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Biomedical subjects

T Deguchi

Publications and source records attributed to T Deguchi.

At least 379 records · Page 21Linked to original sources
PubMed1973

Supersensitivity and subsensitivity of the beta-adrenergic receptor in pineal gland regulated by catecholamine transmitter.

Depletion of neural norepinephrine by reserpine treatment or by denervation resulted in a greater induction of serotonin N-acetyltransferase (EC 2.3.1.5) and a higher elevation of cyclic AMP in postsynaptic pineal cell to small amount of isoproterenol. This increase in responsiveness occurs rapidly within 24 hr after treatment with reserpine. Repeated administration of isoproterenol to the denervated or reserpine-treated rats not only suppressed the superinduction, but also caused a decreased response to isoproterenol in cultured pineal cells. Cultured pineal cells from denervated or reserpine-treated rats were about 10 times more responsive to small amounts of isoproterenol. The response of cultured pineal cells of rats which were repeatedly injected with isoproterenol was markedly reduced after exposure to submaximal amounts of catecholamines. The maximal increase in N-acetyltransferase was the same in denervated, reserpine-treated, isoproterenol-treated, and untreated pineal cells. Exposure of rats to continuous lighting (a procedure that reduces sympathetic nerve activity) resulted in a superinduction of pineal N-acetyltransferase by isoproterenol. These observations indicate that the responsiveness of the postsynaptic beta-adrenergic receptor is conditioned by prior exposure to its agonist, norepinephrine. Decreased norepinephrine results in supersensitivity, and repeated exposure to large amounts of catecholamines causes subsensitivity (tolerance).

Acetyltransferases↗
PubMed1972

Induction and superinduction of serotonin N-acetyltransferase by adrenergic drugs and denervation in rat pineal organ.

Activity of serotonin N-acetyltransferase (EC 2.3.1.5) in rat pineal organ is rapidly and markedly elevated in vivo after administration of beta-(3,4-dihydroxyphenyl)-L-alanine (L-DOPA), norepinephrine, epinephrine, isoproterenol, monoamine oxidase inhibitors, or theophylline. Serotonin or 5-hydroxytryptophan has no effect on the increase in activity of this enzyme. Inhibitors of protein synthesis or propranolol, a beta-adrenergic blocking agent completely inhibit(s) the increase in activity of serotonin N-acetyltransferase induced by drugs, indicating that new enzyme molecules are formed via stimulation of beta-receptors of pineal cells and adenosine 3':5'-cyclic monophosphate. When rat pineal organ is denervated by ganglionectomy, beta-(3,4-dihydroxyphenyl)-L-alanine induces much more serotonin N-acetyltransferase than in the innervated gland. This superinduction by denervation appears to be due to changes of the postsynaptic site, probably the beta-adrenergic receptor on the pineal cell.

5-Hydroxytryptophan↗
PubMed1972

Control of circadian change of serotonin N-acetyltransferase activity in the pineal organ by the beta--adrenergic receptor.

Serotonin N-acetyltransferase (EC 2.3.1.5) activity in the rat pineal organ is enhanced 50-fold at night. Rats exposed to light at night or kept in darkness during the daytime do not show any elevation of enzyme activity. Treatment with reserpine, a compound that depletes norepinephrine from nerves, 1-propranolol, a beta-adrenergic blocking agent, or cycloheximide, an inhibitor of protein synthesis, abolishes the nocturnal increase in serotonin N-acetyltransferase activity, indicating that the enzyme activity is modulated by neural release of norepinephrine from sympathetic nerves via beta-adrenergic receptors, and that the increase in enzyme activity is due to synthesis of new enzyme molecules. When rats are exposed to light at night or injected with 1-propranolol, there is a precipitous fall in serotonin N-acetyltransferase activity (half-life 5 min). Cycloheximide administered at night results in a slow fall in enzyme activity (half-life 60 min). When rats are kept in darkness and then exposed to light for 10 min, L-isoproterenol rapidly initiates the elevation of serotonin N-acetyltransferase activity to the initial level in 60 min. On the other hand, when the rats are kept in continuous light, L-isoproterenol initiates an increase in serotonin N-acetyltransferase activity after a lag phase of 60 min. The results indicate that there are two types of changes in serotonin N-acetyltransferase activity; a rapid increase and decrease mediated by the beta-adrenergic receptor, and a slow increase and decrease in enzyme activity that appears to represent the turnover of the enzyme.

Acyltransferases↗
PubMed1972

The action of phospholipases on the inner and outer surface of the squid giant axon membrane.

1. The effects of phospholipases on resting potential, action potential and membrane ionic conductances of squid giant axons have been studied by means of internal perfusion and voltage clamp techniques. The sample of phospholipases used exhibited both phospholipase A and B activities.2. When applied externally, phospholipases had no effect on the resting and action potentials at a concentration of 100 mug/ml.3. When applied internally, the enzymes effectively suppressed the amplitude and maximum rate of rise of the action potential at a concentration of 100 mug/ml. The resting potential started decreasing appreciably only after the action potential had been suppressed to a considerable extent.4. Under voltage clamp conditions, the peak transient current was suppressed following internal perfusion of phospholipases, 150 mug/ml. The steady-state current began to decrease, and the leakage current to increase only after the transient current had been suppressed to a considerable extent.5. The time course of sodium inactivation was not significantly slowed by internal perfusion of the enzymes.6. The curve relating the peak transient conductance to the membrane potential was shifted in the direction of depolarization after internal perfusion of phospholipases. No appreciable shift of the steady-state conductance curve was observed.7. These experimental results are discussed in connexion with the possible role of membrane phospholipids in the conductance changes associated with excitation.

Action Potentials↗