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T Akasu

Publications and source records attributed to T Akasu.

At least 109 records · Page 6Linked to original sources
PubMed1990

Morphological and electrophysiological properties of C-cells in bullfrog dorsal root ganglia.

Dissociated bullfrog dorsal root ganglion cells were voltage-clamped in the whole-cell configuration. Small spheroidal C-cells had a mean diameter of 14-30 microns and shared about 10% of the total population of the cells. The C-cells were characterized by a prominent calcium-activated potassium current underlying a hyperpolarization following the action potential. In contrast, a hyperpolarization-activated cationic inward rectifier was missing in all C-cells tested. These properties were completely different from those which have been observed for large spheroidal A-cells.

Animals↗
PubMed1990

Alpha 2-adrenoceptors mediate the inhibition of cholinergic transmission in parasympathetic ganglia of the rabbit urinary bladder.

Intracellular recordings were made from neurons of vesical parasympathetic ganglia (VPG) isolated from the rabbit urinary bladder and maintained, in vitro. Bath-application of norepinephrine (NE, 500 nM-5 microM) caused a hyperpolarizing response at the postsynaptic membrane of VPG neurons in a concentration-dependent manner. NE blocked the action potential elicited by an orthodromic stimulation of preganglionic (pelvic) nerve fibers. At a relatively low concentration (5-100 nM), NE depressed the fast excitatory postsynaptic potential (EPSP), without producing the hyperpolarization. NE (100 nM) produced 49 +/- 17% (N = 5) decrease in the amplitude of the fast EPSP. NE did not depress the acetylcholine (ACh) potential produced by iontophoretic application of ACh to the ganglion cells. NE did not affect the amplitude of the miniature EPSP, while it reduced the frequency of miniature EPSPs. These results suggest that NE inhibits the nicotinic transmission in the rabbit VPG, probably reducing the ACh release from presynaptic nerve terminals. Epinephrine (1 microM) was more potent than NE (1 microM) in producing the hyperpolarization as well as the blockade of the fast EPSP amplitude. Isoproterenol was ineffective as an agonist for these inhibitory adrenoceptors. Clonidine mimicked the effect of NE on the fast EPSP. Yohimbine and idazoxan antagonized both the inhibition of the fast EPSP and the hyperpolarization produced by NE. These results suggest that alpha 2-adrenoceptors are responsible for the inhibition of the neuronal activity in parasympathetic ganglia of the rabbit urinary bladder. Immunohistochemical study demonstrated the presence of tyrosine hydroxylase (TH)-labelled neuronal elements in the VPG. They were a small proportion of principal neurons, their dendrites, and many varicose fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1990

Extracellular calcium ions are required for muscarine-sensitive potassium current in bullfrog sympathetic neurons.

Cultured bullfrog sympathetic neurons were voltage-clamped in the whole-cell configuration. The extracellular medium contained tetrodotoxin (3 microM) and cesium (1 mM) to block and inward sodium current and a hyperpolarization-activated cation current Attempts were made to separate the M-current from four other potassium currents. Tetraethylammonium (30 mM) was used to block a classical delayed rectifier current (IK) and a fast calcium-activated current (IC). Apamin (30 nM) was used to block a slow calcium-activated current (IAHP). 4-Aminopyridine (1 mM) was used to reduce the amplitude of a transient current (IA). In these conditions, the maximum M-conductance near 0 mV was reduced by as much as 90% when divalent cations such as cobalt (1 mM) were added to the superfusate. The maximum M-conductance was also reduced by as much as 60% when calcium ions were removed from the superfusate. The half-activation voltage in the steady-state activation curve and the reversal potential of the M-current were not significantly changed in the calcium-free solution. It is suggested that the presence of calcium ions in the extracellular space is required for the M-current activation.

Adrenergic Fibers↗
PubMed1990

Volatile anaesthetics inhibit a cyclic AMP-dependent sodium-potassium current in cultured sensory neurones of bullfrog.

