Somatic ATP release from guinea pig sympathetic neurons does not require calcium-induced calcium release from internal stores

Merriam, Laura A.; Locknar, Sarah A.; Girard, Beatrice M.; Parsons, Rodney L.

doi:10.1152/ajpcell.00036.2010

Cited by 3 publications

(4 citation statements)

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“…Detectable levels of transcript were obtained for TRPC 1, 3, 4, and 5, but not TRPC 6. Recently, we found that transcripts for TRPC 1, 3, 4, 5, and 6 were present in extracts of the guinea pig sympathetic stellate ganglia (Merriam et al 2010). In addition, Beaudet et al (2000) found previously that transcripts for TRPC 1, 3, and 6 were present in extracts from neonatal cultured rat SCG neurons and rat adult SCG.…”

Section: Discussionmentioning

confidence: 99%

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Pretreatment with Nonselective Cationic Channel Inhibitors Blunts the PACAP-Induced Increase in Guinea Pig Cardiac Neuron Excitability

et al. 2012

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Calcium influx is required for the pituitary adenylyl cyclase activating polypeptide (PACAP)-induced increase in guinea pig cardiac neuron sexcitability, noted as a change from a phasic to multiple action potential firing pattern. Intracellular recordings indicated that pretreatment with the nonselective cationic channel inhibitors, 2-aminoethoxydiphenylborate (2-APB), 1-[β-[3-(4-methoxyphenyl)propoxy]-4-methoxy-phenethyl]-1H-imidazole HCl (SKF 96365), and flufenamic acid (FFA) reduced the 20-nM PACAP-induced excitability increase. Additional experiments tested whether 2-APB, FFA, and SKF 96365 could suppress the increase in excitability by PACAP once it had developed. The increased action potential firing remained following application of 2-APB but was diminished by FFA. SKF 96365 transiently depressed the PACAP-induced excitability increase. A decrease and recovery of action potential amplitude paralleled the excitability shift. Since semiquantitative PCR indicated that cardiac neurons express TRPC subunit transcripts, we hypothesize that PACAP activates calcium-permeable, nonselective cationic channels, which possibly are members of the TRPC family. Our results are consistent with calcium influx being required for the initiation of the PACAP-induced increase in excitability, but suggest that it may not be required to sustain the peptide effect. The present results also demonstrate that non-selective cationic channel inhibitors could have other actions, which might contribute to the inhibition of the PACAP-induced excitability increase.

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Section: Discussionmentioning

confidence: 99%

“…The primers used to determine the presence of TRPC transcripts were those used previously to test for TRPC transcripts in extracts of guinea pig stellate ganglia (Merriam et al 2010). …”

Section: Methodsmentioning

confidence: 99%

Pretreatment with Nonselective Cationic Channel Inhibitors Blunts the PACAP-Induced Increase in Guinea Pig Cardiac Neuron Excitability

et al. 2012

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“…Tissue sections (20 μm stellate, 40 μm right atria and guinea pig midbrain) were processed by direct mounting techniques as described previously [23,24] . In a separate set of experiments stellate neurons were dissociated and maintained in culture media for 3 days as described in detail previously [25–27] prior to a 1 hour exposure to fixative (2% paraformaldehyde containing 0.2% picric acid). The fixed tissue sections or dissociated cells were rinsed in PBS, permeabilized with 0.5% Triton X-100, and incubated at 4 °C overnight with a primary antiserum directed against tyrosine hydroxylase (TH) (mouse monoclonal 1:400 from RBI, Natick MA) and a primary antiserum against galanin (rabbit polyclonal 1:1000 from Phoenix Pharmaceuticals, Burlingame CA).…”

Section: Methodsmentioning

confidence: 99%

The cardiac sympathetic co-transmitter galanin reduces acetylcholine release and vagal bradycardia: Implications for neural control of cardiac excitability

