scholarly journals Slow synaptic transmission in frog sympathetic ganglia

1986 ◽  
Vol 124 (1) ◽  
pp. 259-285
Author(s):  
P. R. Adams ◽  
S. W. Jones ◽  
P. Pennefather ◽  
D. A. Brown ◽  
C. Koch ◽  
...  
Keyword(s):  
B Cells ◽  
Synaptic Transmission ◽  
Selective Reduction ◽  
Sympathetic Ganglia ◽  
Repetitive Firing ◽  
C Cells ◽  
Calcium Dependent ◽  
Potassium Conductances ◽  
Voltage Dependent ◽  
Slow Potassium

Bullfrog ganglia contain two classes of neurone, B and C cells, which receive different inputs and exhibit different slow synaptic potentials. B cells, to which most effort has been directed, possess slow and late slow EPSPs. The sEPSP reflects a muscarinic action of acetylcholine released from boutons on B cells, whereas the late sEPSP is caused by a peptide (similar to teleost LHRH) released from boutons on C cells. During either sEPSP there is a selective reduction in two slow potassium conductances, designated ‘M’ and ‘AHP’. The M conductance is voltage dependent and the AHP conductance is calcium dependent. Normally they act synergistically to prevent repetitive firing of action potentials during maintained stimuli. Computer stimulation of the interactions of these conductances with the other five voltage-dependent conductances present in the membrane allows a complete reconstruction of the effects of slow synaptic transmission on electrical behaviour.

scholarly journals Action Potentials in Rhodnius Oocytes: Repolarization is Sensitive to Potassium Channel Blockers

1986 ◽  
Vol 126 (1) ◽  
pp. 119-132
Author(s):  
M. J. O'DONNELL
Keyword(s):  
Potassium Channel ◽  
Action Potentials ◽  
Potassium Conductance ◽  
Channel Blockers ◽  
Calcium Dependent ◽  
Outward Rectification ◽  
Current Voltage ◽  
Potassium Channel Blockers ◽  
Potassium Conductances ◽  
Voltage Dependent

Depolarization of Rhodnius oocytes evokes action potentials (APs) whose rising phase is calcium-dependent. The ionic basis for the repolarizing (i.e. falling) phase of the AP was examined. Addition of potassium channel blockers (tetraethylammonium, tetrabutylammonium, 4-aminopyridine, atropine) to the bathing saline increased the duration and overshoot of APs. Intracellular injection of tetraethyl ammonium had similar effects. These results suggest that a voltage-dependent potassium conductance normally contributes to repolarization. Repolarization does not require a chloride influx, because substitution of impermeant anions for chloride did not increase AP duration. AP duration and overshoot actually decreased progressively when chloride levels were reduced. Current/voltage curves show inward and outward rectification, properties often associated with potassium conductances. Outward rectification was largely blocked by external tetraethylammonium. Possible functions of the rectifying properties of the oocyte membrane are discussed.

On the role of muscarinic and peptidergic receptors in ganglionic transmission in bullfrogs in vivo

1997 ◽  
Vol 272 (5) ◽  
pp. R1501-R1514 ◽  
Author(s):  
A. Y. Ivanoff ◽  
P. A. Smith
Keyword(s):  
B Cells ◽  
Sympathetic Ganglia ◽  
Synaptic Activity ◽  
C Cells ◽  
Postsynaptic Potentials ◽  
C Fibers ◽  
C Fiber ◽  
Paravertebral Sympathetic Ganglia ◽  
Ganglionic Transmission

