Late Slow Excitatory Postsynaptic Potential Research Articles

Serotonin receptor subtypes that depolarize guinea pig inferior mesenteric ganglion neurons

Our previous studies indicated that serotonin (5-HT) depolarized a majority of guinea pig inferior mesenteric ganglion (IMG) neurons and may be another transmitter for the noncholinergic late slow excitatory postsynaptic potential (ls-EPSP) in the IMG. However, the subtypes of 5-HT receptor mediating these responses have not yet been identified. Using intracellular recording, we examined the effect of 5-HT receptor antagonists with specificity to various 5-HT receptor subtypes on the 5-HT-mediated depolarization and ls-EPSP in IMG neurons in vitro. Cyproheptadine, a 5-HT 1/2 receptor antagonist, reversibly inhibited the slow, but not the fast, depolarization and ls-EPSP in the 5-HT-sensitive neurons. Both mianserin and spiperone, 5-HT 2 and 5-HT 1A receptor antagonists, did not significantly alter either the fast or slow depolarizing responses or the ls-EPSP. The 5-HT 3 receptor antagonist MDL 72222 (Bemesetron) completely inhibited the fast depolarization with little diminution of the slow depolarization and ls-EPSP. Superfusion of putative 5-HT 1P receptor antagonist, BRL 24924 (Renzapride), reversibly attenuated both the depolarization and ls-EPSP. However, 5-HT-insensitive neurons with ls-EPSP were found to be insensitive to both cyproheptadine and BRL 24924. In most 5-HT-sensitive neurons, the 5-HT 3 receptor agonist, 2-methyl-5-HT, and the selective 5-HT 1P agonist, MCPP or 5-OHIP, evoked a fast and a slow depolarization in 55.6 and 71.4% of the neurons, respectively, without a significant effect on the membrane potential in 85.7 and 100% of the 5-HT-insensitive neurons. In 5-HT-sensitive neurons, MDL 72222 reversibly abolished the fast depolarization induced by 2-methyl-5-HT; BRL 24924 significantly inhibited the slow depolarization induced by MCPP or 5-OHIP, but not by SP. Prolonged superfusion of 5-HT-sensitive neurons with MCPP abolished the evoked ls-EPSP without inhibition of action potential. These results suggest that the fast and slow depolarizations in these neurons are mediated by 5-HT 3 and 5-HT 1P receptor subtypes, respectively. The latter may also mediate the ls-EPSP in 5-HT-sensitive neurons.

Caffeine and carbonyl cyanide m-chlorophenylhydrazone increased evoked and spontaneous release of luteinizing hormone-releasing hormone from intact presynaptic terminals

In bullfrog sympathetic ganglia, the ryanodine-sensitive Ca 2+ store and mitochondria modulate [Ca 2+] within nerve terminals. We used caffeine (10 mM) and carbonyl cyanide m-chlorophenylhydrazone (10 μM) to assess how these Ca 2+ stores affect release of a neuropeptide, luteinizing hormone-releasing hormone, from these nerve terminals. Release of luteinizing hormone-releasing hormone was evoked by electrical stimulation to presynaptic nerves and was monitored as a late slow excitatory postsynaptic potential in ganglionic neurons. Caffeine increased release of luteinizing hormone-releasing hormone similarly whether the release was evoked by 4 or 20 Hz stimulations (by 2.7±1.1- and 3.2±0.9-fold, mean±S.E.M., n=27, respectively). Carbonyl cyanide m-chlorophenylhydrazone augmented release of luteinizing hormone-releasing hormone evoked by 4 Hz stimulation much more strongly (by 11.8±1.8-fold) than it increased the release evoked by 20 Hz stimulation (by 3.6±1.3-fold, n=25). We detected spontaneous release of luteinizing hormone-releasing hormone as a slow hyperpolarization in response to a brief application of an antagonist to the receptors for luteinizing hormone-releasing hormone in 65% (34 of 52) and 39% (11 of 28) of the ganglionic B and C neurons, respectively. Caffeine increased spontaneous release of luteinizing hormone-releasing hormone by 2.3±0.7-fold ( n=6) whereas carbonyl cyanide m-chlorophenylhydrazone increased this release by 4.27- and 1.76-fold ( n=2). Facilitation of Ca 2+ release from the intracellular store by caffeine and inhibition of mitochondrial Ca 2+ removal by carbonyl cyanide m-chlorophenylhydrazone increased spontaneous as well as evoked release of luteinizing hormone-releasing hormone. Moreover, caffeine increments of evoked release did not depend on the firing frequency of the nerve whereas carbonyl cyanide m-chlorophenylhydrazone augmentations of evoked release strongly depended on the firing frequency.

