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At least 523 records · Page 29Linked to original sources
PubMed1968

Activity of aortic chemoreceptors during electrical stimulation of the stellate ganglion in the cat.

1. In anaesthetized cats, action potentials from aortic chemoreceptors were recorded during electrical stimulation of preganglionic sympathetic fibres to the decentralized right stellate ganglion. The rate of discharge in afferents in the ipsilateral but not in the contralateral aortic nerve increased when stimulus frequency was 4/sec or higher.2. The post-ganglionic fibres in the stimulated pathway originate in the right stellate ganglion. They leave the ganglion in the caudal limb of the ansa subclavia, and the results suggest that the ipsilateral aortic nerve and its branches distribute sympathetic fibres as well as afferents to aortic bodies.3. In contrast, the rate of discharge of chemoreceptor fibres in the contralateral aortic nerve fell as blood pressure increased during sympathetic stimulation. Sympathetic pathways to the aortic bodies can maintain or increase chemoreceptor discharge during hypertension elicited by sympathetic activation.

Journal Article↗
PubMed1993

Vasoactive intestinal peptide and secretin produce long-term increases in tyrosine hydroxylase activity in the rat superior cervical ganglion.

Electrical stimulation of the preganglionic fibers innervating the rat superior cervical ganglion (SCG) produces both short-term and long-term increases in tyrosine hydroxylase (TH) activity that are not completely blocked by nicotinic antagonists. Vasoactive intestinal peptide (VIP) and secretin, two neuropeptides known to produce short-term increases in TH activity, were examined for their ability to produce long-term increases in this enzyme activity. Culturing the SCG in the presence of either peptide produced a 30-50% increase in TH activity measured 2 days later. The results raise the possibility that one of these peptides or a related molecule participates in the transsynaptic induction of ganglionic TH.

Animals↗
PubMed1987

Chronic stimulation of the Gasserian ganglion for treatment of atypical facial neuralgia.

After a trial of percutaneous stimulation of the Gasserian ganglion in 21 patients with atypical facial pain, five patients were selected for chronic implantation. After a follow-up of two years (18 to 32 months), there is stable and excellent analgesia in three patients. There are various complications and problems associated with the method of implantation, either percutaneous or open. The best indication for this procedure is the presence of trigeminal pain and some sensory loss in the painful area. This new application of neurostimulation for pain was described by Myerson in 1980, and this therapy should be considered for any patient who has atypical facial pain that has been resistant to other forms of treatment.

Electric Stimulation Therapy↗
PubMed2001

Effects of electrical stimulation of the Gasserian ganglion on regional cerebral blood flow after induced subarachnoid hemorrhage in pigs evaluated by 99mTc-HMPAO-SPECT.

It could be demonstrated that cervical spinal cord stimulation increases cerebral blood flow. The effects of electrical stimulation of the trigeminal ganglion in the acute phase of SAH in pigs were investigated. The experiments were carried out on 11 domestic pigs divided in two groups (group I: SAH [n = 5]; group II: SAH and trigeminal stimulation [n = 6]). In all animals a native SPECT was performed. The Gasserian ganglion was exposed for inserting the stimulation electrode. SAH was induced by injecting 10 ml autologous blood through a catheter placed in the suprasellar cistern. 30 minutes after SAH-induction electrical stimulation was started for two hours in group II (2.8-4.5 V, 50 Hz, 300 microseconds). 99mTc-HMPAO (400-540 MBq) was injected intravenously 110 minutes later. In group I 99mTc-HMPAO was applied after the same time interval. 80 minutes later SPECT was performed. Data were processed to calculate the uptake of radioactivity (%/kg tissue weight). The mean values were calculated for the different groups: native animal examination (%/kg tissue weight): 0.6343; group I: 0.468; group II: 0.6533. Comparing the mean values a highly significant difference between group I and group II (p < 0.01) and between native examination and group I (p < 0.01) could be found. No statistical significance could be detected on comparing the left/right-ratio in any ROI. The electrical stimulation of the Gasserian ganglion leads to a significantly increased uptake of 99mTc-HMPAO after induced SAH. Maybe the stimulation of the Gasserian ganglion constitutes a new therapeutic modality treating disturbed rCBF after SAH.

