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T Akasu

Publications and source records attributed to T Akasu.

At least 91 records · Page 5Linked to original sources
PubMed1994

Patch-clamp analysis of hypoglycemia-induced inhibition of synaptic transmission in the rat dorsolateral septal nucleus.

The role of glucose in neuronal transmission was examined in the rat dorsolateral septal nucleus (DLSN) by using 'slice-patch' techniques. Removal of glucose from the oxygenated Krebs solution produced an outward current associated with an increased K+ conductance. The glucose-depletion depressed the excitatory postsynaptic current (EPSC), the inhibitory postsynaptic current (IPSC) and the late hyperpolarizing current (LHC) produced by stimulation of the fimbria/fornix pathway. It is hypothesized that glucose regulates neurotransmission in the rat DLSN by modulating the release of transmitters from presynaptic nerve terminals.

Animals↗
PubMed1993

Intracellular ATP changes the voltage-dependence of delayed rectifier potassium current in bullfrog primary afferent neurons.

Dissociated bullfrog dorsal root ganglion cells were voltage-clamped in the whole-cell configuration to study the steady-state activation and inactivation curves for a delayed rectifier potassium current. The 50%-activation of the current occurred at +15 mV when measured with ATP (5 mM) in the pipette solution as opposed to -11 mV with 5'-adenylylimidodiphosphate (AMP-PNP, 5 mM) and -15 mV with adenosine 5'-O-(3-thiotriphosphate) (5 mM). The 50%-inactivation of the current occurred at -6 mV with ATP but at -31 mM with AMP-PNP. The results suggest that intracellular ATP modulates voltage-dependence of the delayed rectifier in amphibian afferent neurons.

Adenosine Triphosphate↗
PubMed1993

Chemosensitivity of C-cells in bullfrog dorsal root ganglia to substance P and adenosine 5'-triphosphate.

Dissociated bullfrog dorsal root ganglion cells were voltage clamped in the whole-cell configuration. In small C-cells having 20 microns as averaged diameter, substance-P (0.1-1 microM) inhibited an M-type potassium current while ATP (1-10 microM) activated a sodium-potassium current. In large A-cells (approximately 65 microns in diameter) in which ATP has been shown to inhibit M-current, substance P (0.1-1 microM) also inhibited this potassium current without activating the sodium-potassium current. Results provided evidence for the distinction between A- and C-cells in terms of their chemosensitivity.

Adenosine Triphosphate↗
PubMed1993

Inward rectifier and low-threshold calcium currents contribute to the spontaneous firing mechanism in neurons of the rat suprachiasmatic nucleus.

Intracellular and voltage-clamp studies were carried out to clarify the mechanism for spontaneous firing activity in neurons of the suprachiasmatic nucleus (SCN) of rat hypothalamic brain slices in vitro. SCN neurons displayed spontaneously firing action potentials that were preceded by a depolarizing pre-potential and followed by a short spike after-hyperpolarization (AHP). Injection of inward current with a duration longer than 50 ms resulted in a depolarizing voltage "sag" on hyperpolarizing electrotonic potentials. The inward rectification was depressed by bath application of caesium (1 mM) but not by barium (500 microM). SCN neurons also showed a rebound depolarization associated with spike discharge (anodal break) in response to relaxation of hyper polarizing current injection. The rebound depolarization was reduced by nominally zero calcium. Cadmium (500 microM), cobalt (1 mM) or caesium (1 mM) but not nicardipine also depressed the rebound depolarization. Under voltage-clamp conditions, hyperpolarizing steps to membrane potentials negative to approximately -60 mV caused an inward rectifier current, probably H current (IH), which showed no inactivation with time. Bath application of caesium (1-2 mM) suppressed IH. Caesium (2 mM) depressed the slope of the depolarizing spike pre-potential, resulting in a prolongation of the interspike interval of tonic firing neurons. We conclude that both the inward rectifier current, IH, and the low-threshold calcium current contribute to the spike prepotential of spontaneous action potentials in firing neurons of the rat SCN.

2-Amino-5-phosphonovalerate↗
PubMed1993

Myosin light chain kinase occurs in bullfrog sympathetic neurons and may modulate voltage-dependent potassium currents.

