent suppressed the Glu response at lower concentrations than required to potentiate responses to gamma-amino butyric acid. Excitatory postsynaptic potentials (EPSPs) elicited by stimulation of mossy fibers were suppressed by Pent. The EPSPs were a little more resistant to Pent than were the Glu responses. These results indicate that Pent blocks receptors for excitatory amino acids in the hippocampus. Of the three different populations of the receptors, Quis receptors are the most sensitive to Pent and KA receptors are the least sensitive. The suppression of the EPSPs is in accordance with the notion that Glu is the transmitter released from mossy fibers.

Amino Acids↗
PubMed1985

Inhibitors of high-affinity uptake augment depolarizations of hippocampal neurons induced by glutamate, kainate and related compounds.

Actions of dihydrokainate (DHKA) and 3-hydroxy-DL-aspartate (HAsp), inhibitors of high-affinity uptake for L-glutamate (Glu), were studied in vitro in thin hippocampal slices of the guinea pig. The amplitude of the depolarizations induced by Glu and by L-aspartate (Asp) in CA3 neurons are markedly augmented by DHKA and HAsp. Depolarizations induced by D-homocysteate (DH) were unaffected by the inhibitors. In about half of the neurons, depolarizations induced by L-homocysteate (LH) and by quisqualate (Quis) were slightly augmented by the inhibitors. Fast responses to kainate (KA) were augmented by the inhibitors to a similar extent as were Glu responses whereas slow KA responses were insensitive to HAsp. HAsp was without effect on excitatory postsynaptic potentials elicited by stimulation of granular layer. These findings are in general agreement with the biochemical data on amino acid uptake processes and are also consistent with the slow time-courses of depolarizations induced by DH, LH and Quis. Augmentation of fast KA responses provides strong evidence for the hypothesis that an KA pulse causes a liberation of Glu and/or Asp from the tissue and the liberated amino acid(s) induces the fast KA response in neurons nearby.

Animals↗
PubMed1985

Some properties of ionic channels activated by excitatory amino acids in hippocampal neurons.

Properties of excitation induced by various excitatory amino acids were studied in thin slices of the guinea pig hippocampus in the presence of Mn2+, tetrodotoxin and tetraethylammonium chloride. Depolarizations induced by L-glutamate (Glu), quisqualate (Quis) and D-homocysteate (DH) were accompanied consistently by decreases in neuron input resistance. In the current-voltage function, increases in input resistance were never observed at any membrane potential. The amplitude of Glu, Quis and DH responses decreased during tonic outward currents and increased during tonic inward currents. Although neuron input resistance decreased with depolarizations induced by L-aspartate (Asp) as well, the magnitude of the resistance reduction was significantly smaller than that induced by Glu. Asp responses changed in amplitude as did Glu responses during tonic inward and outward currents. Depolarizations induced by N-Methyl-D-aspartate (NMDA) were accompanied by apparent increases in input resistance, and their amplitudes increased and decreased during tonic depolarization and hyperpolarization, respectively. Mn2+ was almost without effect at the concentration used (2.7 mM) on responses induced by Glu, DH or Asp. These results suggest that Glu, Quis and DH induce depolarizations in hippocampal neurons by activating only Quis receptors, and that Asp activates Quis receptors preferentially though it activates NMDA receptors as well.

Amino Acids↗
PubMed1985

Two components of long-term potentiation in mossy fiber-induced excitation in hippocampus.

Experiments were made in thin transverse sections of the guinea pig hippocampus to clarify whether tetani to a heterosynaptic input can induce long-term potentiation (LTP) in the absence of seizure discharges and whether the heterosynaptic LTP occurs in a monosynaptic or polysynaptic pathway. Early and late responses were differentiated in field potentials elicited in region CA3 by mossy fiber stimulation. The LTP of the early response was specific to a tetanized pathway, whereas heterosynaptic LTP was observed in the late response in the absence of seizure discharges. The magnitude of LTP of the early response was significantly smaller than that of the late response. LTPs of the early and late responses were not induced at a low Ca2+ concentration. A brief exposure to a high Ca2+ solution resulted in a long-lasting potentiation of both the early and late responses. Counterparts to the early and late responses were recorded from the distal dendritic layer in reversed polarities. The intracellular counterpart to the late response was a slow depolarization superimposed on the peak and falling phase of excitatory postsynaptic potentials. These results suggest that LTP of the early response reflects enhanced transmission through synapses between mossy fibers and CA3 neurons and LTP of the late response reflects modified interaction among postsynaptic neurons.

Action Potentials↗
PubMed1984

Fast and slow depolarizing potentials induced by short pulses of kainic acid in hippocampal neurons.