1. Cultured dorsal root ganglion cells of the bullfrog were voltage-clamped in the whole-cell configuration. 2. An adenosine 3':5'-cyclic monophosphate (cyclic AMP)-dependent cationic inward rectifier (IH) was inhibited by bath application of enflurane (0.2-0.8 mM) and halothane (0.2-0.5 mM), which thereby induced an outward current at the resting potential, and a membrane hyperpolarization in unclamped cells. 3. The main effect of enflurane (0.5 mM) was to displace the steady-state IH activation curve to a hyperpolarizing direction by about 10 mV, as well as to reduce the maximum H-conductance to about 20%. 4. Forskolin (1-10 microM), which enhances IH by producing a depolarizing shift in the IH activation curve and increasing the maximum H-conductance, recruited IH even when the current had already been eliminated by enflurane (1 mM).

Anesthetics↗
PubMed1990

Cyclic AMP regulates an inward rectifying sodium-potassium current in dissociated bull-frog sympathetic neurones.

1. Bull-frog sympathetic neurones in primary culture were voltage clamped in the whole-cell configuration. The pipette solution contained ATP (5 mM). 2. A hyperpolarization-activated sodium-potassium current (H-current: IH) was separated from other membrane currents in a nominally calcium-free solution containing cobalt (2 mM), magnesium (4 mM), barium (2 mM), tetraethylammonium (20 mM), tetrodotoxin (3 microM), apamin (30 nM) and 4-aminopyridine (1 mM). IH was selectively blocked by caesium (10-300 microM). 3. The steady-state activation of IH occurred between -60 and -130 mV. The H-conductance was 4.1-6.6 nS at the half-activation voltage of -90 mV. With the concentrations of potassium and sodium ions in the superfusate at 20 and 70 mM, respectively, the reversal potential of IH was about -20 mV. IH was activated with a time constant of 2.8 s at -90 mV and 22 degrees C. The Q10 between 16 and 26 degrees C was 4.3. 4. A non-hydrolysable ATP analogue in the pipette solution did not support IH activation. Intracellular 'loading' of GTP-gamma-S (30-500 microM) led to a progressive activation of IH. 5. Forskolin (10 microM) increased the maximum conductance of IH by 70%. This was associated with a depolarizing shift in the half-activation voltage (5-10 mV) and in the voltage dependence of the activation/deactivation time constant of IH. 6. Essentially the same results as with forskolin were obtained by intracellular 'loading' with cyclic AMP (3-10 microM) or bath application of 8-bromo cyclic AMP (0.1-1 mM), dibutyryl cyclic AMP (1 mM) and 3-isobutyl-1-methylxanthine (0.1-1 mM). 7. The protein kinase inhibitor H-8 (1-10 microM) decreased the peak amplitude of IH. Phorbol 12-myristate 13-acetate (10 microM), a protein kinase C activator, was without effect. 8. It is concluded that a voltage-dependent cation current can be regulated by the basal activity of adenylate cyclase, presumably through protein kinase A, in vertebrate sympathetic neurones.

1-Methyl-3-isobutylxanthine↗
PubMed1990

Calcium-dependent chloride current in neurones of the rabbit pelvic parasympathetic ganglia.

