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.

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.

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 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.

The significance of adrenaline-induced potentiation of electrogenic sodium pumping in bullfrog sympathetic ganglia

1985 ◽  
Vol 63 (9) ◽  
pp. 1182-1189 ◽  
Author(s):  
Peter A. Smith ◽  
Kochu-Rani Dombro
Keyword(s):  
Sympathetic Ganglia ◽  
Short Term ◽  
Experimental Conditions ◽  
Membrane Hyperpolarization ◽  
Gap Technique ◽  
Electrophysiological Responses ◽  
Sucrose Gap ◽  
Electrophysiological Effects ◽  
Lines Of Evidence ◽  
Stimulation Of

Two different electrophysiological responses in amphibian sympathetic ganglia were studied by means of the sucrose gap technique; (i) the potassium-activated hyperpolarization (KH) which serves as an index of electrogenic Na+ pumping, and (ii) the hyperpolarization induced by adrenaline (AdH). Under appropriate experimental conditions, 0.1 μM adrenaline potentiated the KH to 121.5 ± 7.5% of control (n = 7). This potentiation was blocked by both yohimbine (50 nM) and prazosin (1 μM) but not by propranolol (1 μM). Clonidine (10 nM) potentiated the KH to 113.5 ± 3.4% of control (n = 5), whereas methoxamine (0.1 μM) was ineffective. Several lines of evidence argued against the hypothesis that the AdH may be generated, in whole or in part, by stimulation of the Na+ pump. For example, (i) the AdH was sometimes completely unaffected when the KH was blocked by ouabain, and (ii) the AdH was eliminated by 2 nM Ba2+ even though this cation enhanced membrane hyperpolarization accompanying electrogenic Na+ pumping. These results imply that the electrogenic Na+ pump is not involved in the short-term electrophysiological effects of catecholamines. Despite this, it is possible that the homeostasis of Na+ and K+ in nerve may be regulated by α-adrenergic mechanisms.

Nerve Growth Factor Regulates Sodium But Not Potassium Channel Currents in Sympathetic B Neurons of Adult Bullfrogs

2001 ◽  
Vol 86 (2) ◽  
pp. 641-650 ◽  
Author(s):  
Saobo Lei ◽  
William F. Dryden ◽  
Peter A. Smith
Keyword(s):  
Nerve Growth Factor ◽  
B Cells ◽  
Growth Factor ◽  
Sympathetic Neurons ◽  
Defined Medium ◽  
Sympathetic Ganglia ◽  
Delayed Rectifier ◽  
Inactivation Kinetics ◽  
Nerve Growth ◽  
Paravertebral Sympathetic Ganglia

The TTX-sensitive and -resistant components of the voltage-gated Na+ current (TTX-s I Na and TTX-r I Na) are increased within 2 wk of cutting the axons of B-cells in bullfrog paravertebral sympathetic ganglia (BFSG). Axotomy also increases the noninactivating, voltage-activated K+ current (M current I M), whereas delayed rectifier K+ current ( I K) is reduced. We found that similar effects were produced when BFSG B cells were dissociated from adult bullfrogs and maintained in a defined-medium, neuron-enriched, low-density, serum-free culture. Thus the density of TTX-s I Na, TTX-r I Na, and I M were transiently increased, whereas I K density was decreased. Reduction in voltage-sensitive, Ca2+-dependent K+ current ( I C) was attributed to previously documented decreases in Ca2+ channel current ( I Ca). To test whether axotomy- or culture-induced changes in ion channel function reflect loss of retrograde influence of nerve growth factor (NGF), we examined the effect of murine β-NGF on TTX-s I Na, TTX-r I Na, I K, and I M. Culture of neurons for 15 days in the presence of NGF (200 ng/ml), more than doubled total I Na density but did not enhance neurite outgrowth. The TTX-r I Nadensity was increased about threefold and the TTX-s I Na density increased 2.4-fold. NGF did not affect the activation or inactivation kinetics of the total Na+ conductance. Effects of NGF were blocked by the transcription inhibitors, cordycepin (20 μM) and actinomycin D (0.01 μg/ml). I K and I M were unaffected by NGF, and although I C was enhanced, this likely reflected the known effect of NGF on I Ca in BFSG neurons. Na+ channel synthesis and/or expression in adult sympathetic neurons is therefore subject to selective regulation by NGF. Despite this, the increase in I Na and I M as well as the decrease in I K seen in BFSG neurons in culture or after axotomy cannot readily be explained in terms of alterations in the availability of target-derived NGF.

Effect of sympathectomy on spinal blood flow autoregulation and posttraumatic ischemia

1982 ◽  
Vol 56 (5) ◽  
pp. 706-710 ◽  
Author(s):  
Wise Young ◽  
Vincent DeCrescito ◽  
John J. Tomasula
Keyword(s):  
Blood Flow ◽  
Spinal Injury ◽  
Sympathetic Ganglia ◽  
Control Group ◽  
Content Type ◽  
Systemic Pressure ◽  
Sympathetic Regulation ◽  
Mean Systemic Pressure ◽  
Paravertebral Sympathetic Ganglia ◽  
Fine Print

✓ The hypothesis that the paravertebral sympathetic ganglia play a role in spinal blood flow regulation was tested in cats. Five cats were subjected to paravertebral sympathectomy, two to combined sympathectomy-adrenalectomy, three to adrenalectomy alone, and five controls received no treatment. Laminectomy was carried out to expose the T4–10 cord, and autoregulation was tested by measuring blood flow from the lateral columns with the hydrogen clearance technique during manipulation of systemic pressure with intravenous saline infusion and nitroprusside administration. The cord was then contused at T-7 with a 400 gm-cm impact injury. Posttraumatic blood flow was recorded, and neurophysiological function was assessed with somatosensory evoked potential (SEP) monitoring. Before injury, blood flow in the untreated (control) group had no consistent relationship with mean systemic pressure over the range 80 to 160 mm Hg. In contrast, in all cats with paravertebral sympathectomy, whether accompanied by adrenalectomy or not, blood flows increased with systemic pressure (correlation coefficient 0.86, p < 0.01). After injury, the control and adrenalectomized cats showed blood flow decreases of > 60% to 4 to 6 ml/100 gm/min (p < 0.01) by 2 to 3 hours. However, cats with paravertebral sympathectomy maintained blood flow above 9 ml/100 gm/min for up to 3 hours after injury. All the sympathectomized cats recovered their SEP by the 3rd hour after injury, compared with none of the controls. Thus, in the absence of the paravertebral sympathetic ganglia, spinal blood flow autoregulation was impaired and the typical posttraumatic loss in blood flow did not occur. The sympathectomy also protected the spinal cords from the neurophysiological loss usually seen in 400 gm-cm injury. The data suggest the need for caution in using acetylcholine blocking agents to paralyze animals in experimental spinal injury, since these agents alter sympathetic activity and may influence the injury process. The spinal cord is an excellent model in which to investigate sympathetic regulation of central nervous system blood flow.

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