Electrophysiological effects of nitric oxide in mouse superior mesenteric ganglion

Effects of nitric oxide (NO) generated from sodium nitroprusside (SNP) on neurons of mouse superior mesenteric ganglion (SMG) were studied in vitro using intracellular recording techniques. SNP solutions caused a membrane hyperpolarization in the majority (64%) of the neurons tested or a hyperpolarization followed by a depolarization in 8% of the neurons tested. The SNP-induced hyperpolarization persisted in a low-Ca2+ high-Mg2+ solution, indicating a direct effect of NO on the postsynaptic membrane. The hyperpolarizing effect of SNP was reduced or abolished by oxyhemoglobin. Electrical stimulation of the colonic nerves evoked a late slow excitatory postsynaptic potential (late sEPSP) in a population of neurons in normal Krebs solution. The amplitude of the late sEPSP was significantly enhanced in the presence of NG-nitroL-arginine, a NO synthase inhibitor. The results, particularly those observed with the NO synthase inhibitor, suggest that endogenous NO was released in the mouse SMG by repetitive nerve stimulation and that it modulated slow synaptic transmission, presumably by a direct action on ganglionic neurons.

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 < 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.

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.

Pharmacological studies in frog sympathetic ganglion: support for the cholinergic monosynaptic hypothesis for slow IPSP mediation

The slow inhibitory postsynaptic potential (slow IPSP), the slow excitatory postsynaptic potential (slow EPSP), the late slow excitatory postsynaptic potential (late slow EPSP), and the fast excitatory postsynaptic potential/compound action potential (fast EPSP) were recorded from the 9th or 10th paravertebral sympathetic ganglia of bullfrogs (and some Rana pipiens frogs) by the sucrose-gap technique. The adrenergic antagonists phentolamine, dihydroergotamine and propranolol did not show any antagonistic effect on the slow IPSP when used at concentrations of up to 10, 100 and 10 μM, respectively. U-0521 (3′,4′-dihydroxy-2-methylpropriophenone, 50 μg/ml), a specific inhibitor of catechol- OM-methyltransferase, did not show any potentiating effect on the slow IPSP. The cholinesterase inhibitor neostigmine (0.5–1 μM) induced a large increase in the duration and amplitude of slow IPSP. When phentolamine and propranolol at concentrations greater than 10 μM were used the slow IPSP (and all other synaptic potentials) were non-specifically reduced in amplitude by these drugs. The results reported in this paper do not lend any support to the hypothesis that the slow IPSP in frog sympathetic ganglia is mediated by an adrenergic interneuron. The results are consistent with the proposal that the slow IPSP in this ganglion is mediated by a direct action of acetylcholine released from cholinergic preganglionic fibers.

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.

The facilitation of nicotinic receptor sensitivity during the late slow excitatory postsynaptic potential

The facilitation of nicotinic receptor sensitivity during the late slow excitatory postsynaptic potential

Synaptic transmission in the rabbit inferior mesenteric ganglion

Electrical properties, cholinergic neurotransmission and non-cholinergic neurotransmission in the rabbit inferior mesenteric ganglion (IMG) in vitro were examined with intracellular recording techniques. A single ganglionic neuron received an average of 42 nicotinic cholinergic synaptic inputs. An atropine-sensitive slow excitatory postsynaptic potential not followed by a non-cholinergic late slow excitatory postsynaptic potential (LS-EPSP) was observed in 7% of the cells. In 63% of the cells a LS-EPSP insensitive to antagonism of nicotinic and muscarinic receptors was observed following repetitive nerve stimulation. The involvement of substance P (SP) in the genesis of the LS-EPSP was tested by applications of SP, applications of SP antagonists and applications of capsaicin. Neither SP, SP antagonists nor capsaicin affected the LS-EPSP. These findings distinguish the LS-EPSP in the rabbit IMG from its counterpart in the guinea pig IMG where SP has been proposed as the mediator of the LS-EPSP. A late slow inhibitory postsynaptic potential was observed in 13% of the cells. This hyperpolarization followed repetitive nerve stimulation and was insensitive to blockade of cholinergic receptors. There is a marked convergence of subthreshold fast excitatory postsynaptic potentials (F-EPSPs) of both central and peripheral origin onto these cells. The LS-EPSP could provide a mechanism for increasing the likelihood of temporal and/or spatial summation of these fast synaptic inputs, thereby increasing the probability of action potential generation in the ganglion cells.