1. Voltage-clamp recordings were made from neurones in rabbit vesical pelvic ganglia by using single microelectrodes filled with 2 M-caesium chloride. Neurones were superfused with Krebs solution containing 300 nM-tetrodotoxin and 50 mM-tetraethylammonium. 2. Depolarizing voltage jumps activated inward currents followed by slowly decaying inward tail currents at -30 to +30 mV, which were accompanied by a large increase in membrane conductance. Both the inward current and tail current were blocked by cobalt (2 mM) or in a Krebs solution containing zero calcium and 12 mM-magnesium. 3. Substitution of barium for calcium enhanced the inward current, while it strongly reduced the tail current. Strontium substitution still exhibited both the inward current and the tail current. 4. Lowering external chloride activity increased the tail current amplitudes without affecting an initial calcium current. The reversal potentials of the tail current, measured using a twin-pulse protocol, were -18 +/- 5 mV (mean +/- S.E.M., n = 8) and +5 +/- 3 mV (n = 5) in Krebs solution and low-chloride (62 mM) solution, respectively, suggesting a calcium-dependent chloride current. 5. Stilbene derivatives, 4-acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid (SITS, 0.01-1 mM) and 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS, 0.01-1 mM), reversibly and concentration dependently depressed the tail current without affecting the calcium current. 6. Transient (T) and sustained (N and L) types of calcium current were likely to co-exist in neurones of the rabbit pelvic ganglia. Calcium-dependent chloride current was activated by N- and L-type calcium currents but not by T-type current. 7. Activation of the tail current at 0 to +20 mV was described by a single-exponential function. The tail current decayed exponentially at a holding membrane potential of -70 mV. Tail decay time constants were dependent on voltage and duration of the step command. 8. Substantial activation of the calcium-dependent chloride conductance could occur during a post-tetanic after-potential when pelvic ganglia neurones fired action potentials repetitively.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1990

ATP regulates muscarine-sensitive potassium current in dissociated bull-frog primary afferent neurones.

1. Bull-frog dorsal root ganglion cells in primary culture were voltage clamped in the whole-cell configuration. The pipette solution contained ATP (5 mM). 2. Step depolarizations (5-70 mV, 0.1-1 s) from a holding potential close to the resting potential (range, -64 to -79 mV) evoked a non-inactivating potassium current with properties indistinguishable from those which have been reported for the M-current of bull-frog sympathetic neurones. 3. An unhydrolysable ATP analogue APP(NH)P (5 mM), substitute with ATP in the pipette solution, did not support the M-current activation. 4. Bath application of ATP (30 nM-30 microM) reduced the amplitude of the M-current in a concentration-dependent manner, congruent to 50% inhibition of the current occurring with 1 microM-ATP. The main effect of ATP was to reduce the maximum M-conductance without changing the activation and deactivation kinetics of the M-current. 5. Essentially the same results were obtained with ADP (0.1-30 microM) and alpha, beta-methylene-ATP (10-30 microM). AMP (10-100 microM) and adenosine (10-30 microM) were without effect on the M-current. 6. The ATP-induced inhibition of the M-current was irreversible when an unhydrolysable GTP analogue GTP-gamma-S (10-30 microM) was present in the pipette solution. ATP (3 microM) reduced the amplitude of the M-current only by about 10% when GDP-beta-S (100 microM) was present in the pipette solution. Pre-treatment of the cells with pertussis toxin (IAP; 500 ng ml-1) for 24 h at 24 degrees C did not prevent the ATP-induced M-current inhibition. 7. Phorbol 12-myristate 13-acetate (PMA; 1-3 microM) reduced the amplitude of the M-current to about 50%. A reduction in the M-current amplitude by PMA (3 microM) and ATP (10 microM) was attenuated when staurosporine (200 nM) was present in the pipette solution. Forskolin (10 microM) was without effect on the M-current. 8. It is concluded that ATP acting at P2 receptors, associated with an IAP-insensitive GTP-binding protein, inhibits the M-current in amphibian primary afferent neurones.

Adenosine Diphosphate↗
PubMed1990

Reduction of the N-type calcium current by noradrenaline in neurones of rabbit vesical parasympathetic ganglia.