Animals↗
PubMed1995

Increased acetylcholine content induced by antidromic stimulation of a sympathetic ganglion: a possible retrograde action of adenosine.

Prolonged high-frequency orthodromic stimulation of superior cervical ganglia is known to result in increased acetylcholine (ACh) synthesis and ACh content after the period of stimulation. In a previous study, we provided evidence to suggest that adenosine acts as an extracellular signal to activate this increased ACh synthesis and we proposed that the source of that adenosine might be postsynaptic. Thus, the purpose of the present study was to test whether direct stimulation of the post-ganglionic nerves could affect ganglionic ACh content. Antidromic conditioning of ganglia (15 Hz, 45 min) did not affect significantly their ACh content. However, if ganglia were allowed a 15-min rest period after this antidromic conditioning, their ACh stores were increased by 20%; a similar increase was induced by 4-Hz stimulation before the rest period. During the 15-Hz antidromic stimulation, ACh release was not clearly increased above the basal level, suggesting that preganglionic nerve endings were not stimulated to an extent that could explain the increased ACh content. Orthodromic stimulation (5 Hz) of ganglia 15 min after they had been subjected to antidromic conditioning (15 Hz, 45 min) showed increased ACh release in comparison with that from control unconditioned ganglia. Moreover, the extra ACh released by the conditioned ganglia was quantitatively similar to the increase in the ACh stores, as if most, or all, of the additional ACh was released by preganglionic stimulation. If the antidromic conditioning and the rest period were done during perfusion with Ca(2+)-free medium, the ganglia did not accumulate extra ACh.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1999

The continuing search for outer hair cell afferents in the guinea pig spiral ganglion.

Antidromic stimulation of the stump of the VIIIth nerve was combined with microelectrode recording in the spiral ganglion of the guinea pig cochlea in an attempt to identify a sub-population of neurons with long-latency antidromic action potentials that might correspond to the thin unmyelinated afferent neurons emanating from the outer hair cells. The techniques used were similar but not identical to those employed in an earlier study by Brown (1994). By far the largest population of cells contacted had short antidromic latencies (0.58+/-0.12 ms, 76 units) and also responded to acoustic stimulation. These were assumed to be type I afferents emanating from inner hair cells. Eight cells had antidromic latencies larger than 1 ms, all but one of which had a zero spontaneous rate. All eight of these longer-latency cells were unresponsive to acoustic stimulation despite the fact that short-latency neurons in the same cochleas showed robust responses to sound before and after they were contacted. Four of these longer-latency cells had their antidromic thresholds accurately measured and two had significantly higher thresholds to electrical stimulation (0.1 ms duration) than type I cells in the same animal while two had similar electrical thresholds. Attempts to trace the eight long-latency neurons to the outer hair cells using intracellular injection of horseradish peroxidase were unsuccessful. On the basis of present evidence, we cannot conclude definitively that the long-latency neurons found in the spiral ganglion belong to the outer hair cell afferent population.

Animals↗
PubMed1978

[Reaction of peripheral vestibular ganglion cells on experimental stimulation in guinea pigs].

The effects of adequate stimuli upon the ganglion cells of the ganglion vestibulare and ganglion geniculi n. facialis were studied in the guinea pig labyrinth. During experimental examination, swelling up to 112% as well as shrinkage up to 35% were noticed. These volume changes do not coincide with the changes occurring in the corresponding sensory nuclei during the same stimulus. As the ganglion cells receive their impulses from various sensularies, they are responsible for several types of movement. A periodical increase and decrease of the nuclear volume are assumed to be an expression of the general total activity. The cells of the ganglion geniculi respond very strongly to these movement stimuli, which are not regarded to be adequate. Consequently it was proved that strong inadequate excitations can also influence the neighboring ganglion cells. In the cytoplasm, strong excitations lead to variations in the Nissl content. An intensive material exchange between the cytoplasm and the karyoplasm is assumed to be a cause for the changes of the nuclei volumes. But only the relation between the cell nuclei and the cell somata is altered. The volume of the whole cell remains approximately constant.

Animals↗
PubMed1996

Induction of HELLP syndrome-like biochemical parameters by stimulation of the celiac ganglion in rats.