A polyclonal antibody against myosin light chain kinase (MLCK) of chicken gizzard recognized a 130 kd peptide of bullfrog sympathetic ganglia as MLCK. MLCK immunoreactivity was confined to the neuronal cell body. A synthetic peptide corresponding to an inhibitory domain of MLCK (Ala783-Gly804) was applied intracellularly to isolated sympathetic neurons during whole-cell recordings of ionic currents. The peptide inhibitor reversibly decreased M-type potassium current (IM) while not affecting A-type of delayed rectifier-type potassium currents. Intracellular application of an active fragment of MLCK enhanced IM, whereas application of an inactive MLCK fragment did not. The results suggest that IM can be modulated by MLCK-catalyzed phosphorylation.

Amino Acid Sequence↗
PubMed1993

Effects of vasoactive intestinal contractor on voltage-activated Ca2+ currents in feline parasympathetic neurons.

Intracellular current-clamp and single-electrode voltage-clamp techniques were used to study in vitro action potentials and the action of vasoactive intestinal contractor (VIC; 0.03-1 microM) on the high-voltage-activated Ca2+ currents (ICa) of neurons in feline colonic parasympathetic ganglia. In the current-clamp recording mode, action potential amplitude was depressed by cobalt (1 mM) and omega-conotoxin (300 nM) or in nominally Ca(2+)-free Krebs solutions. In the single-electrode voltage-clamp recording mode, the ICa was isolated by blocking the voltage-gated Na+ current with tetrodotoxin (1-3 microM) and by Krebs solutions containing a low Na+ concentration. The voltage-activated K+ currents were blocked by intracellular injection of cesium through a recording electrode filled with 2 M CsCl and external application of tetraethylammonium (30-50 mM) and barium (2 mM). The Ca(2+)-dependent Cl- current was blocked by replacement of Ca2+ (2 mM) with equimolar barium. Anomalous rectification was blocked by external application of 2 mM cesium. The ICa was evoked by depolarizing step commands more positive than -40 mV from holding potentials ranging between -80 and -60 mV. ICa was depressed by cobalt (1 mM), cadmium (100 microM), and omega-conotoxin (500 nM) but not by nifedipine (10 microM), nicardipine (10 microM), and verapamil (10 microM). BAY K 8644 (3-10 microM) also did not affect the ICa. VIC (0.1-1 microM), one of the endothelin (ET) isopeptides, caused an inward current followed by an outward current. The VIC-induced inward and outward currents were associated with an increase and decrease in membrane conductance, respectively. VIC also caused an initial depression followed by a long-lasting augmentation of the ICa. ET-1, ET-2, and ET-3 equally mimicked the action of VIC on both holding current and ICa. These data suggest that VIC activates a receptor-operated channel and modulates the omega-conotoxin-sensitive voltage-activated Ca2+ channels through ETB receptor subtypes of neurons in feline colonic parasympathetic ganglia.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1992

Presynaptic facilitation of excitatory postsynaptic potential by glucagon in neurons of rat ventromedial hypothalamic slices.

Intracellular recordings were made from neurons in rat ventromedial hypothalamus (VMH), in vitro. Application of glucagon (100 nM to 5 microM) for 2-5 min increased the amplitude of excitatory postsynaptic potential (EPSP) lasting for 10-20 min. Forskolin and 8-bromo-cyclic AMP mimicked glucagon in producing a long-lasting facilitation of the EPSP. These drugs did not affect depolarizing response produced by glutamate. 3-Isobutyl-1-methylxanthine (IBMX) potentiated the time course of glucagon-induced facilitation of the EPSP. These results suggest that glucagon facilitates the EPSP probably by increasing transmitter release through activation of adenylate cyclase.

Animals↗
PubMed1992

Adenosine inhibits the synaptic potentials in rat septal nucleus neurons mediated through pre- and postsynaptic A1-adenosine receptors.

Intracellular and voltage-clamp recordings were made from neurons in rat brain slices containing dorsolateral septal nucleus (DLSN), in vitro. Bath application of adenosine (100 microM) produced a hyperpolarization (2-15 mV) in 46% of DLSN neurons (AH-neurons); in the remaining 54% neurons (non-AH-neurons), no hyperpolarization to adenosine was observed. Adenosine (1-300 microM) depressed not only the excitatory postsynaptic potential (EPSP) but also the inhibitory postsynaptic potential (IPSP) and the late hyperpolarizing potential (LHP) evoked by stimulation of the hippocampal CA3 area or the fimbria/fornix pathway in both AH- and non-AH-neurons. In non-AH-neurons, adenosine did not block current responses resulting from glutamate, muscimol or baclofen applied directly to DLSN neurons. In AH-neurons, adenosine partially depressed the baclofen-induced outward current. Adenosine did not block the directly-evoked IPSP (monosynaptic IPSP) as well as the glutamate-induced (hyperpolarizing) postsynaptic potential (PSP) that is mediated by GABA released from interneurons. These results suggest that adenosine does not directly inhibit the release of GABA. The effects of adenosine was mimicked by selective A1-receptor agonists and was blocked by selective A1-receptor antagonists. Pertussis toxin (PTX) blocked the hyperpolarization induced by adenosine or baclofen applied exogenously. Adenosine consistently produced presynaptic inhibition of the EPSP even in DLSN neurons treated with PTX. We conclude that adenosine inhibits neurotransmission between the hippocampus and septum through activation of pre- and postsynaptic A1-receptors which couple with G-proteins of different PTX-sensitivity or with distinct transduction processes at pre- vs. postsynaptic sites.