Herring

Cranley

Lokale

et al. 2012

Journal of Molecular and Cellular Cardiology

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The autonomic phenotype of congestive cardiac failure is characterised by high sympathetic drive and impaired vagal tone, which are independent predictors of mortality. We hypothesize that impaired bradycardia to peripheral vagal stimulation following high-level sympathetic drive is due to sympatho-vagal crosstalk by the adrenergic co-transmitters galanin and neuropeptide-Y (NPY). Moreover we hypothesize that galanin acts similarly to NPY by reducing vagal acetylcholine release via a receptor mediated, protein kinase-dependent pathway. Prolonged right stellate ganglion stimulation (10 Hz, 2 min, in the presence of 10 μM metoprolol) in an isolated guinea pig atrial preparation with dual autonomic innervation leads to a significant (p < 0.05) reduction in the magnitude of vagal bradycardia (5 Hz) maintained over the subsequent 20 min (n = 6). Immunohistochemistry demonstrated the presence of galanin in a small number of tyrosine hydroxylase positive neurons from freshly dissected stellate ganglion tissue sections. Following 3 days of tissue culture however, most stellate neurons expressed galanin. Stellate stimulation caused the release of low levels of galanin and significantly higher levels of NPY into the surrounding perfusate (n = 6, using ELISA). The reduction in vagal bradycardia post sympathetic stimulation was partially reversed by the galanin receptor antagonist M40 after 10 min (1 μM, n = 5), and completely reversed with the NPY Y2 receptor antagonist BIIE 0246 at all time points (1 μM, n = 6). Exogenous galanin (n = 6, 50–500 nM) also reduced the heart rate response to vagal stimulation but had no effect on the response to carbamylcholine that produced similar degrees of bradycardia (n = 6). Galanin (500 nM) also significantly attenuated the release of 3H-acetylcholine from isolated atria during field stimulation (5 Hz, n = 5). The effect of galanin on vagal bradycardia could be abolished by the galanin receptor antagonist M40 (n = 5). Importantly the GalR1 receptor was immunofluorescently co-localised with choline acetyl-transferase containing neurons at the sinoatrial node. The protein kinase C inhibitor calphostin (100 nM, n = 6) abolished the effect of galanin on vagal bradycardia whilst the protein kinase A inhibitor H89 (500 nM, n = 6) had no effect. These results demonstrate that prolonged sympathetic activation releases the slowly diffusing adrenergic co-transmitter galanin in addition to NPY, and that this contributes to the attenuation in vagal bradycardia via a reduction in acetylcholine release. This effect is mediated by GalR1 receptors on vagal neurons coupled to protein kinase C dependent signalling pathways. The role of galanin may become more important following an acute injury response where galanin expression is increased.

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“…Compared with group N, the hemodynamic parameters of group S decreased at some time points, and significant difference was presented. The overall trend indicated the perioperative hemodynamic parameters of group S tended to be more stable than that of group N. The mechanism may be associated with the following reactions: SGB can, to some extent, suppress the conduction of cardiopulmonary sympathetic nerves, surgically stimulate the nerve conduction and lower the sympathetic tension to decrease the sympathetic excitability (Merriam et al, 2010), while the general anesthesia suppresses the relative excitation of vagus nerves so that the haemodynamic parameters can remain stable.…”

Section: Discussionmentioning

confidence: 96%

Effects of Stellate Ganglion Block on the Peri-operative Vasomotor Cytokine Content and Intrapulmonary Shunt in Patients with Esophagus Cancer

Guo

Jin²,

Yu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Asian Pac J Cancer Prev, 15 (21), 9505-9509 IntroductionOne-lung ventilation (OLV) has been widely applied to cardiothoracic surgery. In spite of unilateral lung ventilation during OLV, bilateral lungs are perfused, which is bound to result in reduced oxygenation, even hypoxemia (Karzai et al., 2009). Hypoxic pulmonary vasoconstriction (HPV) is a phenomenon that the body regulates respiratory and circulatory functions to maintain the oxygen supply within the normal range under the conditions of decreased oxygen partial pressure. The formation mechanism is relatively complicated. Most studies believe that HPV is the direct effect of hypoxia on pulmonary arterial smooth muscle cells and endothelial cells (Evans et al., 2011;Swenson, 2013), but the effect of intrapulmonary During OLV, ET contents were increased significantly in two groups (P<0.05), and no significant difference was presented (P>0.05). NO content in group S was obviously higher than in group N at T3 (P<0.05), whereas CGRP content in group N was markedly lower than in group S at each time point (P<0.05). Qs/Qt was significantly increased in both groups after OLV, but there was no statistical significant regarding the Qs/Qt at each time point between two groups. Conclusions: Total intravenous anesthesia combined with SGB is conducive to regulation of perioperative vasomotor cytokines in thoracotomy, and has little effect on intrapulmonary shunt at the time of OLV.

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Somatic ATP release from guinea pig sympathetic neurons does not require calcium-induced calcium release from internal stores

Abstract: Merriam LA, Locknar SA, Girard BM, Parsons RL. Somatic ATP release from guinea pig sympathetic neurons does not require calcium-induced calcium release from internal stores.

Cited by 3 publications

References 31 publications

Pretreatment with Nonselective Cationic Channel Inhibitors Blunts the PACAP-Induced Increase in Guinea Pig Cardiac Neuron Excitability

Pretreatment with Nonselective Cationic Channel Inhibitors Blunts the PACAP-Induced Increase in Guinea Pig Cardiac Neuron Excitability

The cardiac sympathetic co-transmitter galanin reduces acetylcholine release and vagal bradycardia: Implications for neural control of cardiac excitability

Effects of Stellate Ganglion Block on the Peri-operative Vasomotor Cytokine Content and Intrapulmonary Shunt in Patients with Esophagus Cancer

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