OBJECTIVE: An animal model of HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome was developed by means of stimulation of the celiac ganglion in rats. METHODS: The celiac ganglion in pregnant or non-pregnant rats was exposed to endotoxin (lipopolysaccharide, LPS) (500 micrograms/50 microliters), potassium chloride (0.2 mol/l/50 microliters), or saline solution (50 microliters). In another group of rats the bifurcation of the abdominal aorta was exposed to LPS (500 micrograms/50 microliters). Blood pressure, platelet count, hematocrit, serum aspartate transaminase (AST), alanine transaminase (ALT), lactate dehydrogenase (LDH), and plasma norepinephrine and epinephrine were measured for 6 h after treatment. Histopathologic studies were also performed in these rats. RESULTS: A significant increase in blood pressure, AST, ALT, LDH, norepinephrine, and epinephrine was found in the endotoxin-treated pregnant rats compared with control rats treated with the saline solution. A significant decrease in platelet count was found in endotoxin-treated pregnant rats compared with the control rats. A significant increase in blood pressure, AST, norepinephrine, and epinephrine was found in the potassium chloride-treated pregnant rats compared with control rats. Blood pressure and biochemical parameters remained unchanged in the pregnant rats treated with LPS at the bifurcation of the abdominal aorta, as in those treated with saline at the celiac ganglion. Histologic examination of liver tissues treated with LPS or potassium chloride showed varying degrees of ischemic necrosis of hepatocytes similar to that observed in the human HELLP syndrome. Blood pressure, biochemical parameters, and histologic findings in non-pregnant rats were almost the same as those in pregnant rats. CONCLUSION: This study suggests that exogenous stimulation of the celiac ganglion causes an increase in the blood pressure and liver ischemia, resulting in HELLP syndrome-like disease in pregnant and non-pregnant rats.

Animals↗
PubMed1982

Acetylcholine release during burst-patterned stimulation of a sympathetic ganglion: its relation to transmission efficiency.

The time-course of increase in acetylcholine (ACh) output during burst-patterned preganglionic stimulation of the cat superior cervical ganglion has been determined. The increase in output corresponded closely with the increase in transmission efficiency found earlier in the stellate ganglion subjected to similar preganglionic stimulation. ACh output however continued to increase following the time of attainment of full neuronal recruitment. The results indicate that the increase in ACh output may largely account for the increase in transmission; but they leave unexplained the synaptic function of the continuing increase in transmitter release.

Acetylcholine↗
PubMed1991

Dihydroergotamine and sumatriptan attenuate levels of CGRP in plasma in rat superior sagittal sinus during electrical stimulation of the trigeminal ganglion.

Vasoactive neuropeptides, present in unmyelinated C-fibers, can be released from perivascular sensory axons by antidromic stimulation, to mediate vasodilation and extravasation of plasma protein (neurogenic inflammation). In this report, the effects of antidromic trigeminal stimulation on levels of calcitonin gene-related peptide (CGRP) in plasma were examined in the superior sagittal sinus and the effects of drugs that have been shown previously to block extravasation of neurogenic plasma determined. The levels of immunoreactive CGRP in plasma were measured both before and during electrical stimulation of the trigeminal ganglion (0.1-1.0 mA, 5 msec, 5 Hz, 3-5 min), using a highly specific and sensitive immunochemiluminometric assay. Levels of CGRP increased and became maximal within the first minute of stimulation. The increases were detectable at intensities of current as small as 0.1 mA. Peak levels related to the intensity of the stimulus. Samples from femoral arterial blood did not show concomitant increases at 1 min. Pretreatment with dihydroergotamine (DHE) (50 micrograms/kg i.v.) did not change the baseline levels but decreased levels of CGRP during stimulation (0.3 mA), by 55% at 1 min and 50% at 3 min. Sumatriptan (GR43175) (300 micrograms/kg) attenuated the increase by 57% at 3 min (0.1 mA, 5 msec, 5 Hz) but not after 1 min of stimulation, although decreases were observed at the latter time during an individual experiment. Drug-induced attenuation of levels of CGRP in plasma may reflect inhibition of release, to thereby provide evidence to explain blockade of neurogenic extravasation of plasma.

Animals↗
PubMed2001

Possible involvement of calcium-calmodulin pathways in the positive chronotropic response to angiotensin II on the canine cardiac sympathetic ganglia.