Modulation of action potential during the late slow excitatory postsynaptic potential in bullfrog sympathetic ganglia

The spike peak and after-hyperpolarization of the action potential of bullfrog sympathetic ganglion cells were depressed during the late slow excitatory postsynaptic potential (EPSP). These changes in the action potential were mimicked by luteinizing hormone-releasing hormone (LH-RH), a neurotransmitter candidate for the late show EPSP. LH-RH (5 μM) suppressed the voltage-dependent K + currents, both the delayed rectifier K + current (I K1) and the M current (I K2). It is suggested that the depression of the after-hyperpolarization of the action potential during the late slow EPSP may be due to suppression of I K1 and I K2.

Voltage-clamp analysis of peptidergic slow depolarizations in bullfrog sympathetic ganglion cells.

1. The membrane currents during the late slow excitatory post-synaptic potential (late slow e.p.s.c.s) and luteinizing hormone-releasing hormone (LHRH)-induced depolarization of nicotinized and atropinized bullfrog lumbar sympathetic ganglion cells were studied with voltage-clamp methods. 2. Two types of late slow e.p.s.c. were observed. The Type I response was associated with a decreased conductance and was depressed by membrane hyperpolarization. The Type II response was accompanied by an increased conductance and was augmented by membrane hyperpolarization. 3. LHRH also induced two types of responses. The nature of the LHRH-induced current and the late slow e.p.s.c. in each neurone was similar, if not identical. 4. The Type I response appeared to be produced primarily by a suppression of the M current (Brown & Adams, 1980) and partially by a depression of the resting K+ conductance. The Type II response is probably due to an increased conductance to Na+ or Na+ and some other cations.

Peptidergic transmitters in synaptic boutons of sympathetic ganglia

In sympathetic ganglia of the bullfrog, a slow synaptic potential lasting for minutes--the late slow excitatory postsynaptic potential (e.p.s.p.)--was discovered. This slow response, unlike other previously known synaptic potentials in the autonomic nervous system, is not mediated by acetylcholine or monoamines. Similar non-cholinergic, non-adrenergic slow synaptic potentials have since been found in several other vertebrate autonomic ganglia. We found that the late slow e.p.s.p. is probably mediated by a peptide that is identical to, or closely resembles, mammalian luteinizing hormone releasing hormone (LHRH), because (1) when applied directly to sympathetic neurones, LHRH and its agonists elicit a slow depolarization, associated with similar changes in membrane conductance and excitability as those occurring during the late slow e.p.s.p. Furthermore, both peptide-induced and nerve-evoked responses are blocked by antagonists of LHRH; and (2) radioimmunoassays indicate that a chain of sympathetic ganglia contains 100-800 pg of a LHRH-like peptide. Its distribution among spinal nerves, the great reduction of this substance following denervation, and its release from ganglia following isotonic KCl treatment or nerve stimulation suggest that the LHRH-like material is contained in preganglionic nerve fibres. Here we report that immunohistochemical staining of sympathetic ganglia shows that LHRH-like immunoreactivity is indeed present in synaptic boutons. We also show that the two types of ganglion cells (B cells and C cells) receive strikingly different patterns of peptidergic innervation.

Further evidence for peptidergic transmission in sympathetic ganglia.