Adenosine↗
PubMed1992

Guanosine 3',5'-cyclic monophosphate regulates calcium channels in neurones of rabbit vesical pelvic ganglia.

1. The effects of dibutyryl guanosine 3',5'-cyclic monophosphate (db-cyclic GMP) were studied in vitro on calcium channels of neurones in rabbit vesical parasympathetic ganglia, using intracellular and single-electrode voltage-clamp recordings. 2. Db-cyclic GMP (100 microM) caused membrane depolarization associated with a decrease in membrane input resistance and an after-hyperpolarization associated with an increase in membrane input resistance. 3. Db-cyclic GMP (0.01-1 mM) caused a concentration-dependent, transient inward current followed by a long-lasting outward current. Membrane conductance was increased and decreased during the inward and outward currents, respectively. 4. The db-cyclic GMP-induced inward current was depressed in nominally calcium-free solutions, by cobalt (1 mM) and nicardipine (10 microM). The mean reversal potentials of the inward current were +42 and -20 mV in the presence and absence of calcium in the external solution, respectively. 5. The db-cyclic GMP-induced inward current was not altered by lowering the external sodium concentration, raising external potassium concentration or by intracellular injection of caesium. 6. A calcium-insensitive component of the db-cyclic GMP-induced current was increased by lowering the external chloride concentration and blocked by 4-acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid, a chloride channel blocker. 7. Voltage-dependent, high-threshold calcium currents were depressed during the db-cyclic GMP-induced inward current and facilitated during the outward current. 8. Cyclic GMP was less potent than db-cyclic GMP in causing both inward and outward currents or modulation of calcium currents. GTP, GDP, GMP, guanosine, 8-bromoadenosine 3',5'-cyclic monophosphate and forskolin did not alter the holding current or voltage-dependent calcium currents. 9. It is concluded that intracellular cyclic GMP causes not only activation of resting calcium and chloride channels but also a transient depression followed by long-lasting facilitation of voltage-dependent calcium currents in neurones of vesical parasympathetic ganglia.

Animals↗
PubMed1992

Cellular metabolism regulating H and M currents in bullfrog sympathetic ganglia.

Much evidence has accumulated suggesting that neurons in autonomic and dorsal root ganglia possess voltage-dependent currents that link with transmitter receptors through intracellular signal transduction systems. The M current (IM), a voltage-dependent potassium current, was activated at potentials more positive than -65 mV, while the H current (IH), a voltage-dependent nonselective cationic current, was activated at potentials more negative than -50 mV. The hydrolyzable form of ATP was required to activate IM and IH. Intracellular application of calmodulin enhanced the amplitude of IM in a calcium-dependent manner. IM was reduced by W-7, a calmodulin antagonist, and by ML-9, an inhibitor of calmodulin-dependent protein kinase. IH was enhanced by intracellular loading with cyclic adenosine monophosphate (AMP) or bath application of forskolin and membrane-permeable cyclic AMP analogues. Isobutylmethylxanthine also increased the maximal conductance of IH. IH was depressed by H-8 but not by phorbol ester. It is concluded that the resting membrane conductance of these ganglion cells can be regulated by basal activities of calmodulin-dependent protein kinase and A kinase.

Animals↗
PubMed1991

DNA ploidy pattern in rectal carcinoid tumors.

The nuclear DNA pattern of 22 rectal carcinoids was determined by cytophotometry of paraffin embedded tissues. The results were compared with clinical as well as histopathologic features of the tumor. Three of the carcinoids with synchronous or metachronous metastasis had aneuploid DNA pattern, whereas 19 tumors with no metastasis showed diploid DNA pattern. No other single clinical or pathologic feature of the tumor could predict more accurately the malignant potential and the subsequent course of the rectal carcinoid. It is concluded that DNA aneuploidy in rectal carcinoid tumors is not so rare as indicated by earlier studies and that it is a factor of significant prognostic value.

