Inhibitory effects of galanin on evoked [Ca2+]i responses in cultured myenteric neurons

2004 ◽  
Vol 286 (6) ◽  
pp. G1009-G1014 ◽  
Author(s):  
Giovanni Sarnelli ◽  
Pieter Vanden Berghe ◽  
Petra Raeymaekers ◽  
Jozef Janssens ◽  
Jan Tack
Keyword(s):  
Electrical Stimulation ◽  
Inhibitory Effect ◽  
Enteric Neurons ◽  
Myenteric Neurons ◽  
High K ◽  
Excitatory Neurotransmitters ◽  
Before And After ◽  
Electrical Pulses ◽  
Intracellular Ca ◽  
Excitatory Responses

Galanin modulates gastrointestinal motility by inhibiting the release of ACh from enteric neurons. It is, however, not known whether galanin also inhibits neuronal cholinergic transmission postsynaptically and whether galanin also reduces the action of other excitatory neurotransmitters. The aim of the present study was thus to investigate the effect of galanin on the evoked intracellular Ca2+ concentration ([Ca2+]i) responses in myenteric neurons. Cultured myenteric neurons from small intestine of adult guinea pigs were loaded with the Ca2+ indicator fluo-3 AM, and the [Ca2+]i responses following the application of different stimuli were quantified by confocal microscopy and expressed as a percentage of the response to high-K+ solution (75 mM). Trains of electrical pulses (2 s, 10 Hz) were applied to stimulate the neuronal fibers before and after a 30-s superfusion with galanin (10−6 M). Substance P (SP), 5-HT, 1,1-dimethyl-4-phenyl-piperazinium iodide (DMPP), and carbachol were used as direct postsynaptic stimuli (10−5 M, 30 s) and were applied alone or after galanin perfusion. Galanin significantly reduced the responses induced by electrical fiber stimulation (43 ± 2 to 35 ± 3%, P = 0.01), SP (15.4 ± 1 to 8.0 ± 0.3%, P < 0.01), and 5-HT (26 ± 2 to 21.4 ± 1.5%, P < 0.05). On the contrary, galanin did not affect the responses induced by local application of DMPP and carbachol. We conclude that in cultured myenteric neurons, galanin inhibits the excitatory responses induced by electrical stimulation, SP, and 5-HT. Finally, the inhibitory effect of galanin on electrical stimulation, but not on DMPP- and carbachol-induced responses, suggests that, at least for the cholinergic component, galanin acts at the presynaptic level.

Cross-talk along gastrointestinal tract during electrical stimulation: effects and mechanisms of gastric/colonic stimulation on rectal tone in dogs

2005 ◽  
Vol 288 (6) ◽  
pp. G1195-G1198 ◽  
Author(s):  
Shi Liu ◽  
Lijie Wang ◽  
J. D. Z. Chen
Keyword(s):  
Electrical Stimulation ◽  
Inhibitory Effect ◽  
Adrenergic Blockade ◽  
Rectal Compliance ◽  
Rectal Tone ◽  
Before And After ◽  
Sensory Functions ◽  
Sympathetic Pathway ◽  
Colonic Electrical Stimulation ◽  
Stimulation Of

Gastric electrical stimulation (GES) has been shown to alter motor and sensory functions of the stomach. However, its effects on other organs of the gut have rarely been investigated. The study was performed in 12 dogs implanted with two pairs of electrodes, one on the serosa of the stomach and the other on the colon. The study was composed of two experiments. Experiment 1 was designed to study the effects of GES on rectal tone and compliance in nine dogs compared with colonic electrical stimulation (CES). Rectal tone and compliance were assessed before and after GES or CES. Experiment 2 was performed to study the involvement of sympathetic pathway in 8 of the 12 dogs. The rectal tone was recorded for 30–40 min at baseline and 20 min after intravenous guanethidine. GES or CES was given for 20 min 20 min after the initiation of the infusion. It was found that both GES and CES reduced rectal tone with comparable potency. Rectal compliance was altered neither with GES, nor with CES. The inhibitory effect of GES but not CES on rectal tone was abolished by an adrenergic blockade, guanethidine. GES inhibited rectal tone with a comparable potency with CES but did not alter rectal compliance. The inhibitory effect of GES on rectal tone is mediated by the sympathetic pathway. It should be noted that electrical stimulation of one organ of the gut may have a beneficial or adverse effect on another organ of the gut.