We previously proposed that, in sympathetic ganglia of the bullfrog, a peptide which resembles luteinizing hormone-releasing factor (LH-RF, luliberin) functions as the transmitter for the late slow excitatory postsynaptic potential (epsp), a signal that may last 5-10 min. To test this hypothesis further, we have compared the physiological andpharmacological effects of LH-RF with those of the natural transmitter and have found a close parallel. (i) LH-RF, when ejected with a brief pulse of pressure through a micropipette near a ganglion cell, produces a depolarizing response lasting for minutes. (ii) The LH-RF-induced response is associated with changes in input resistance similar to thoe during a late slow epsp. (iii) The amplitudes of the LH-RF-induced response and the late slow epsp vary in parallel as the membrane potential is shifted over a wide range. (iv) Both responses increase the excitability of ganglion cells. (v) The two responses interact with the cholinergic epsps in a parallel manner: they cause diminution of the slow epsp but not of the fast epsp. (vi) Both responses are blocked by an analog of LH-RF that antagonizes the effects of LH-RF in the rat.

Effects of physostigmine on the afterdischarge and slow postsynaptic potentials of bullfrog sympathetic ganglia.

1. The effects of anticholinesterases (anti-ChEs) (physostigmine, prostigmine and TEPP) on the afterdischarges and the extracellular and intracellular slow potentials of bullfrog sympathetic ganglia were studied.2. The anti-ChEs augmented the early afterdischarge, the late negative potential and the slow excitatory postsynaptic potential. This indicated that the nature of the early afterdischarge was cholinergic (muscarinic) and that the late negative potential or the slow excitatory postsynaptic potential generated the early afterdischarge.3. Since the anti-ChEs increased the positive potential, the depression of the early afterdischarge observed in the presence of an antiChE was explained to be caused by the increased inhibitory effect of the enhanced positive potential.4. Prostigmine and tetraethyl pyrophosphate did not show any appreciable effects on the late afterdischarge, the late late negative potential nor the late slow excitatory postsynaptic potential. This indicated that the nature of the late afterdischarge was non-cholinergic and that the late late negative potential or the late slow excitatory postsynaptic potential generated the late afterdischarge.5. Physostigmine reversibly depressed the late afterdischarge, the late late negative potential and the late slow excitatory postsynaptic potential. The depressant action of physostigmine was not due to its anti-ChE action.

Early and late after discharges of amphibian sympathetic ganglion cells.