Adult↗
PubMed1991

Endothelin modulates calcium channel current in neurones of rabbit pelvic parasympathetic ganglia.

1. The effects of endothelin were studied, in vitro, on neurones contained in the rabbit vesical pelvic ganglion by use of intracellular and single-electrode voltage clamp techniques under conditions where sodium and potassium channels were blocked. 2. In the current-clamp experiments, endothelin (1 microM) caused a depolarization followed by a hyperpolarization of the membrane potential. In the voltage-clamp experiments, endothelin (0.01-1 microM) caused an inward current followed by an outward current in a concentration-dependent manner. 3. Membrane conductance was increased during the endothelin-induced depolarization and inward current. Membrane conductance was decreased during the endothelin-induced hyperpolarization and outward current. 4. The endothelin-induced inward and outward currents were not altered by lowering external sodium concentration or raising external potassium concentration. 5. The endothelin-induced inward current was depressed (mean 72%) in a Krebs solution containing nominally zero calcium and high magnesium. These results suggest that a predominent component of the endothelin-induced inward current is mediated by calcium ions. 6. The calcium-insensitive component of the inward current was abolished by a chloride channel blocker, 4-acetamide-4'-isothiocyanostilbene-2,2'-disulphonic acid. The mean reversal potential for the calcium-insensitive component of the inward current was -18 mV. This value is near the equilibrium potential for chloride. Thus, it is presumed that the calcium-insensitive component of the inward current is carried by chloride ions. 7. Endothelin caused an initial depression followed by a long lasting facilitation of both rapidly and slowly decaying components of high-threshold calcium channel currents (N- and L-type). 8. In summary, the data show that for neurones in the vesical pelvic ganglia, endothelin causes membrane depolarization and activates an inward current. The ionic mechanisms involve receptor-operated calcium and chloride currents. Also, endothelin causes an initial depression followed by a long-lasting facilitation of the voltage-dependent calcium current.

Animals↗
PubMed1991

Slowly inactivating potassium current in cultured bull-frog primary afferent and sympathetic neurones.

1. Cultured bull-frog dorsal root ganglion cells were voltage clamped in the whole-cell configuration. The cells were superfused with a nominally calcium-free Ringer solution containing tetrodotoxin (3 microM), magnesium (10 mM), cobalt (1 mM), barium (2 mM), 4-aminopyridine (3 mM) and caesium (2 mM). 2. Step depolarizations (10-40 mV, 100-300 ms) from a holding potential close to the rest (typically -70 mV) evoked an outward current (IK) followed by an outward tail current. The peak amplitude of the current was reduced to less than 10% by tetraethylammonium (30 mM). 3. IK developed to its peak in 200 ms at -30 mV. Tail currents reversed at potentials that changed according to the logarithm of the extracellular potassium concentrations. 4. Tail currents declined to the baseline according to an exponential function of time (tau congruent to 40 ms at -60 mV) and its reciprocal time constant increased e-fold with a 13 mV hyperpolarization. 5. The current inactivated during sustained (1-20 s) depolarizing pulses according to a single exponential function (tau congruent to 3 s). 6. The peak amplitude of IK at -30 mV was progressively increased as the holding potential was made more negative than -70 mV reaching the maximum with step depolarizations from -120 mV. Reversed phenomenon was observed as the holding potential was made less negative than -70 mV. 7. The removal of the steady-state inactivation occurred along with a single exponential function and the time constant was decreased from 70 ms at -70 mV to 10 ms at -120 mV. 8. It is suggested that a slowly inactivating potassium current which we called IK in amphibian sensory neurones could be a class of a 'delayed' rectifier potassium current. A potassium current with properties indistinguishable from those which have been described for the sensory IK also occurred in cultured bull-frog sympathetic neurones. 9. Forskolin (1-30 microM) and 1,9-dideoxy forskolin (10 microM) reduced the amplitude of IK by up to 85% but these actions were not mimicked by any of 8-bromo-cyclic AMP (1 mM), dibutyryl cyclic AMP (1 mM) and 3-isobutyl-1-methylxanthine (1 mM). A hydrophilic forskolin analogue, 7-O-hemisuccinyl-7-deacetyl forskolin (10 microM), was about one-tenth as potent as forskolin (10 microM).

Animals↗