The GABAergic Innervation of Paravertebral Sympathetic Ganglia

1992 ◽  
pp. 45-63 ◽  
Author(s):  
J. R. Wolff ◽  
P. Kása ◽  
E. Dobó ◽  
Á. Párducz ◽  
F. Joó
Keyword(s):  
Sympathetic Ganglia ◽  
Gabaergic Innervation ◽  
Paravertebral Sympathetic Ganglia

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.

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.

Inhibitory effects of catecholamines in the paravertebral sympathetic ganglia of the anesthetized dog

1990 ◽  
Vol 185 (1) ◽  
pp. 61-68 ◽  
Author(s):  
Guiseppe Mercuro ◽  
Patrick T. Horn ◽  
Erik R. Orelind ◽  
Jai D. Kohli
Keyword(s):  
Sympathetic Ganglia ◽  
Inhibitory Effects ◽  
Paravertebral Sympathetic Ganglia

scholarly journals Multiple effects of artemin on sympathetic neurone generation, survival and growth

Development ◽  
2001 ◽  
Vol 128 (19) ◽  
pp. 3685-3695
Author(s):  
Rosa Andres ◽  
Alison Forgie ◽  
Sean Wyatt ◽  
Qi Chen ◽  
Frederic J. de Sauvage ◽  
...  
Keyword(s):  
Sympathetic Ganglia ◽  
Stages Of Development ◽  
Physiological Relevance ◽  
Mitogenic Action ◽  
Sympathetic Neurones ◽  
Survival And Growth ◽  
Paravertebral Sympathetic Ganglia ◽  
Neuroblast Proliferation ◽  
Cultured Neurones

To define the role of artemin in sympathetic neurone development, we have studied the effect of artemin on the generation, survival and growth of sympathetic neurones in low-density dissociated cultures of mouse cervical and thoracic paravertebral sympathetic ganglia at stages throughout embryonic and postnatal development. Artemin promoted the proliferation of sympathetic neuroblasts and increased the generation of new neurones in cultures established from E12 to E14 ganglia. Artemin also exerted a transient survival-promoting action on newly generated neurones during these early stages of development. Between E16 and P8, artemin exerted no effect on survival, but by P12, as sympathetic neurones begin to acquire neurotrophic factor independent survival, artemin once again enhanced survival, and by P20 it promoted survival as effectively as nerve growth factor (NGF). During this late period of development, artemin also enhanced the growth of neurites from cultured neurones more effectively than NGF. Confirming the physiological relevance of the mitogenic action of artemin on cultured neuroblasts, there was a marked reduction in the rate of neuroblast proliferation in the sympathetic ganglia of mice lacking the GFRα3 subunit of the artemin receptor. These results indicate that artemin exerts several distinct effects on the generation, survival and growth of sympathetic neurones at different stages of development.

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.

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