Early and late after discharges of amphibian sympathetic ganglion cells.S Nishi, and K KoketsuS Nishi, and K KoketsuPublished Online:01 Jan 1968https://doi.org/10.1152/jn.1968.31.1.109MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByExcitatory Muscarinic Modulation Strengthens Virtual Nicotinic Synapses on Sympathetic Neurons and Thereby Enhances Synaptic GainPaul H. M. Kullmann, and John P. Horn1 December 2006 | Journal of Neurophysiology, Vol. 96, No. 6Voltage- and Activity-Dependent Chloride Conductance Controls the Resting Status of the Intact Rat Sympathetic NeuronOscar Sacchi, Maria Lisa Rossi, Rita Canella, and Riccardo Fesce1 August 2003 | Journal of Neurophysiology, Vol. 90, No. 2A Model for Pleiotropic Muscarinic Potentiation of Fast Synaptic TransmissionHermann Schobesberger, Diek W. 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Horn1 April 2000 | Journal of Neurophysiology, Vol. 83, No. 4Amphibian sympathetic ganglia: An owner's and operator's manualProgress in Neurobiology, Vol. 43, No. 4-5Vasoactive intestinal peptide and secretin produce long-term increases in tyrosine hydroxylase activity in the rat superior cervical ganglionBrain Research, Vol. 607, No. 1-2Acetylcholine-activated ionic currents in isolated paratracheal ganglion cells of the ratBrain Research, Vol. 558, No. 1Thyrotropin-releasing hormone given intrathecally to the rat increases arterial pressure and heart rate.Circulation Research, Vol. 65, No. 4Neurotoxicological effects of trimethyltin on the stellate ganglionNeurotoxicology and Teratology, Vol. 11, No. 5Enhancement of peptidergic synaptic transmission by catecholamines in the bullfrog sympathetic ganglionJournal of the Autonomic Nervous System, Vol. 23, No. 2Regulation of two ion channels by a common muscarinic receptor-transduction system in a vertebrate neuronNeuroscience Letters, Vol. 81, No. 1-2Cholinergic excitatory synaptic potentials of neurones in mammalian lumbar paravertebral gangliaJournal of the Autonomic Nervous System, Vol. 18, No. 3Slow postsynaptic potentials in neurones of submucous plexus of guinea-pig caecum and their mimicry by noradrenaline and various peptidesNeuroscience, Vol. 16, No. 4Significance of slow synaptic potentials for transmission of excitation in guinea-pig myenteric plexusNeuroscience, Vol. 14, No. 2Biochemical consequences of synaptic stimulation:Trends in Neurosciences, Vol. 8Muscarinic agonists depress calcium-dependent gK in bullfrog sympathetic neuronsJournal of the Autonomic Nervous System, Vol. 10, No. 2A late slow depolarization unmasked in the presence of tetraethylammonium in neonatal rat sympathetic neurons in vitroBrain Research, Vol. 293, No. 2Modulation of action potential during the late slow excitatory postsynaptic potential in bullfrog sympathetic gangliaBrain Research, Vol. 280, No. 2Luteinizing hormone-releasing hormone modulates nicotinic ACh-receptor sensitivity in amphibian cholinergic transmissionBrain Research, Vol. 279, No. 1-2Physiology of sexual behaviorUrology, Vol. 22, No. 5Substance P inhibits the action potentials in bullfrog sympathetic ganglion cellsNeuroscience Letters, Vol. 41, No. 1-2A LHRH-like peptidergic neurotransmitter capable of ‘action at a distance’ in autonomic gangliaTrends in Neurosciences, Vol. 6Distribution of (3H) QNB binding in dog gastric smooth muscle pre- and post vagotomyLife Sciences, Vol. 31, No. 8Modulation of slow postsynaptic potentials by dopamine, in rabbit sympathetic ganglionBrain Research, Vol. 217, No. 1Does γ-aminobutyric acid in blood control transmitter release in bullfrog sympathetic ganglia?Brain Research, Vol. 195, No. 1Characterization of LRF-like immunoreactivity in the frog sympathetic ganglia: Non-identity with LRF decapeptideNeuropeptides, Vol. 1, No. 1Effects of erabutoxins on the cholinergic receptors of bullfrog sympathetic ganglion cellsBrain Research, Vol. 191, No. 1Effects of nicotine and hexamethonium on discharges in the stellate ganglionEuropean Journal of Pharmacology, Vol. 54, No. 3Actions of substance P on sympathetic neuronsNeuropharmacology, Vol. 18, No. 2Slowly-developing depolarization of neurones in the guinea-pig inferior mesenteric ganglion following repetitive stimulation of the preganglionic nervesBrain Research, Vol. 140, No. 2Synaptic events in sympathetic gangliaProgress in Neurobiology, Vol. 11, No. 2Post-tetanic spontaneous spike activity in rat sympathetic neurons exposed to low potassium ion concentrationBrain Research, Vol. 123, No. 2Actions of ketamine on synaptic transmission in frog sympathetic gangliaNeuropharmacology, Vol. 15, No. 2Unusual cholinergic response of bullfrog sympathetic ganglion cellsEuropean Journal of Pharmacology, Vol. 31, No. 2Is inactivation of potassium conductance involved in slow postsynaptic excitation of sympathetic ganglion cells? Effects of nicotineLife Sciences, Vol. 14, No. 10Non-nicotinic transmission during ganglionic block with chlorisondamine and nicotineEuropean Journal of Pharmacology, Vol. 24, No. 1Acetylcholine and slow synaptic inhibition in frog sympathetic ganglion cellsBrain Research, Vol. 55, No. 1The effect of adrenaline on sympathetic ganglion cells of bullfrogsLife Sciences, Vol. 11, No. 24A functional connection between postganglionic neurons in a bullfrog sympathetic ganglionLife Sciences, Vol. 11, No. 17Unusual nature of ganglionic slow EPSP studied by a voltage-clamp methodLife Sciences, Vol. 8, No. 1Acetylcholine-potential of sympathetic ganglion cell membraneLife Sciences, Vol. 7, No. 13 More from this issue > Volume 31Issue 1January 1968Pages 109-21 https://doi.org/10.1152/jn.1968.31.1.109PubMed4295893History Published online 1 January 1968 Published in print 1 January 1968 Metrics