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T Akasu

Publications and source records attributed to T Akasu.

At least 127 records · Page 7Linked to original sources
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↗
PubMed1989

Electrophysiological properties of cultured dog myocytes obtained by endomyocardial biopsy.

Right ventricular cardiac tissue (10-20 mg wet weight) was obtained from anesthetized adult dogs by endomyocardial biopsy. The biopsy could be repeated in one dog every 2 weeks for up to 3 months. Fifty to 200 cardiomyocytes, dispersed with collagenase and trypsin, were collected by centrifugation of the cells with 50% polysucrose-sodium diatrizoate solution (Ficoll-Paque). Single cardiomyocytes were suspended in a minimum essential medium containing 20% fetal bovine serum and 8-bromoadenosine 3': 5'-cyclic monophosphate (0.1 mM) for up to 3 weeks. Approximately 70-80% of the cultured cardiomyocytes were rod shaped after 24 hours (10-20% after 7 days). Cytoplasmic organelles of the cultured cells, examined with a transmission electron microscope, were within the normal range of canine heart morphology in vivo. Resting membrane potential of the cells was about -80 mV when superfused with a Krebs' solution containing 4.7 mM potassium ions. The action potential lasted for 300 msec and had a peak amplitude of about 120 mV. Voltage-clamp experiments demonstrated the presence of an inward calcium current (congruent to 0.9 nA at +9 mV), which was facilitated by isoproterenol (0.1-1 microMs). The background potassium current showed typical inward rectification at potentials more negative than -80 mV. The results indicate that morphological, electrophysiological, and pharmacological properties of the cultured cardiomyocytes were intact. We propose that the culture techniques we have developed can be useful for repeated investigation on functional aspects of cardiac muscles in myocardial disease.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1989

Delayed rectifier potassium current in dissociated bullfrog primary afferent neurons.

Cultured bullfrog dorsal root ganglion cells were voltage-clamped in the whole-cell configuration. The classical delayed rectifier potassium current (IK) was separated from other ionic currents. Tetraethylammonium (1-50 mM) depressed the amplitude of IK in a concentration-dependent manner, a complete block occurring with 30 mM. With the concentration of potassium ions in the superfusate at 20 mM, the reversal potential of IK amounted to about -30mV. IK was activated between -30 and +70 mV. The half activation of IK occurred at +15 mV. The amplitude of IK was increased e-fold with 13.6 mV depolarization. The time constant of IK de-activation was shortened with membrane hyperpolarization (tau congruent to 4 ms at -100 mV). Finally, reciprocal time constant (tau -1) of the de-activating IK was increased e-fold with congruent to 13 mV hyperpolarization. It appears that the properties of IK in amphibian afferent neurons are comparable to those which have been observed with respect to the IK of the squid giant axons (Hodgkin and Huxley, 1952).

Action Potentials↗
PubMed1988

5-Hydroxytryptamine facilitates GABA-induced depolarization in bullfrog primary afferent neurons.

Intracellular and voltage-clamp recordings were made from sensory neurons in bullfrog dorsal root ganglia (DRG). Bath-application of 5-hydroxytryptamine (5-HT, 10 microM to 1 mM) reversibly increased the amplitude of depolarizing responses to gamma-aminobutyric acid (GABA) and muscimol. 5-HT also increased the amplitude of chloride current activated by GABA. An analysis with dose-response curves revealed that 5-HT potentiated the maximum GABA current (Vmax), while it produced no significant change in the apparent dissociation constant (Km). It is suggested that 5-HT increases the sensitivity of the GABAA receptor, acting on an allosteric site for the receptor-ionophore complex.

Animals↗
PubMed1988

Propranolol blocks recurrent synaptic activation in paravertebral sympathetic ganglia of bullfrogs.

Intracellular recordings were made from neurons in bullfrog sympathetic ganglia. Orthodromic, intracellular and antidromic stimulations evoked recurrent depolarizing responses accompanied by a spontaneous firing of the action potential in type 2 neurons. The depolarizing response elicited by intracellular and antidromic stimulations was selectively blocked by propranolol (1 microM), but not by yohimbine and phenoxybenzamine. Propranolol did not block the 'nicotinic' fast excitatory postsynaptic potential evoked by orthodromic stimulation. These results suggest that excitatory beta-adrenoceptors mediate the recurrent synaptic facilitation of nicotinic transmission in type 2 neurons of bullfrog sympathetic ganglia.

Action Potentials↗
PubMed1988

5-hydroxytryptamine inhibits cholinergic transmission through 5-HT1A receptor subtypes in rabbit vesical parasympathetic ganglia.

Intracellular recordings were made from parasympathetic neurons of the rabbit vesical pelvic ganglia (VPG) maintained in vitro. 5-Hydroxytryptamine (5-HT) inhibited cholinergic transmission in the VPG by reducing the fast excitatory postsynaptic potential (EPSP) evoked by stimulations of pelvic nerves. 8-Hydroxy-2-(di-n-propyl-amino) tetralin hydrochloride mimicked the inhibitory effect of 5-HT on the ganglionic transmission. 5-HT-induced inhibition of the fast EPSP was antagonized by spiperone. The results suggest that 5-HT1A receptor subtypes mediate the inhibition of cholinergic transmission in the rabbit VPG.