We investigated the ganglionic effects of angiotensin II (Ang II) and the signal transduction involved in the cardiac sympathetic ganglia by the direct administration of agents to the ganglia through the right subclavian artery and monitoring the heart rate as an indicator of the ganglionic function in pithed dogs. Ang II given i.a. caused increases in the heart rate, which was inhibited by the treatment with the AT1-receptor antagonist forasartan, but not by the AT2-receptor antagonist PD-123319. The stimulation by Ang II, but not by acetylcholine, was inhibited after treatment with an inhibitor of phospholipase C, U-73122; a cell-permeant modulator of the Ins(1,4,5)P3 receptors, 2-aminoethoxydiphenyl borate; an intracellular calcium and calcium-associated protein kinase inhibitor, HA-1077; calmodulin (CaM) inhibitor, W-7; Ca2+/CaM-dependent protein kinase II inhibitor, KN-93; a selective protein kinase C inhibitor, calphostin C; and Na+H+ exchange inhibitor, dimethylamiloride. These results suggest that Ang II stimulates the ganglionic transmission at postsynaptic sites via the activation of AT1 receptor coupled to either activation of phospholipase C, phosphoinositide hydrolysis and subsequent increase in intracellular Ca2+ and activation of protein kinase C and Ca2+/CaM kinase II, although this ganglionic stimulation seems to involve, at least in part, the protein kinases-dependent increase of amiloride-sensitive Na+ inflow.

Amiloride↗
PubMed1991

[Responses of toad spinal ganglion neurons in vitro to peripheral repetitive stimulation].

Responses of toad ganglion neurons in vitro to repetitive stimulation of their peripheral processes (sciatic nerve) were intracellularly recorded. The conduction velocity, threshold and resting membrane potential of the 66 recorded neurons ranged 5.3-20.0 m/s, 0.02-0.10 mA, and -50-(-)80 mV, respectively. As the stimulation frequency increased, jitter or delay in onset latency, reduction in amplitude, prolongation in duration, and decrease in afterhyperpolarization occurred in evoked responses of the spinal ganglion neurons. The responses decomposed into three subwaves of S, NM, and M and then missed. The ability of these three components to follow stimulation frequency was in the order of S less than NM less than M; the frequency range during which the spike potential or wave S misses was from 16.7 Hz to 250 Hz. These results indicate that there are three distinct zones in excitability in type A toad spinal ganglion neurons, and some of them may exhibit synaptic or junctional activity.

Animals↗
PubMed2003

Differential modulation of light-evoked on- and off-EPSCs by paired-pulse stimulation in salamander retinal ganglion cells.

Short-term plasticity of On- and Off-EPSPs, and its potential role in regulation of signal processing was studied in salamander retinal On-Off ganglion cells by whole-cell recording. Paired-pulse light stimulation resulted in a depression of On-, and an enhancement of Off-EPSCs. Recovery from depression and enhancement was exponential and complete by 20 s. Paired-pulse enhancement, but not depression, was abolished with increasing stimulus duration. Blockade of On-EPSC by L-2-amino-4-phosphonobutyrate (AP-4), an agonist at group III mGluRs, significantly increased Off-EPSCs evoked by short (<2 s) duration conditioning light stimuli, resulting in a reversal of the paired-pulse enhancement to depression. The acetylcholinesterase inhibitor eserine reduced Off-EPSC1 and increased the ratio of enhancement. An opposite effect was observed in the presence of the nACh receptor antagonist d-tubocurarine. AP-7, an antagonist of NMDA receptors attenuated the enhancement of Off-EPSCs. In current clamp mode paired-pulse stimulation resulted in a modulation of light evoked, as well as the depolarization-induced spike firing pattern of ganglion cells. The present study suggests that paired light stimulation differently modulates On and Off EPSPs, and the light-evoked spike firing pattern of On-Off ganglion cells.

Action Potentials↗
PubMed1990

Responses of type A cat spinal ganglion neurons to repetitive stimulation of their central and peripheral processes.