1. Intracellular and single-electrode voltage-clamp recordings were made from neurones of vesical parasympathetic ganglia (VPG) isolated from the rabbit urinary bladder. 2. Noradrenaline (NA, 0.5-5 microM) shortened the duration of the action potentials and depressed the amplitudes of both spike after-hyperpolarization and after-current. 3. Voltage-dependent calcium currents (ICa) were recorded by using microelectrodes filled with 2 M-caesium chloride in a superfusing solution containing tetraethylammonium (TEA, 50 mM) and tetrodotoxin (TTX, 500 nM). Noradrenaline (0.5-5 microM) depressed both the ICa and the tail current evoked by depolarizing voltage jumps from -100 to -50 mV to -30 to +20 mV. 4. Substitution of barium for calcium also produced an inward current (IBa) with no obvious tail current. Noradrenaline (1 microM) reduced the magnitude of the IBa without affecting the voltage dependence of the current-voltage relationship for IBa. 5. Yohimbine (1 microM), but not prazosin (1 microM) or propranolol (1 microM), antagonized the NA-induced inhibition of the IBa. UK 14304, a potent alpha 2-adrenoceptor agonist, mimicked NA in depressing the IBa. 6. The transient low-threshold (T), the transient high-threshold (N) and the slowly inactivating high-threshold (L) calcium currents co-existed in VPG neurones. 7. Noradrenaline reduced the IBa evoked at clamp potentials more positive than -20 mV from holding potentials near the resting membrane potential (-70 to -50 mV). Under these conditions, the IBa consisted primarily of N- and L-current components. In contrast, NA had no effect on the isolated T- and L-currents. It is concluded that NA selectively inhibits the N-type calcium channels by an action at alpha 2-adrenoceptors in the rabbit VPG neurones.

Action Potentials↗
PubMed1990

Properties of voltage-dependent barium currents in neurons of pelvic parasympathetic ganglia of rabbit.

Properties of voltage-dependent barium current (IBa) were examined in parasympathetic neurons of the rabbit urinary bladder, in vitro. Transient low-threshold IBa was evoked by voltage jump from a holding potential (Vh) of -100 to -50 mV. Additional transient high-threshold IBa appeared at potentials more positive than -30 mV. Long-lasting high-threshold IBa was evoked at 0 to -20 mV. High-threshold currents were blocked by omega-conotoxin but not by dihydropyridines.

Animals↗
PubMed1990

Adenosine inhibits a GABAB receptor-mediated hyperpolarizing postsynaptic potential in neurons of rat septal nuclei.

Intracellular recordings were made from neurons of rat dorsolateral septal nucleus (DLSN), in vitro. Adenosine and 2-chloroadenosine (1-500 microM) hyperpolarized DLSN neurons and blocked the excitatory postsynaptic potential (EPSP) and the late hyperpolarizing potential (LHP) in the presence of bicuculline. Adenosine did not depress the glutamate-induced potential. Bath-application of adenosine depressed the baclofen-induced potential in 60% of the neurons. Adenosine also inhibited the LHP in the remaining 40% of neurons, while it did not depress the baclofen-induced potential in these neurons. These results indicate that adenosine inhibits the EPSP pre-synaptically whereas it inhibits the LHP both pre- and postsynaptically in rat septal nuclei.

Adenosine↗
PubMed1989

Frequency dependent inhibition of the nicotinic transmission by serotonin in vesical pelvic ganglia of the rabbit.

Intracellular recordings were made from neurons in rabbit vesical pelvic ganglia (VPG), in vitro. Increasing the frequency of preganglionic-nerve stimulations from 0.1-1 Hz to 10-20 Hz facilitated fast excitatory postsynaptic potentials (EPSPs), resulting in a generation of action potentials. Acetylcholine-induced response was not altered during the facilitation of the fast EPSP. Serotonin blocked action potentials elicited by preganglionic-nerve stimulations at 0.1 Hz, while it caused no blockade at 10 Hz. Serotonin may potentiate the feature of high-pass filter in transmission of VPG. Immunohistochemical study demonstrated serotonin-like varicose terminals in rabbit VPG.

Acetylcholine↗
PubMed1989

Modulation of the sensitivity of nicotinic receptors in autonomic ganglia.

This article reviews some of the evidence suggesting that a variety of endogenous substances either facilitates or inhibits the sensitivity of nicotinic acetylcholine (ACh) receptors at the subsynaptic membrane of cholinergic synapses. It is noteworthy that 5-hydroxytryptamine and histamine act as competitive antagonists, like curare, presumably changing the affinity of ACh for the specific binding site on the nicotinic receptor. Catecholamine, neuropeptides, prostaglandin and glucocorticoids act as non-competitive antagonists on an allosteric site on the receptor-ionic channel complex. ATP and LH-RH (in a subpopulation of sympathetic neurons) caused a facilitation of the sensitivity of nicotinic receptors. The mode of actions of endogenous substances which modulate the nicotinic receptor-sensitivity is similar to those of pharmacological agents. Therefore, these neurotransmitters and neurohormones have been termed endogenous 'antagonists' or 'sensitizers'.