Animals↗
PubMed1988

Adrenaline depolarization in paravertebral sympathetic neurones of bullfrogs.

Responses to adrenaline (Ad) and their ionic mechanisms were analysed using intracellular recording and voltage-clamp methods in neurones of bullfrog sympathetic ganglia. Ad (5 microM-1 mM) applied directly to sympathetic neurones by pressure ejection through a micropipette produced three types of depolarizing responses (2-20 mV). Under voltage-clamp conditions, Ad (100 microM) produced fast, slow and mixed types of inward currents (AdIs) with amplitude of 2.9 +/- 1.3 nA. beta-Adrenoceptors may be responsible for the generation of these AdDs. The slow AdI which lasted for 1-5 min was associated with a decreased membrane conductance. The slow AdI decreased at hyperpolarized potential level and eventually nullified at -70 mV. No reversal of the slow AdI polarity was observed in the Ringer solution. Injection of Cs2+ into the ganglion cells produced a marked depression of the amplitude of the slow AdI. The slow AdI was blocked by bath-applied Ba2+ but not by TEA. Ad reduced the slow current relaxation, the M current, associated with voltage jumps in the membrane potential range -35 to -55 mV. The fast Ad response was associated with an increase in membrane conductance. When the membrane was depolarized, the fast AdI decreased and reversed its polarity at -36 +/- 8.3 mV. Removal of Cl ion from superfusing solution depressed the fast AdI, suggesting that activation of Cl- conductances may be involved in the generation of the fast AdI. The mixed type of Ad response exhibited characteristics of both the fast and slow Ad responses. The results suggest that Ad increases the excitability of neurones in bullfrog sympathetic ganglia.

Animals↗
PubMed1988

Presynaptic inhibition of cholinergic transmission by peptidergic neurons in bullfrog sympathetic ganglia.

Intracellular recordings were made from sympathetic B neurons to investigate an interaction between peptidergic and cholinergic responses in bullfrog sympathetic ganglia. Simultaneous stimulations of 3rd-5th and 8th spinal nerves evoked the fast excitatory postsynaptic potential (EPSP) superimposed with the late slow EPSP at the same sympathetic neuron. The amplitude of fast EPSPs was reduced during the course of the late slow EPSP in a majority of sympathetic neurons. A nicotinic depolarization produced by an ionophoretic application of ACh (ACh potential) was not significantly affected during the late slow EPSP. The quantal content of the fast EPSP calculated by the variance method was depressed during the late slow EPSP. Luteinizing hormone-releasing hormone (LH-RH), a putative transmitter for the late slow EPSP decreased the amplitude and the quantal content of the fast EPSP. [D-Phe2,6, Pro3]-LH-RH, and [D-pGlu1, D-Phe2, D-Trp3,6]-LH-RH, antagonists for LH-RH receptors prevented the inhibition of the fast EPSP induced by the late slow EPSP and LH-RH. These results suggest that cholinergic nicotinic transmission is inhibited during the late slow EPSP by a decreased ACh-release from nerve terminals in bullfrog sympathetic ganglia.

Acetylcholine↗
PubMed1988

Calcium-activated chloride conductance in parasympathetic neurons of the rabbit urinary bladder.

Intracellular recordings were made from vesical pelvic ganglion cells of the rabbit in a Krebs solution containing tetrodotoxin (1 microM). Experiments were carried out during complete suppression of the calcium-dependent potassium conductance by tetraethylammonium (greater than or equal to 20 mM) and/or intracellular injection of cesium ions. The action potential was followed by a depolarizing afterpotential which lasted for 0.3-10 s and had a peak amplitude of 5-20 mV at about -50 mV. The afterdepolarization (ADP) could not be observed when the preceding calcium-dependent action potential was blocked in a nominally calcium-free solution. Intracellular injection of ethyleneglycol-bis(beta-aminoethyl ether)N,N'-tetraacetic acid (EGTA) or total substitution of extracellular calcium ions with barium ions selectively blocked the ADP. The ADP, associated with an increased membrane conductance, reversed its polarity at -17 mV, when ganglion cells were impaled with microelectrodes filled with potassium chloride or cesium chloride. This reversal level was similar to that of the depolarization induced by gamma-aminobutyric acid. The reversal potential shifted to about -50 mV when acetate or sulphate were injected as counter anions. The peak amplitude and the total duration of the ADP was increased by substitution of external sodium chloride with sucrose or sodium isethionate. These results suggest that the ADP results from calcium entry during the spike and subsequent opening of chloride channels in parasympathetic neurons of the rabbit.

Action Potentials↗
PubMed1988

Calcium-dependent potassium conductance in neurons of rabbit vesical pelvic ganglia.

