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R C Ma

Publications and source records attributed to R C Ma.

At least 19 recordsLinked to original sources
PubMed1991

Effect of nifedipine on neurons of guinea pig celiac ganglion.

The effect of nifedipine on electrophysiological membrane properties and nicotinic neurotransmission of guinea pig celiac ganglion neurons was studied using intracellular recordings in vitro. Nifedipine in concentrations of 0.1-10 microM did not affect membrane potential, membrane input resistance or the amplitude and duration of action potentials induced by intracellular current injection. Higher doses of nifedipine (0.1-1 mM) significantly reduced the amplitude and extended the duration of action potentials induced by intracellular current injection. Superfusion of the ganglia with nifedipine in concentrations of 0.1-10 microM significantly inhibited nicotinic fast excitatory postsynaptic potentials (f-EPSPs) and orthodromic action potentials evoked by nerve stimulation. This depressant effect of nifedipine on synaptic transmission was eliminated with high Ca2+ (12.5 mM). Nifedipine (10 microM) did not affect the postsynaptic effect of exogenous acetylcholine (ACh), but significantly reduced the quantal content but not the quantal size of evoked f-EPSPs in a low Ca2+ (0.5 mM), high Mg2+ (5.5 mM) Krebs solution. Nifedipine in concentration of 10 microM did not affect afterspike hyperpolarization (AH) and post-tetanic hyperpolarization (PTH), which have been recognized to be generated mainly by an increase of calcium-dependent potassium conductance. Higher doses of nifedipine (0.1-1 mM) significantly depressed AH and PTH. These experimental results suggest that nifedipine in concentrations of 0.1-10 microM exerts an inhibitory effect on nicotinic neurotransmission without affecting the membrane properties of the guinea pig celiac ganglion neurons. This inhibitory effect of nifedipine on synaptic transmission may result from blocking L-type calcium channels and reducing the quantal release of ACh from the presynaptic nerve terminals.

Animals↗
PubMed1991

[Serotonin mediated synaptic transmission of inferior mesenteric ganglion of the guinea pig].

By means of intracellular recording technique, it was observed that: (1) Application of serotonin (5-HT) caused in a portion of the neurons of the guinea pig inferior mesenteric ganglia (IMG) a slow depolarization similar to non-cholinergic late slow excitatory postsynaptic potential (ls-EPSP). (2) Prolonged superfusion of 5-HT markedly suppressed the ls-EPSP in 5-HT sensitive neurons. (3) The ls-EPSP elicited in 5-HT sensitive neurons as well as the 5-HT depolarization could be enhanced by fluoxetine 5-HT reuptake inhibitor; In contrast, the ls-EPSP of 5-HT insensitive neurons was not appreciably changed by this drug. (4) Pretreating the guinea pigs with para-chlorophenylalanine (PCPA), a 5-HT biosynthesis inhibitor, markedly reduced the occurrence rate and amplitude of ls-EPSP. These results indicate that ls-EPSP of the guinea pig IMG is possibly mediated by several transmitters including 5-HT.

Animals↗
PubMed1991

[Nifedipine inhibits calcium-dependent potentials in guinea pig sympathetic neurons].

Reversible effects of nifedipine, a calcium channel blocker, on 3 types of calcium-dependent potentials in the celiac ganglion cells of the guinea pigs in vitro were investigated by means of intracellular recordings. Nifedipine (0.1-1 mmol/L) inhibited the spike afterhyperpolarization, the post-tetanic membrane potential in dose-dependent manner. Nifedipine (0.1 mumol/L) also depressed the Ca2+ spike potential in a Na(+)-free/high Ca2+ solution plus TEA. Thus the results indicate that nifedipine in clinical therapeutic dosage may directly reduce Ca2+ conductance and then in higher concentration may also depress secondarily Ca(2+)-dependent potassium conductance. These actions of nifedipine may underlie the mechanism of blockade of quantal release of ACh from presynaptic membrane as well as the modulation of excitability of sympathetic postganglionic neuron.

Animals↗
PubMed1990

The role of serotonin in non-cholinergic excitatory transmission in the guinea pig inferior mesenteric ganglion.