Synaptic activity of individual B and C cells in the paravertebral sympathetic ganglia of urethan-anesthetized bullfrogs was monitored with intracellular electrodes. Postganglionic activity from the B and C fiber populations was monitored with suction electrodes. Intravenous infusion of muscarine (0.1 ml of 8 microM) excited individual B cells and increased the amplitude and rate of spontaneous, postganglionic B fiber population discharges. Muscarine also increased the number of action potentials (APs) within each burst of synaptic activity in individual C cells. Because atropine (0.1 ml of 0.1 microM) had little or no effect on postganglionic population B or C fiber activity, the muscarinic slow inhibitory postsynaptic potentials and slow excitatory postsynaptic potentials (EPSPs) are unlikely to be involved in the transmission, modulation, or integration of postganglionic outflow in vivo. Atropine did, however, decrease the number of APs per burst in individual C cells, an effect that could be explained if excitatory presynaptic muscarinic receptors exist on C fiber terminals. Stimulation of preganglionic C fibers at "physiological" frequencies evoked a lasting afterdischarge in postganglionic B fibers that was blocked by a combination of atropine and [D-pyro-Glu1,D-Phe2,D-Trp3,6]-luteinizing hormone-releasing hormone (LHRH). Release of LHRH from C fiber terminals and activation of the peptidergic, late-slow EPSP mechanism in B cells may therefore play a role in ganglionic transmission in vivo.

scholarly journals The Effects of Spike Frequency Adaptation and Negative Feedback on the Synchronization of Neural Oscillators

2001 ◽  
Vol 13 (6) ◽  
pp. 1285-1310 ◽  
Author(s):  
Bard Ermentrout ◽  
Matthew Pascal ◽  
Boris Gutkin
Keyword(s):  
Cortical Neurons ◽  
Potassium Current ◽  
Spike Frequency ◽  
Repetitive Firing ◽  
Spike Frequency Adaptation ◽  
Calcium Dependent ◽  
M Current ◽  
Frequency Adaptation ◽  
Voltage Dependent ◽  
Standard Models

There are several different biophysical mechanisms for spike frequency adaptation observed in recordings from cortical neurons. The two most commonly used in modeling studies are a calcium-dependent potassium current Iahp and a slow voltage-dependent potassium current, Im. We show that both of these have strong effects on the synchronization properties of excitatorily coupled neurons. Furthermore, we show that the reasons for these effects are different. We show through an analysis of some standard models, that the M-current adaptation alters the mechanism for repetitive firing, while the after hyperpolarization adaptation works via shunting the incoming synapses. This latter mechanism applies with a network that has recurrent inhibition. The shunting behavior is captured in a simple two-variable reduced model that arises near certain types of bifurcations. A one-dimensional map is derived from the simplified model.

The pathway for the slow inhibitory postsynaptic potential in bullfrog sympathetic ganglia

1986 ◽  
Vol 56 (3) ◽  
pp. 823-834 ◽  
Author(s):  
P. A. Smith ◽  
F. F. Weight
Keyword(s):  
B Cells ◽  
Ringer Solution ◽  
Sympathetic Ganglia ◽  
Sympathetic Chain ◽  
C Cells ◽  
Inhibitory Postsynaptic Potential ◽  
Postsynaptic Potential ◽  
Sucrose Gap ◽  
Paravertebral Sympathetic Ganglia ◽  
Stimulation Of