Acetylcholine↗
PubMed1989

Adrenaline inhibits muscarinic transmission in bullfrog sympathetic ganglia.

The effect of adrenaline (Ad) on muscarinic transmission was examined in B neurones of bullfrog sympathetic ganglia by using intracellular and voltage-clamp recording methods. Bath-application of Ad (5-500 microM) caused a depression of the slow excitatory postsynaptic potential (EPSP) elicited by repetitive stimulations of preganglionic nerve fibres in the presence of curare (30 microM). Ad also depressed the 'muscarinic' ACh potential induced by ionophoretic application of ACh directly to curarized sympathetic neurones in a concentration-dependent manner. Isoprenaline mimicked the effect of Ad in producing the inhibition of the 'muscarinic' ACh potential. Propranolol antagonized the inhibitory action of Ad. Dibutyryl adenosine 3',5'-monophosphate had no significant effect on the 'muscarinic' ACh potential. Under voltage-clamp conditions, Ad caused an inward current associated with inhibition of the M-current (Brown and Adams 1980). Ad depressed the amplitude of slow postsynaptic currents produced by applications of ACh and muscarinic. At a concentration of 100 microM, Ad produced a 68 +/- 8% (n = 12) depression of the amplitude of the muscarinic ACh current. The inhibition of muscarinic transmission induced by Ad is due to a direct suppression of the muscarinic current at the postsynaptic membrane in bullfrog sympathetic ganglia.

Acetylcholine↗
PubMed1989

5-Hydroxytryptamine produces presynaptic facilitation of cholinergic transmission in rabbit parasympathetic ganglia.

Intracellular recordings were made from neurons of rabbit vesical pelvic (parasympathetic) ganglia (VPG). Application of 5-hydroxytryptamine (5-HT, 0.3-30 microM) produced an initial depression followed by a long-lasting facilitation of the fast excitatory postsynaptic potential (e.p.s.p.) evoked by stimulation of the pelvic preganglionic nerve. The facilitation of nicotinic transmission lasted for 30-120 min, even when 5-HT was removed from the superfusing solution. 5-HT (0.3-30 microM) did not change the depolarization induced by a direct application of acetylcholine (ACh) to the VPG neurons pretreated with 1 microM atropine. 5-HT also caused an initial depression followed by an increase in the quantal content of the fast e.p.s.p. It is, therefore, suggested that diphasic effect of 5-HT on the nicotinic transmission is due mainly to a modulation of the ACh-release from presynaptic nerve terminals. Methysergide (5 microM), mianserin (5-30 microM) and ICS 205-930 (100-300 nM) did not antagonize the presynaptic actions of 5-HT on the nicotinic transmission, suggesting that the presynaptic 5-HT receptor may belong to a class of 5-HT1 subtypes. Spiperone (1 microM), a selective 5-HT1A antagonist, blocked the 5-HT-induced inhibition of the fast e.p.s.p. Under the effect of spiperone, the facilitation appeared soon after application of 5-HT. The facilitation of the fast e.p.s.p. may be mediated through a 5-HT1B or 5-HT1C subtype. Lowering temperature of the external solution eliminated the 5-HT-induced facilitation of the nicotinic transmission. Forskolin produced a presynaptic facilitation of the fast e.p.s.p., without producing an initial depression. 3-Isobutyl-1-methylxanthine (10 microM) potentiated the facilitatory action of 5-HT. Bath-application of dibutyryl cyclic adenosine monophosphate (cAMP) (1-6 mM) and 8-bromo-cyclic AMP (2-5 mM) mimicked the effect of 5-HT in producing the facilitation of the fast e.p.s.p.s. All data presented are consistent with the hypothesis that 5-HT, acting on presynaptic 5-HT1 receptors, causes a facilitation in the release of ACh from preganglionic nerve terminals possibly mediated through an activation of adenylate cyclase.