The non-cholinergic late slow excitatory postsynaptic potential (ls-EPSP) of the guinea pig inferior mesenteric ganglion (IMG) was previously believed to be mediated by substance P (SP) or several other neuropeptides. Yet, the pharmacological evidence presented here indicates that serotonin (5-HT) may be another transmitter for the ls-EPSP in the guinea pig IMG. Repetitive stimulation of the presynaptic nerves elicited ls-EPSP in about half of the IMG neurons. Application of 5-HT or SP caused, in a portion of the IMG neurons, a slow depolarization similar to ls-EPSP. Fifty-six out of 88 (63.6%) neurons with ls-EPSP and 13 out of 35 (37.1%) neurons with ls-EPSP were sensitive to 5-HT and SP, respectively. Superfusion of the ganglia with 5-HT markedly suppressed the ls-EPSP evoked in 5-HT sensitive neurons. Similarly, exogenously applied SP attenuated the ls-EPSP of SP-sensitive neurons. However, prolonged superfusion of 5-HT or SP had no effect on the ls-EPSP elicited in 5-HT or SP-insensitive neurons, respectively. Furthermore, the ls-EPSPs elicited in 5-HT-sensitive neurons as well as the 5-HT-induced depolarization were reversibly suppressed by cyproheptadine, a 5-HT antagonist, and enhanced by fluoxetine, a 5-HT reuptake inhibitor. In contrast, the ls-EPSP of 5-HT insensitive neurons and SP-induced depolarization were not appreciably changed by those two drugs. Pretreatment with p-chlorophenylalanine, a 5-HT biosynthesis inhibitor, did not change the general electrophysiological characteristics of the neurons and did not suppress nicotinic neurotransmission, but markedly reduced the occurrence rate of ls-EPSP from 53.8% to 15.1% (P less than 0.005). Collectively, our results indicate that, besides SP, 5-HT may be involved in mediating the ls-EPSP in a subpopulation of neurons in the guinea pig IMG. The type of transmitter mediating ls-EPSP is apparently not limited to 5-HT and SP, as about 30% of the neurons with ls-EPSP were found to be insensitive to both 5-HT and SP and prolonged superfusion with both did not affect appreciably the ls-EPSP elicited in these neurons.

Animals↗
PubMed1990

[Depressant effect of nifedipine on synaptic transmission in celiac ganglion].

The effect of nifedipine, a calcium channel blocker, on nicotinic transmission, was studied in the isolated celiac ganglia of the guinea pig by means of intracellular recordings. Nifedipine in concentration of 0.1-10 mumol/L did not affect resting membrane potential, input membrane resistance and action potential induced by intracellular stimulation in all cells tested, but obviously inhibited nicotinic transmission. The depressant effect of nifedipine on synaptic transmission could be limited by low Ca2+ and antagonized by high Ca2+. Nifedipine did not affect acetylcholine (ACh) sensitivity of postsynaptic membrane, but decreased frequency of miniature excitatory postsynaptic potentials (mEPSPs) in high K+ Kreb's solution and reduced quantal content without effect on quantal size of evoked EPSPs in low Ca2+ /high Mg2+ kreb's solution. The results indicate that nifedipine in therapeutic dose exerts depressant effect on synaptic transmission through blocking Ca2+ entry into presynaptic membrane and reducing quantal release of ACh from presynaptic nerve terminals.

Acetylcholine↗
PubMed1989

[Electrophysiological properties of the cells in intermediolateral nucleus of neonatal rat spinal cord slices in vitro].

Intracellular recordings were made from the cells in the interm ediolateral nucleus (IML) of neonatal rat spinal cord slices in vitro. Both resting and active electrophysiological properties of the cellular membrane were investigated. Resting membrane potential ranged from -46 to -70 mV. The means of input resistance, time constant and membrane capacitance were 108.3 +/- 67.9 M omega (mean +/- SD), 9.9 +/- 5.6 ms and 138.6 +/- 124.2 pF, respectively. Repetitive firing at high frequency (up to 150 Hz) could be produced in thirty five cells (85.4%) in response to intracellular injection of depolarizing current, while single spike firing produced in the remaining cells (15.6%). The amplitude and duration of action potentials evoked by intracellular stimulation were 63.4 +/- 9.0 mV and 2.4 +/- 0.6 ms, respectively. The threshold at the level of 18.7 +/- 6.2 mV was more depolarized than the resting potential. In most of cells, spikes induced by intracellular stimulation were followed by afterhyperpolarization, whose peak amplitude and duration were 5.1 +/- 2.7 mV and 90 +/- 31.8 ms, respectively. EPSP, orthodromic action potentials and, rarely, IPSP could be evoked by dorsal root stimulation, and antidromic action potentials were obtained by ventral root stimulation. Identification of sympathetic preganglionic neuron and functional significance of electrophysiological properties were discussed.

Animals↗
PubMed1987

Neurokinin A in capsaicin-sensitive neurons of the guinea-pig inferior mesenteric ganglia: an additional putative mediator for the non-cholinergic excitatory postsynaptic potential.

The presence of neurokinin-A-like immunoreactivity in guinea-pig inferior mesenteric ganglia was detected by radioimmunoassay procedures. Pretreating the animals with capsaicin 7 days prior to experimentations reduced the mean content of neurokinin-A-like immunoreactivity by 85% from its control value of 150 +/- 31.3 fmol per ganglion. High-performance liquid chromatography revealed that neurokinin-A-like immunoreactivity was heterogenous as in addition to neurokinin A, peaks corresponding to the amphibian tachykinin eledoisin and to neuropeptide K were detected, and they too were depleted by capsaicin. Electrophysiological studies showed that neurokinin A applied either by superfusion or by pressure ejection evoked a slow depolarization in the majority of inferior mesenteric ganglia neurons in vitro. Neurokinin-A-evoked depolarizations in the majority of cells tested were associated with a small increase in membrane input resistance. However, the responses were increased by membrane hyperpolarization: the extrapolated mean equilibrium potential of neurokinin-A-induced depolarization was -36 mV. Removal of extracellular sodium but not chloride ions suppressed the neurokinin-A-induced depolarization. The slow depolarization elicited either by exogenously applied substance P or by repetitive stimulation of hypogastric nerves was reversibly eliminated in the presence of neurokinin A. Collectively, our studies suggest that neurokinin-A-like immunoreactivity may coexist with substance-P-like immunoreactivity in capsaicin-sensitive fibers in the guinea-pig prevertebral ganglia and that the similarity of the actions of neurokinin A on the one hand and substance P on the other raises the possibility that non-cholinergic excitatory potentials elicited in the inferior mesenteric ganglia may be generated by not one but a number of closely related tachykinins.