Intracellular and sucrose gap recording techniques were used to examine synaptically evoked potentials and the response of neurons in bullfrog paravertebral sympathetic ganglia to muscarinic agonists. These neurons were defined as either B or C cells on the basis of the conduction velocity of antidromically evoked action potentials. Following stimulation of preganglionic C-fibers in the rostral portion of the VIIIth spinal nerve, a fast nicotinic excitatory postsynaptic potential (EPSP) and a slow atropine-sensitive inhibitory postsynaptic potential (IPSP) could be recorded intracellularly in C cells of the IXth and Xth paravertebral ganglia treated with 70 microM d-tubocurarine chloride (dTC). Under these conditions, local iontophoretic application of acetylcholine (ACh) could produce a slow hyperpolarization of C cell membrane potential. ACh hyperpolarizations or slow IPSPs were not detected in ganglionic B cells. Stimulation of the preganglionic B-fibers in the sympathetic chain produced a fast nicotinic EPSP and a slow muscarinic EPSP in ganglionic B cells. A small population of C cells also received cholinergic B-fiber innervation from the sympathetic chain and exhibited a slow IPSP upon tetanic stimulation of this pathway. When curarized ganglia were examined by means of sucrose gap recording, superfusion of the muscarinic agonist, methacholine (MCh), produced an initial hyperpolarization (MChH) followed by a depolarization (MChD). Both responses were blocked by atropine and therefore presumably reflect the activation of muscarinic receptors involved in the generation of the slow IPSP and the slow EPSP, respectively. Although synaptic transmission was blocked by Ringer solution containing 4 mM Co2+, neither this solution nor 10 microM tetrodotoxin reduced the amplitude of the MChH. The MChH was slightly reduced by Ringer solution containing 0.1 mM Ca2+, however, the response could be restored by the addition of 6 mM Mg2+. These results indicate that the MChH in curarized bullfrog sympathetic ganglia results from a direct muscarinic action on ganglionic cells. This suggests that the slow IPSP is mediated by ACh released from cholinergic preganglionic fibers that make synaptic contact with ganglionic C cells.

Development of Potassium Conductances in Perinatal Rat Phrenic Motoneurons

2000 ◽  
Vol 83 (6) ◽  
pp. 3497-3508 ◽  
Author(s):  
Miguel Martin-Caraballo ◽  
John J. Greer
Keyword(s):  
Action Potential ◽  
Potassium Currents ◽  
Perinatal Period ◽  
Repetitive Firing ◽  
Respiratory Drive ◽  
Calcium Dependent ◽  
Phrenic Motoneurons ◽  
Potential Shape ◽  
Potassium Conductances ◽  
Firing Properties

Prior to the inception of inspiratory synaptic drive transmission from medullary respiratory centers, rat phrenic motoneurons (PMNs) have action potential and repetitive firing characteristics typical of immature embryonic motoneurons. During the period spanning from when respiratory bulbospinal and segmental afferent synaptic connections are formed at embryonic day 17 ( E17) through to birth (gestational period is ∼21 days), a pronounced transformation of PMN electrophysiological properties occurs. In this study, we test the hypothesis that the elaboration of action potential afterpotentials and the resulting changes in repetitive firing properties are due in large part to developmental changes in PMN potassium conductances. Ionic conductances were measured via whole cell patch recordings using a cervical slice-phrenic nerve preparation isolated from perinatal rats. Voltage- and current-clamp recordings revealed that PMNs expressed outward rectifier ( I KV) and A-type potassium currents that regulated PMN action potential and repetitive firing properties throughout the perinatal period. There was an age-dependent leftward shift in the activation voltage and a decrease in the time-to-peak of I KV during the period from E16 through to birth. The most dramatic change during the perinatal period was the increase in calcium-activated potassium currents after the inception of inspiratory drive transmission at E17. Block of the maxi-type calcium-dependent potassium conductance caused a significant increase in action potential duration and a suppression of the fast afterhyperpolarizing potential. Block of the small conductance calcium-dependent potassium channels resulted in a marked suppression of the medium afterhyperpolarizing potential and an increase in the repetitive firing frequency. In conclusion, the increase in calcium-mediated potassium conductances are in large part responsible for the marked transformation in action potential shape and firing properties of PMNs from the time between the inception of fetal respiratory drive transmission and birth.