Intracellular recordings were made from L7-S1 type A spinal ganglion neurons of anesthetized cats while electrical stimulation was delivered repetitively to their associated dorsal root and the sciatic nerve. The general response pattern of these neurons changed during stimulation at progressively higher rates. The changes were observable as jitter in onset latency of the evoked spikes, inability of evoked responses to follow electrical stimuli in a 1:1 manner (spike failure), reduction in action potential amplitude, and decomposition of the full spike into its non-myelinated and myelinated components. The frequency following ability of these spike components was in the order of full spike less than non-myelinated less than myelinated. In jitter in onset latency and inability to follow high frequency stimulation was determined only for the full spike, as is typical for antidromicity criteria, a wide frequency following spectrum was obtained for our sample of spinal ganglion neurons. Less than a third of the cells were able to follow stimulation rates in excess of 200 Hz, and about a fifth of the neurons failed to follow any rates greater than 20 Hz. Most of the neurons activated from both the dorsal root and sciatic nerve responded with the same pattern of stimulus-evoked responses. However, some of these cells exhibited strikingly different patterns to dorsal root and sciatic stimulation, including the presence of prepotentials following stimulation of one, but not the other, process. These prepotentials occurred in the depolarizing direction, at threshold stimulation were all-or-none in nature, generated spikes that varied in onset latency, and failed to occur at even low-to-moderate rates of stimulation. The results indicate that the frequency following spectrum of cat type A ganglion neurons is wide, and that it is their somata that are most vulnerable to high frequency stimulation. It is possible that some of the observed prepotentials are functional manifestations of synaptic contacts in spinal ganglia.

Action Potentials↗
PubMedDate not supplied

[The effect of clofelin on the transudation of plasma proteins into the dura mater induced by stimulation of the trigeminal ganglion].

Intravenous administration of clofelin blocks transudation of 131I-albumin into the dura mater of rats in electrical stimulation of the trigeminal ganglion. Preliminary injection of the alpha-adrenoblocker yohimbine and the antagonist of serotonin receptors 5-NT1 mianserin completely removes the blocking effect of clofelin. Naloxon and the alpha 1-adrenoblocker prazosin had no effect on the degree of expression of albumin transudation and the clophelin effect. The role of the adrenergic system, the presynaptic alpha 2-adrenoceptors in particular, in functioning of the trigeminovascular system and the development of neurogenic inflammation in the dura mater is discussed.

Adrenergic alpha-Agonists↗
PubMed2001

Depletion of substance P, neurokinin A and calcitonin gene-related peptide from the contralateral and ipsilateral caudal trigeminal nucleus following unilateral electrical stimulation of the trigeminal ganglion; a possible neurophysiological and neuroanatomical link to generalized head pain.

Primary trigeminal neurons of the trigeminal ganglion (TG) innervate major parts of the face and head, including the dura. Electrical stimulation of the TG at specific parameters, can activate its nociceptive neurons and may serve as an experimental pain model. Markowitz [J. Neurosci. 7 (1987) 4129] reported that electrical stimulation of the trigeminal ganglion (TG) causes extravasation of plasma proteins from venules of the trigeminally innervated domain possibly due to the release of vasoactive substances. Neurogenic inflammation (vasodilatation, plasma protein extravasation, release of vasoactive peptides) in dura may serve as one of the possible pathomechanisms underlying vascular head pain [Moskowitz, Ann. Neurol. 16 (1984) 157]. We performed a unilateral electrical stimulation (7.5 Hz, 5 ms, 0.8-1.4 mA for 5 min) of the TG in rat, to induce a neurogenic inflammation in the peripheral trigeminal domain including the dura, looking for calcitonin gene related peptide (CGRP), substance P (SP) and neurokinin A (NKA) immunoreactivity (IR) in the caudal trigeminal nucleus (CTN) into which massive central trigeminal processes terminate. Here, we show patchy depletion(s) of CGRP-, SP- and NKA-IRs in the contralateral CTN of the rat in addition to their ipsilateral depletion. Such depletion is due to the release of these neuropeptides in the CTN leading to the activation of bilateral trigeminal nociceptive pathway. These data afford the possibility that under specific frequencies (which may roughly correlate to the intensity of the painful stimulus) and/or specific intensities (may correlate to specific areas of the peripheral trigeminal domain) of stimulation, activation of one side of the TG may activate bilateral trigeminal nociceptive pathway leading to the perception of an ill localized/generalized pain or headache rather than a unilateral one.

Animals↗