Animals↗
PubMed1986

Excitation of lateral horn neurons of the neonatal rat spinal cord by 5-hydroxytryptamine.

The effects of 5-hydroxytryptamine (5-HT) on lateral horn cells contained in thin in vitro slices of neonatal rat spinal cord were investigated by means of intracellular recording techniques. Superfusion of 5-HT (1-100 microM) to lateral horn cells caused a concentration-dependent membrane depolarization leading to, in some instances, repetitive cell discharges. A number of lateral horn cells could be activated antidromically by stimulating the ventral rootlets. The conduction velocity of the antidromic spikes was estimated to be 0.3-2 m/s which corresponds to that of the axons of rat sympathetic preganglionic neurons reported by others. The 5-HT depolarization evoked in neurons that could be activated antidromically was similar to that elicited from unidentified lateral horn cells. The depolarization induced by 5-HT could be partially eliminated by low Ca/high Mg solution or tetrodotoxin in a portion of lateral horn cells and was accompanied by an increase in membrane resistance. The response was nullified near the membrane potential at which the spike after hyperpolarization was abolished; a clear reversal of polarity was not observed at a more negative potential level. The 5-HT depolarization was reversibly blocked by methysergide and cyproheptadine and enhanced by fluoxetine, a 5-HT-uptake inhibitor. The results indicate that the indoleamine primarily exerted an excitatory action on lateral horn cells, including those tentatively identified as sympathetic preganglionic neurons, by a direct depolarization which appears to be mediated by decrease of a voltage-sensitive K conductance and partly by an indirect effect via the release of an excitatory substance(s).

Animals↗
PubMed1985

Vasopressin depolarizes lateral horn cells of the neonatal rat spinal cord in vitro.

The effects of vasopressin (VP) on lateral horn cells including a number of sympathetic preganglionic neurons contained in thin in vitro slices of neonatal rat spinal cord were investigated by means of intracellular recording techniques. Superfusion of (Arg8)-vasopressin (AVP, 0.01-1 microM) caused a depolarization leading, in the majority of lateral horn cells, to repetitive discharges. The AVP depolarization which could be partially reduced by low Ca/high Mg solution or tetrodotoxin, was accompanied by an increase in membrane resistance and the response was nullified near the membrane potential at which the spike afterhyperpolarization was abolished. A clear reversal of the response was not observed upon further hyperpolarization. The AVP response was blocked by the VP1 antagonist, D-(CH2)5 Tyr (Me)-AVP, whereas, deamino (D-Arg8-vasopressin), a VP2 agonist, at high concentrations (greater than or equal to 50 microM) was either ineffective or produced a small depolarization. The results indicate that AVP, acting mainly on VP1 receptors, excited lateral horn cells by a direct depolarization and an indirect effect via the release of an excitatory transmitter(s). A reduction of a voltage-dependent K conductance may underlie the depolarizing effect of AVP.

Animals↗
PubMed1985

Neurokinin A depolarizes neurons of the guinea pig inferior mesenteric ganglia.

Neurokinin A (NKA) applied either by superfusion (0.1-10 microM) or by pressure ejection evoked a slow membrane depolarization in neurons of the inferior mesenteric ganglia in vitro. The NKA-induced depolarization which was not significantly affected by reducing the Ca concentration or by tetrodotoxin was associated in most cases by a small-to-moderate increase in membrane resistance; however, conditioning hyperpolarization increased rather than decreased the response. The depolarization elicited by NKA was eliminated in the presence of substance P (SP) and the depolarization by SP in the presence of NKA. The results suggest that the actions of NKA on prevertebral neurons are similar to that of SP and that these two peptides may act on the same receptors or share similar ionic channels.

Animals↗
PubMed1985

Norepinephrine depolarizes lateral horn cells of neonatal rat spinal cord in vitro.

Superfusion of norepinephrine (NE) (1-50 microM) onto lateral horn cells, including antidromically identified sympathetic preganglionic neurons (SPNs), situated in thin transverse neonatal rat thoracolumbar spinal cord slices caused a membrane depolarization and repetitive cell discharges. The NE depolarization was associated with an increase in membrane resistance, and the response became smaller upon conditioning hyperpolarization; a clear reversal of polarity, however, was not observed. Pretreating the slices with phentolamine and prazosin but not yohimbine or propranolol prevented the depolarizing effect of NE. This finding, in conjunction with the evidence of the presence of noradrenergic fibers in the spinal cord, suggests that NE may serve as an excitatory neurotransmitter to neurons of the lateral horn.

Animals↗