Presynaptic inhibition of calcium-dependent and -independent release elicited with ionomycin, gadolinium, and alpha-latrotoxin in the hippocampus

1996 ◽  
Vol 75 (5) ◽  
pp. 2017-2028 ◽  
Author(s):  
M. Capogna ◽  
B. H. Gahwiler ◽  
S. M. Thompson
Keyword(s):  
Synaptic Transmission ◽  
Presynaptic Inhibition ◽  
Receptor Agonist ◽  
Gabab Receptor ◽  
Gaba Release ◽  
Presynaptic Receptors ◽  
Gamma Aminobutyric Acid ◽  
Calcium Dependent ◽  
Opioid Receptor Agonist ◽  
Voltage Dependent

1. Presynaptic inhibition of synaptic transmission in the hippocampus was investigated by comparing the effects of several agonists on miniature excitatory and inhibitory postsynaptic currents (mEPSCs and mIPSCs). 2. The Ca2+ ionophore ionomycin increased the frequency of mEPSCs and mIPSCs but did not affect their amplitude. Ionomycin-induced release required extracellular Ca2+ and was prevented by pretreatment with botulinum neurotoxin serotype F, like evoked synaptic transmission. Unlike evoked transmission, however, this increase did not involve activation of voltage-dependent Ca2+ channels because it was insensitive to Cd2+. 3. Both the lanthanide gadolinium and alpha-latrotoxin produced increases in the frequency of mEPSCs and mIPSCs, but their actions were independent of extracellular Ca2+. 4. Adenosine, the gamma-aminobutyric acid-B (GABAB) receptor agonist baclofen, and a mu-opioid receptor agonist strongly reduced the frequency of synaptic currents triggered by all three secretagogues. 5. We conclude that activation of these presynaptic receptors can reduce high frequencies of vesicular glutamate and GABA release by directly impairing transmitter exocytosis. Presynaptic inhibition of gadolinium- and alpha-latrotoxin-induced release indicates that this impairment occurs without changes in intraterminal Ca2+ homeostasis and when vesicle fusion is rendered Ca2+ independent, respectively. 6. The inhibition of ionomycin-induced release provides additional evidence for a direct, neurotransmitter receptor-mediated modulation of the proteins underlying vesicular docking or fusion as an important component of presynaptic inhibition of evoked synaptic transmission.

scholarly journals Role of Apamin-Sensitive KCa Channels for Reticulospinal Synaptic Transmission to Motoneuron and for the Afterhyperpolarization

2002 ◽  
Vol 88 (1) ◽  
pp. 289-299 ◽  
Author(s):  
Lorenzo Cangiano ◽  
Peter Wallén ◽  
Sten Grillner
Keyword(s):  
Synaptic Transmission ◽  
Nmda Receptors ◽  
Time Course ◽  
Frequency Regulation ◽  
Similar Time ◽  
Calcium Dependent ◽  
Before And After ◽  
Voltage Dependent ◽  
Intracellular Ca

Single motoneurons and pairs of a presynaptic reticulospinal axon and a postsynaptic motoneuron were recorded in the isolated lamprey spinal cord, to investigate the role of calcium-dependent K+ channels (KCa) during the afterhyperpolarization following the action potential (AHP), and glutamatergic synaptic transmission on the dendritic level. The AHP consists of a fast phase due to transient K+ channels (fAHP) and a slower phase lasting 100–200 ms (sAHP), being the main determinant of spike frequency regulation. We now present evidence that the sAHP has two components. The larger part, around 80%, is abolished by superfusion of Cd2+ (blocker of voltage-dependent Ca2+ channels), by intracellular injection of 1,2-bis-( 2-aminophenoxy)-ethane- N,N,N′,N′-tetraacetic acid (BAPTA; fast Ca2+ chelator), and by apamin (selective toxin for KCa channels of the SK subtype). While 80% of the sAHP is thus due to KCa channels, the remaining 20% is not mediated by Ca2+, either entering through voltage-dependent Ca2+ channels or released from intracellular Ca2+ stores. This Ca2+-independent sAHP component has a similar time course as the KCa portion and is not due to a Cl− conductance. It may be caused by Na+-activated K+ channels. Glutamatergic excitatory postsynaptic potentials (EPSPs) evoked by single reticulospinal axons give rise to a local Ca2+ increase in the postsynaptic dendrite, mediated in part by N-methyl-d-aspartate (NMDA) receptors. The Ca2+ levels remain elevated for several hundred milliseconds and could be expected to activate KCa channels. If so, this activation should cause a local conductance increase in the dendrite that would shunt EPSPs following the first EPSP in a spike train. We have tested this in reticulospinal/motoneuronal pairs, by stimulating the presynaptic axon with spike trains at different frequencies. We compared the first EPSP and the following EPSPs in the control and after blockade with apamin. No difference was observed in EPSP amplitude or shape before and after apamin, either in normal Ringer or in Mg2+-free Ringer removing the voltage-dependent block of NMDA receptors. In conclusion, the local Ca2+ entry during reticulospinal EPSPs does not cause an activation of KCa channels sufficient to affect the efficacy of synaptic transmission. Thus the integration of synaptic signals at the dendritic level in motoneurons appears simpler than would otherwise have been the case.

