Search PubMed⌕ Search

Biomedical subjects

Y Katayama

Publications and source records attributed to Y Katayama.

At least 811 records · Page 45Linked to original sources
PubMed1980

Slow synaptic potentials in neurones of the myenteric plexus.

1. Intracellular recordings were made in vitro from neurones in the myenteric plexus of the guinea-pig ileum. Potential changes were recorded in response to focal stimulation of the surface of the myenteric ganglion at a distance of 30-100 microM from the impaled cell. 2. Stimuli comprising single pulses evoked cholinergic excitatory post-synaptic potentials ('fast' e.p.s.p.s) in S cells. In a small proportion (20%) of both S and AH cells such stimuli also evoked depolarizing potentials with a time course about 1000 times slower than that of the fast e.p.s.p. 3. Stimuli comprising repeated pulses (up to 20 Hz for 2 sec) evoked the slow depolarizing potentials in a higher proporton of neurones (42%). These stimuli caused a hyperpolarizing potential change in 9% of cells, and in a very few cells biphasic changes i membrane potential were observed. 4. Both the slow depolarizing and the slow hyperpolarizing responses persisted in atropine (up to 5 microM) and hexamethonium (up to 200 microM), but were reversibly abolished by changing to calcium-free solutions. 5. Evidence is presented which suggests that the slow depolarizing response is caused by inactivation of the membrane potassium conductance, and the slow hyperpolarizing response is due to activaton of the potassium conductance.

Animals↗
PubMed1980

The action of somatostatin on neurones of the myenteric plexus of the guinea-pig ileum.

1. Intracellular recordings were made from neurones in ganglia of the myenteric plexus of the guinea-pig ileum. 2. Somatostatin (10-300 nM) was applied to the neurones by adding it to the perfusing solution or by ejecting it (charges up to 500 nC) from an ionophoresis electrode onto the soma membrane. 3. By both methods of application, somatostatin either hyperpolarized or depolarized a proportion of neurones. Depolarizing responses were more often observed with ionophoretic application, and hyperpolarizing responses were more often observed with application by perfusion. Both responses were preserved in solutions containing zero Ca and elevated (6 mM) Mg. Some cells were both hyperpolarized and depolarized, depending on the method of administration. 4. The depolarizing responses to somatostatin were associated with an increase in cell input resistance; they became larger with membrane depolarization and smaller with membrane hyperpolarization, and reversed in polarity at a potential close to the potassium equilibrium potential. The hyperpolarizing responses to somatostatin were accompanied by a fall in cell input resistance.

Animals↗
PubMed1980

Multiple actions of 5-hydroxytryptamine on myenteric neurones of the guinea-pig ileum.

1. Intracellular recordings were made from neurones lying within ganglia isolated from the myenteric plexus of the guinea-pig ileum. 2. 5-hydroxytryptamine (5-HT) (200 nM-10 microM) was applied to 160 neurones by adding it to the perfusing solution. Depolarizations were observed in 27% of neurones, and were more likely to be observed in S-cells. Hyperpolarizations were observed in 30% of neurones, and were more likely to be seen in AH cells. 52% of neurones were unaffected. 2. 5-HT was applied to 104 neurones by micro-electrophoresis from an electrode with its tip placed close to the soma membrane. Depolarizations were observed in 35% of cells, and hyperpolarizations 13%; 10% of neurones showed biphasic responses in membrane potential and the remaining cells were unaffected. 4. The depolarizing responses to 5-HT were associated with an increase in neuronal input resistance and were probably due to inactivation of the membrane potassium conductance. The responses declined in amplitude during prolonged or repeated applications of 5-HT. 5. The hyperpolarizing responses to 5-HT were associated with a fall in neuronal input resistance and were probably due to activation of the membrane potassium conductance. These responses persisted throughout the duration of application of 5-HT and did not show marked tachyphylaxis. The hyperpolarizing responses were reversibly abolished by calcium-free solutions. 6. The depolarizing responses to 5-HT may underlie the release of acetylcholine caused by 5-HT in the guinea-pig ileum. The hyperpolarizing responses may contribute to the inhibition of the peristaltic reflex which has been observed when 5-HT is applied to the serosal aspect of the intestine.

Animals↗
PubMed1980

Assessment of brainstem damage by the auditory brainstem response in acute severe head injury.

In 64 cases suffering from severe head injury (Glasgow coma scale: less than seven- the auditory brainstem responses (FARs) recorded at the vertex, which are thought to be volumet conducted far-field potentials reflecting the sequential electrical activities of the auditory afferen) system in the brainstem, were recorded in the neurosurgical intensive care room immediately after admission. The alterations in the responses were compared with the types of primary injury, neurological signs., CT findings and outcome following treatment. Based on the results obtained, it is concluded that the FAR is a useful indicator for predicting the effects of treatment on brainstem damage in patients with severe head injury, and that it provides more reliable information about the function of the brainstem than the neurological signs or CT findings. Moreover, it also offers a diagnostic method for primary brainstem injury. Three cases or primary brainstem injury without lesions in the supratentorial region were diagnosed by means of combined CT and FAR recording.

Adult↗
PubMed1980

[Diagnostic value of the far field acoustic response (FAR) as an objective evaluating method for brainstem injury (author's transl)].