Acetylcholine↗
PubMed1989

Histamine H2 receptor mediates postsynaptic excitation and presynaptic inhibition in submucous plexus neurons of the guinea-pig.

Intracellular recordings were made from submucous plexus neurons of the guinea-pig cecum maintained in vitro. Histamine (0.3-10 microM) produced a dose-dependent membrane depolarization (congruent to 13 mV with 3 microM) in about 28% of the cells tested; most of these cells showed a prominent calcium-activated potassium conductance (AH cells). The depolarization was due primarily to an inactivation of potassium conductance which is available at the resting membrane potential of -60 mV. Peak amplitude of the fast excitatory postsynaptic potential was depressed by histamine (0.1-10 microM) in a dose-dependent manner (congruent to 62% depression with 1 microM). This was observed even in those cells in which histamine did not produce any membrane depolarizations (mostly S cells). The depression of the fast excitatory postsynaptic potential resulted from the presynaptic inhibition of acetylcholine release. Histamine also reduced the amplitude of the non-cholinergic, presumably peptidergic, slow excitatory postsynaptic potential by suppressing peptide release from presynaptic nerve terminals. Peak amplitude of the adrenergic inhibitory synaptic potential was not depressed by histamine suggesting that histamine receptors are not present on presynaptic terminals of sympathetic nerve fibres. Both postsynaptic and presynaptic actions of histamine were blocked by cimetidine or ranitidine but not by pyrilamine implying that H2 receptors are involved.

Action Potentials↗
PubMed1989

Potassium currents in submucous neurones of guinea-pig caecum and their synaptic modification.

1. Intracellular recordings were made from submucous neurones of the guinea-pig caecum. In most experiments, membrane currents were measured using a single-electrode voltage clamp. 2. A potassium current dependent on calcium influx occurred at rest (approximately equal to 200 pA at -60 mV). The amplitude of the current was increased up to 1 nA at -35 mV and decreased to zero at -100 mV; when fully activated the current did not show any inactivation. An inward calcium current, of 15-25 pA in amplitude near -60 mV and insensitive to omega-conotoxin (0.5 microM), probably activated the potassium current. 3. Step depolarizations from potentials negative to -80 mV evoked a transient (less than or equal to 200 ms at -40 mV) potassium current which was blocked by 4-aminopyridine (1-3 mM). Hyperpolarizing commands to potentials negative to -87 mV evoked an inwardly rectifying potassium current which was selectively blocked by caesium (1-2 mM). The residual cell current between -100 and -40 mV in calcium-free solution containing tetraethylammonium (20 mM), caesium (2 mM) and 4-amino-pyridine (3 mM) conformed to constant field assumptions. This current was called a background potassium current. 4. Decrease in membrane conductance during the slow excitatory postsynaptic current (EPSC) was due predominantly (greater than or equal to 90%) to a reduction in the calcium-activated potassium current at -35 mV, but due almost exclusively to a reduction in the background potassium current at potentials more negative than -100 mV. The relative contribution of the two currents to the slow EPSC was entirely dependent on the relative contribution of the currents to the membrane conductance at given potentials. 5. The transient potassium current was unaffected or slightly enhanced during the slow EPSC. The inwardly rectifying potassium current was unaffected during the slow EPSC. 6. Three tachykinins (substance P, substance K and neurokinin B; 3-800 nM), forskolin (1-30 microM), 8-bromoadenosine 3':5'-cyclic monophosphate (8-bromo cyclic AMP; 1-3 mM), 3-isobutyl-1-methylxanthine (0.3-1 mM) mimicked the conductance changes during the slow EPSC in a concentration-dependent manner. 7. It is concluded that the slow excitatory synaptic potential in the submucous plexus, presumably mediated by peptidergic transmitters, results from an inactivation of two distinct potassium currents, at least one of which is controlled by intracellular calcium ions.

1-Methyl-3-isobutylxanthine↗