Phase Space Analysis of Neuronal Excitability

1998 ◽  
Author(s):  
Christof Koch
Keyword(s):  
Neuronal Excitability ◽  
Dynamical Behavior ◽  
Ionic Currents ◽  
Basins Of Attraction ◽  
Mathematical Framework ◽  
Calcium Dependent ◽  
Potassium Conductances ◽  
Slow Potassium ◽  
Quantitative Changes ◽  
The Individual

The previous chapter provided a detailed description of the currents underlying the generation and propagation of action potentials in the squid giant axon. The Hodgkin-Huxley (1952d) model captures these events in terms of the dynamical behavior of four variables: the membrane potential and three state variables determining the state of the fast sodium and the delayed potassium conductances. This quantitative, conductance-based formalism reproduces the physiological data remarkably well and has been extremely fertile in terms of providing a mathematical framework for modeling neuronal excitability throughout the animal kingdom (for the current state of the art, see McKenna, Davis, and Zornetzer, 1992; Bower and Beeman, 1998; Koch and Segev, 1998). Collectively, these models express the complex dynamical behaviors observed experimentally, including pulse generation and threshold behavior, adaptation, bursting, bistability, plateau potentials, hysteresis, and many more. However, these models are difficult to construct and require detailed knowledge of the kinetics of the individual ionic currents. The large number of associated activation and inactivation functions and other parameters usually obscures the contributions of particular features (e.g., the activation range of the sodium activation particle) toward the observed dynamic phenomena. Even after many years of experience in recording from neurons or modeling them, it is a dicey business predicting the effect that varying one parameter, say, the amplitude of the calcium-dependent slow potassium current (Chap. 9), has on the overall behavior of the model. This precludes the development of insight and intuition, since the numerical complexity of these models prevents one from understanding which important features in the model are responsible for a particular phenomenon and which are irrelevant. Qualitative models of neuronal excitability, capturing some of the topological aspects of neuronal dynamics but at a much reduced complexity, can be very helpful in this regard, since they highlight the crucial features responsible for a particular behavior. By topological aspects we mean those properties that remain unchanged in spite of quantitative changes in the underlying system. These typically include the existence of stable solutions and their basins of attraction, limit cycles, bistability, and the existence of strange attractors.

The α1- and α2-adrenoceptor and muscarinic responses of normal and axotomized bullfrog sympathetic ganglia

1990 ◽  
Vol 68 (9) ◽  
pp. 1189-1193 ◽  
Author(s):  
P. A. Smith ◽  
T. Gordon ◽  
M. P. Kehoe ◽  
K. C. Marshall
Keyword(s):  
B Cells ◽  
Sympathetic Ganglia ◽  
C Cells ◽  
Muscarinic Agonists ◽  
Biphasic Response ◽  
Selective Agonist ◽  
Gap Technique ◽  
Adrenoceptor Agonists ◽  
Sucrose Gap ◽  
Paravertebral Sympathetic Ganglia