Far Field Acoustic Response (FAR) was repeatedly studied from acute stage to chronic stage of severe head injury in 64 patients for evaluation of the degree of brainstem injury. (1) In acute stage within 7 days after trauma, FAR abnormalities are found in 56% of the subjects with severe head injury. These abnormalities are as follows: (i) Prolongation of latency, disappearance of the 5th wave. (ii) Disappearance of the 1st-5th waves or 2nd-5th waves. The incidence of FAR abnormalities is not correlated to disease categories and age of the subjects. (2) FAR findings reveal more precisely the level of brainstem dysfunction than by clinical assessments of brainstem reflexes and posture, and by computerized tomography. (3) Evaluating results of the FAR recorded within 7 days after trauma are correlated to the outcome 3 or more months after injury in the subjects. Almost of them with alteration of only the 5th wave in FAR improve clinically and electrophysiologicaly at 2-3 weeks after trauma. However any patients with disappearance of the 1st-5th waves in FAR are fatal or fell into the state of vegetation. According to these results, it was concluded that FAR has a important diagnostic value as an objective evaluating method for brainstem dysfunction in patients with severe closed head injury.

Adolescent↗
PubMed1979

The action of substance P on neurons of the myenteric plexus of the guinea-pig small intestine.

Extracellular and intracellular recordings were made in vitro from single neurons of the myenteric plexus of the guinea-pig small intestine. Synthetic substance P was applied to the neurons by means of the perfusing solution or by electrophoresis from micropipettes. Extracellular recording showed that substance P (100 pm-30 nm), applied by perfusion, increased the firing rate of myenteric neurons. Intracellular recording indicated that perfusion with substance P caused a dose-dependent membrane depolarization which was unaffected by hexamethonium, hyoscine, naloxone or baclofen. The depolarization was also evoked by electrophoretic application of substance P. It was associated with an increase in membrane resistance, augmented by membrane depolarization and reduced by membrane hyperpolarization. The relation between the substance P reversal potential and the logarithm of the extracellular potassium concentration was linear with a slope of 54 mV/log10[K+], which indicates that substance P inactivates the resting potassium conductance of the myenteric neurons. This effect on ion conductance is the same as that of an unknown substance that mediates slow synaptic excitations with the myenteric plexus.

Action Potentials↗
PubMed1979

The action of neurotensin on single myenteric neurones.

The action of neurotensin was studied on single myenteric neurones within ganglia of the myenteric plexus isolated from the guinea-pig ileum. Drugs were applied by adding them to the perfusing Krebs solution. Extracellular recording with glass suction electrodes indicated that neurotensin (100 pM-300 nM) caused a dose-dependent excitation of about 50% of myenteric neurones; the remaining neurones were unaffected. This effect persisted in calcium-free solutions. Intracellular recording showed that a similar proportion of Type 1 myenteric neurones were depolarized by neurotensin: this was associated with an increase in membrane resistance. Type 2 cells were either depolarized or hyperpolarized by neurotensin. The depolarization persisted in calcium-free solutions. The hyperpolarization disappeared in calcium-free solutions, suggesting either that the potential change itself is calcium-dependent or that it was due to release by neurotensin of a hyperpolarizing substance.

Animals↗
PubMed1979

On the mechanism and site of action of enkephalin on single myenteric neurons.

Intracellular recordings were made from neurons in the isolated myenteric plexus of the guinea-pig ileum. Methionine- and leucine-enkephalin were applied to the neurons either by adding them to the perfusing solution in known concentrations or be ejecting them by microiontophoresis. When applied in the perfusion solution, the enkephalin (1 nM-1micron) hyperpolarized the soma membrane of less than half the neurons. The hyperpolarization was of rapid onset and reversed fully when the enkephalin was washed out; in a proportion of cells the hyperpolarization was associated with a fall in neuronal input resistance. This hyperpolarization was reversed or prevented by naloxone. When applied by iontophoresis to the soma membrane, enkephalin never hyperpolarized the myenteric neurons. Hyperpolarization in response to iontophoretic application of enkephalin was observed only when the enkephalin was applied to the surface of the ganglion away from the soma membrane; such hyperpolarization was prevented by addition of naloxone to the perfusion solution. The results indicate that the site at which enkephalin causes the naloxone-reversible hyperpolarization is not the soma membrane. The possibility is discussed that enkephalin may cuase presynaptic inhibition in this preparation by hyperpolarizing or increasing the conductance sites on the cellular processes from which acetylcholine is released.

Animals↗
PubMed1979

Some lipogenic enzyme activities in rat livers in which an excessive fat accumulation occurred due to feeding low-level amino acid mixture diets.

In liver homogenates of rats fed a low-level diet of Wheat-Rice- or Miyazaki-pattern amino acid mixture, some enzymes such as glucose-6-phosphate dehydrogenase, ATP citrate lyase, fatty acid-synthesizing enzymes, malic enzyme and L-alpha-glycerophosphate dehydrogenase, whose activities are indicators of lipogenesis have been determined from the viewpoint of the mechanisms producing fatty liver. In the early experimental period, malic enzyme activity increased more markedly in rats fed low amino acid mixture diets than in the control group, and L-alpha-glycerophosphate dehydrogenase activity in the liver increased slightly. Conversely, ATP citrate lyase and fatty acid-synthesizing enzyme activities remained almost at control levels, or glucose-6-phosphate dehydrogenase activity tended to decrease. These results suggest that some other associated factors, such as depression of the lipid transfer system in the liver rather than accelerated lipogenesis itself, may be the main cause of the fatty livers produced under these nutritional conditions.

ATP Citrate (pro-S)-Lyase↗