Intracellular recordings were made from neurons of vesical pelvic (parasympathetic) ganglia (VPG) isolated from the rabbit urinary bladder. Spontaneous hyperpolarizations (SH), occurring at intervals of 30 s to 5 min, could be recorded from 53% of VPG neurons in Krebs solution. The action potential was associated with inward sodium and calcium currents and was followed by fast and slow afterhyperpolarizations (AHPs). The action potential also evoked an additional hyperpolarization which was identical to the SH. The SH and the AHPs were associated with a decrease in the input resistance and reversed their polarity close to the potassium equilibrium potential. Intracellular cesium ions blocked the AHPs and the SH. Superfusing the preparation with a calcium-free solution produced a depolarization associated with an increased input resistance. The outward rectification activated at the resting membrane potential was depressed in the calcium-free solution. The removal of extracellular calcium ions also depressed both the SH and the spike AHPs. Bath-application of caffeine (1-3 mM) increased the frequency of the appearance of the SH. Injection of EGTA into VPG neurons caused a depolarization due to a blockade of the outward rectification. EGTA also depressed the slow AHP and the SH. These results suggest that the neuronal membrane of the rabbit VPG is endowed with a calcium-dependent potassium conductance (gKCa). Apamin (0.3-5 nM) and (+)-tubocurarine (30-300 microM) blocked the slow AHP and the SH without affecting the fast AHP and the resting membrane potential. Tetraethylammonium (TEA, 0.3-5 mM) suppressed the fast AHP and the SH without affecting the outward rectification. TEA augmented the slow AHP. Barium ions (0.1-1 mM) depressed the AHPs, the SH and the outward rectification. These pharmacological properties imply that at least 3 kinds of gKCa systems underlie the generation of the outward rectification, the spike AHPs and the SH.

Action Potentials↗
PubMed1988

Norepinephrine inhibits calcium action potential through alpha 2-adrenoceptors in rabbit vesical parasympathetic neurons.

Intracellular and voltage-clamp recordings were made from neurons in rabbit vesical parasympathetic ganglia (VPG) maintained in vitro. Norepinephrine (NE, 10 nM-10 microM) reduced the Ca2+ component of the action potential and the afterhyperpolarization. Clonidine and UK14304, the selective alpha 2-adrenoceptor agonists, mimicked the inhibitory effects of NE on the action potential. NE and UK14304 blocked the Ca2+ spike elicited in the presence of tetrodotoxin and tetraethylammonium. UK14304 suppressed the inward Ca2+ current induced by depolarizing step command under the voltage-clamp condition. These inhibitory actions were antagonized by yohimbine and idazoxan but not by prazosin and propranolol. It is suggested that alpha 2-adrenoceptors mediate the inhibition of voltage-dependent Ca2+ entry during the action potential.

Action Potentials↗
PubMed1988

Peptidergic inhibition of cholinergic transmission in bullfrog sympathetic ganglia.

Intracellular and voltage-clamp recordings were made from sympathetic B neurons to investigate an interaction between peptidergic and cholinergic responses in bullfrog sympathetic ganglia. Stimulations of both 3rd-5th (0.2 Hz) and 8th (30 Hz) spinal nerves evoked the fast excitatory postsynaptic potential (EPSP) superimposed with the late slow EPSP at the same sympathetic neuron. The amplitude of fast EPSPs was decreased during the course of the late slow EPSP in a majority of sympathetic neurons. The mean depression of the fast EPSP amplitude was 51 +/- 4% (n = 24). The quantal content of the fast EPSP was also depressed by 54 +/- 3% (n = 10) during the late slow EPSP. Acetylcholine-induced depolarization (ACh potential) and current (ACh current) produced by an ionophoretic application of ACh were not reduced during the late slow EPSP. Bath-application of LH-RH (40 nM-4 microM) depressed the fast EPSP in a concentration-dependent manner; at a concentration of 1 microM, it produced a 63 +/- 8% (n = 8) depression of the quantal content of the fast EPSP. LH-RH (1-4 microM) depressed the frequency of the miniature (M) EPSPs by 25 +/- 4% (n = 5) of control. Antagonists for luteinizing hormone-releasing hormone (LH-RH) receptor, [D-Phe2,6, Pro3]-LH-RH and [D-pGlu1, D-Phe2, D-Trp3,6]-LH-RH, prevented the presynaptic inhibition of the fast EPSP induced by LH-RH. These results suggest that the fast EPSP is depressed during the late slow EPSP by decreasing the evoked release of ACh from presynaptic nerve terminals in bullfrog sympathetic ganglia.

Acetylcholine↗
PubMed1988

Postsynaptic modulation of cholinergic transmission by endogenous substances.

1. Recent concept of postsynaptic modulation is reviewed on the basis of literature data and the results of our investigation using conventional intracellular and voltage-clamp recording methods, in vitro. 2. Experimental evidence provided that the sensitivity of nicotinic ACh receptors endowed on the postsynaptic membrane of the bullfrog sympathetic ganglia and of the frog skeletal muscle end-plate is either facilitated or inhibited by other neurotransmitters or neurohormones. 3. We propose that one neurotransmitter not only initiates its own postsynaptic potential but also regulates the efficacy of synaptic transmission mediated by a distinct neurotransmitter, as an endogenous "antagonist" or "sensitizer".

Animals↗