When neurones in bullfrog paravertebral sympathetic ganglia are studied by means of the sucrose-gap technique, muscarinic agonists produce a biphasic response (an initial hyperpolarization of ganglionic C cells followed by a depolarization of ganglionic B cells). Activation of ganglionic α2-adrenoceptors promotes hyperpolarization. The present experiments with selective α1- and α2-adrenoceptor agonists and antagonists provided evidence for the existence of hitherto undescribed α1-adrenoceptors, which are responsible for the production of depolarizing responses in these ganglia. Fifteen to twenty-five days after cutting postganglionic axons (axotomy), there was a nonselective depression of both α1- and α2-adrenoceptor mechanisms but little change in muscarinic responses. These results argue against the hypothesis that C cells assume all the properties of B cells after axotomy. Since the α-selective agonist phenylephrine failed to depolarize axotomized ganglia, it is unlikely that an α1-adrenoceptor mechanism is prominent in axotomized neurones as it is in some immature adrenergic neurones. The data are consistent with the idea that axotomy selectively affects the properties of certain types of cation channels and raise questions as to the mechanisms involved in regulating the expression and maintenance of specific neurotransmitter responses on ganglionic neurones.Key words: axotomy, α-adrenoceptor mechanisms, muscarinic receptors, sympathetic ganglion, frog.

Reciprocal inhibition of voltage-gated potassium currents (IK(V)) by activation of cannabinoid CB1and dopamine D1receptors in ON bipolar cells of goldfish retina

2005 ◽  
Vol 22 (1) ◽  
pp. 55-63 ◽  
Author(s):  
SHIH-FANG FAN ◽  
STEPHEN YAZULLA
Keyword(s):  
G Protein ◽  
Receptor Agonist ◽  
Lucifer Yellow ◽  
Reciprocal Inhibition ◽  
Receptor Activation ◽  
Light Signal ◽  
Bipolar Cells ◽  
Protein G ◽  
Calcium Dependent ◽  
Voltage Dependent

Cannabinoid CB1receptor (viaGs) and dopamine D2receptor (viaGi/o) antagonistically modulate goldfish cone membrane currents. As ON bipolar cells have CB1and D1receptors, but not D2receptors, we focused on whether CB1receptor agonist and dopamine interact to modulate voltage-dependent outward membrane K+currentsIK(V)of the ON mixed rod/cone (Mb) bipolar cells. Whole-cell currents were recorded from Mb bipolar cells in goldfish retinal slices. Mb bipolar cells were identified by intracellular filling with Lucifer yellow. The bath solution was calcium-free and contained 1 mM cobalt to block indirect calcium-dependent effects. Dopamine (10 μM) consistently increasedIK(V)by a factor of 1.57 ± 0.12 (S.E.M.,n= 15). A CB receptor agonist, WIN 55212-2 (0.25–1 μM), had no effect, but 4 μM WIN 55212-2 suppressedIK(V)by 60%. IfIK(V)was first increased by 10 μM dopamine, application of WIN 55212-2 (0.25–1 μM) reversibly blocked the effect of dopamine even though these concentrations of WIN 55212-2 had no effect of their own. If WIN 55212-2 was applied first and dopamine (10 μM) was added to the WIN-containing solution, 0.1 μM WIN 55212-2 blocked the effect of dopamine. All effects of WIN 55212-2 were blocked by coapplication of SR 141716A (CB1antagonist) and pretreatment with pertussis toxin (blocker of Gi/o) indicating actionviaCB1receptor activation of G protein Gi/o. Coactivation of CB1and D1receptors on Mb bipolar cells produces reciprocal effects onIK(V). The CB1-evoked suppression ofIK(V)is mediated by G protein Gi/o, whereas the D1-evoked enhancement is mediated by G protein Gs. As dopamine is a retinal “light” signal, these data support our notion that endocannabinoids function as a “dark” signal, interacting with dopamine to set retinal sensitivity.

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