Responses of hippocampal neurons to short pulses of alpha-kainic acid (KA) were studied intracellularly in thin brain slices of the guinea pig. A KA pulse induced a slow depolarizing potential either with or without a preceding much faster depolarization. Large fast responses were induced only at the center of glutamate-sensitive spots, where short pulses of L-glutamate (Glu) induced large depolarizations in the impaled neuron. The fast responses resembled Glu-induced depolarizations in time-course, in sensitivity to movement of the tips of amino acid-pipettes, in sensitivity to Glu-antagonists and in reversal potential. The slow response was much more resistant to movement of the amino acid-pipettes and to Glu-antagonists. Mn2+ was without effect on the fast as well as the slow responses. Glu-induced depolarizations super-imposed on the slow response were simply depressed. These results indicate that two different types of receptors are activated by administration of KA, and suggest that the slow response results from a direct action of KA and the fast response is produced as a consequence of either the direct action of KA on the Glu receptors or a calcium-independent release of Glu by KA.

Acetates↗
PubMed1984

The possible involvement of adenylate cyclase inhibition in the field potential suppression through alpha-2 adrenergic receptors in the bed nucleus of the stria terminalis.

Catecholamines, such as norepinephrine (NE), cause a field potential suppression through alpha-2 adrenergic receptors in thin sections of the bed nucleus of the stria terminalis. Phosphodiesterase inhibitors or cyclic AMP (cAMP) analogues attenuate the NE-induced suppression. These results suggest that the NE-induced suppression is mediated by adenylate cyclase inhibition and a resultant decrease of intracellular cAMP content.

1-Methyl-3-isobutylxanthine↗
PubMed1984

Gamma-D-glutamylglycine and cis-2,3-piperidine dicarboxylate as antagonists of excitatory amino acids in the hippocampus.

The actions of gamma-D-glutamylglycine (DGG) and cis-2,3-piperidine dicarboxylate (PDA) were studied in thin hippocampal sections of the guinea pig by intracellular recording. DGG and PDA suppressed depolarizations induced in CA3 neurons by short pulses of L-aspartate (Asp), D-homocysteate (DH) or L-glutamate (Glu). Asp- and DH-responses were more susceptible to the antagonists than were Glu-responses. The sensitivity difference between Glu-responses and Asp- or DH-responses was not so pronounced that these antagonists could be used to differentiate between Glu-mediated and Asp-mediated synapses. Glu and Asp pulses induced long hyperpolarizing deflections in some neurons. In about half of these neurons, PDA and DGG were without effect on the hyperpolarizing responses. The depolarizing action of gamma-amino butyric acid was unaffected by DGG and PDA. These antagonists blocked excitatory postsynaptic potentials induced by fimbrial stimulation. These results suggest that DGG and PDA are relatively specific antagonists of excitatory amino acids in the hippocampus, and that Glu (or Asp) is the neurotransmitter released from axons of CA3 neurons.

Amino Acids↗
PubMed1984

A sensitive fluorometric assay for dopamine-beta-hydroxylase activity by high-performance liquid chromatography.

A sensitive and specific fluorometric assay for dopamine-beta-hydroxylase (DBH) activity is described. The main natural substrate, dopamine (DA), was used and incubated under optimal conditions. Norepinephrine (NE) formed enzymatically from DA was isolated by an aluminum oxide column and was analyzed by high-performance liquid chromatography (HPLC) with trihydroxyindole fluorescence. Epinephrine (EN) was added to the incubation mixture as an internal standard after incubation, and this assay was therefore highly reproducible. HPLC conditions were settled to elute the product, NE, prior to the substrate, DA, and the internal standard, EN, between NE and DA. Only catecholamines produced significant peaks, and therefore, this assay is highly specific. We applied this method to measure the DBH activity in human serum and cerebrospinal fluid.

Chromatography, High Pressure Liquid↗
PubMed1984

Neuronal sensitivity to opiate and opioid peptides in the bed nucleus of the stria terminalis. Effects of chronic treatment with morphine.

To characterize the phenomenon of morphine tolerance in central nervous system, the neuronal sensitivity to opiate and opioid peptides in the bed nucleus of the stria terminalis (BST) and the effects of chronic treatment with morphine were examined with thin slices of the brain of guinea pigs. Both morphine and enkephalins (D-Ala2-Met5-enkephalinamide and D-Ala2-D-Leu5-enkephalin) suppressed neuronal activity in the stria terminalis. Three days after implantation of morphine pellets the guinea pigs became tolerant to morphine and EC50 (the morphine concentration required for causing 50% of the maximal effect) was 79 microM, nearly six times the value in the control animals (EC50 = 13 microM). Cross-tolerance between morphine and enkephalins was not observed. Results of radioreceptor assay, using [3H]dihydromorphine as a ligand, showed that the binding capacity of the morphine-tolerant animals was not statistically different from that of the controls. These results suggested that tolerance to morphine cannot be explained by changes in number and/or affinity of opiate receptors, and that tolerance probably results from modification of the intracellular mechanisms mediating between the binding of morphine with the receptors and neuronal inhibition.

Amygdala↗