Effect of calcium and cAMP on Goα expression in neonatal rat cardiac myocytes

1991 ◽  
Vol 261 (4) ◽  
pp. 15-20
Author(s):  
Karen A. Foster ◽  
Janet D. Robishaw
Keyword(s):  
Cardiac Myocytes ◽  
Inhibitory Effect ◽  
Neonatal Rat ◽  
Intracellular Camp ◽  
Dibutyryl Camp ◽  
High K ◽  
Neonatal Rat Cardiac Myocytes ◽  
Intracellular Ca ◽  
The Mean ◽  
Rat Cardiac Myocytes

Culturing neonatal rat cardiac myocytes in 50 mM KCl inhibits the accumulation of Go that occurs when myocytes are placed in culture. The mechanism by which high extracellular K+ inhibits Go accumulation in myocytes was investigated by measurement of the concentration of intracellular Ca2+ ([Ca2+]) and adenosine 3',5'-cyclic monophosphate concentration ([cAMP]) of control and K+-depolarized myocytes. Although intracellular [Ca2++] in K+-depolarized myocytes was twofold higher than basal intracellular [Ca2+] in control cells, the mean intracellular [Ca2+] in contracting control myocytes was comparable to that of K+-depolarized myocytes. Furthermore, myocytes cultured in low Ca2+ plus high K+ exhibited an inhibition of Go accumulation, even though intracellular [Ca2+] was 10-fold lower than that of cells cultured in normal Ca2+ plus high K+. In addition, intracellular [cAMP] of K+-depolarized myocytes was comparable to that of control cells. Moreover, dibutyryl cAMP inhibited Go accumulation in myocytes to the same extent as high K+, even though intracellular [cAMP] differed 10-fold. Thus neither intracellular Ca2+ nor cAMP appear to mediate the inhibitory effect of high K+ on Go accumulation. However, cAMP has an inhibitory effect on Goα expression that is independent of K+. dibutyryl cAMP; fura-2; immunoblotting

scholarly journals Functional Electrical Stimulation for Upper Limbs Flexion-Extension and Prehension Movements in Rehabilitation

2020 ◽  
Author(s):  
Lullo Francesco ◽  
Coccia Armando ◽  
Saltalamacchia Anna Maria ◽  
Cesarelli Mario ◽  
Lanzillo Bernardo ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Functional Electrical Stimulation ◽  
Upper Limbs ◽  
Clinical Environment ◽  
Flexion Extension ◽  
Before And After ◽  
Electrical Pulses ◽  
Prehension Movements ◽  
The Central Nervous System ◽  
Complex Movement

Functional Electrical Stimulation (FES), is a tecnique that uses low-energy electrical pulses to artificially generate muscle contractions, in individuals with damages regarding the central nervous system. The application of FES in clinical environment involves both patients care and rehabilitation. Aim of this work is to introduce a clinical FES protocol for upper limbs rehabilitation, in order to assist and train the execution of complex movement, such as flexion- extension of wrist and fingers and palmar prehension. The new FES protocol has been tested on a cohort of five subjects with different upper limb neuromotor deficits, during their rehabilitation. The benefits deriving from the application of the new FES protocol have been evaluated by comparing specific quantitative electromyographic parameters assessed before and after the treatment. Results show effective improvements in performances of 4 patients out of 5.

Receptor-induced Ca2+ signaling in cultured myenteric neurons

2000 ◽  
Vol 278 (6) ◽  
pp. G905-G914 ◽  
Author(s):  
Pieter vanden Berghe ◽  
Jan Tack ◽  
Antonius Andrioli ◽  
Ludwig Missiaen ◽  
Jozef Janssens
Keyword(s):  
Substance P ◽  
Receptor Antagonist ◽  
Muscarinic Receptors ◽  
Serotonin Receptors ◽  
Slow Component ◽  
Myenteric Neurons ◽  
Excitatory Neurotransmitters ◽  
Intracellular Ca

We studied the effect of excitatory neurotransmitters (10− 5 M) on the intracellular Ca2+ concentration ([Ca2+]i) of cultured myenteric neurons. ACh evoked a response in 48.6% of the neurons. This response consisted of a fast and a slow component, respectively mediated by nicotinic and muscarinic receptors, as revealed by specific agonists and antagonists. Substance P evoked a [Ca2+]i rise in 68.2% of the neurons, which was highly dependent on Ca2+ release from intracellular stores, since after thapsigargin (5 μM) pretreatment only 8% responded. The responses to serotonin, present in 90.7%, were completely blocked by ondansetron (10− 5M), a 5-HT3 receptor antagonist. Specific agonists of other serotonin receptors were not able to induce a [Ca2+]i rise. Removing extracellular Ca2+ abolished all serotonin and fast ACh responses, whereas substance P and slow ACh responses were more persistent. We conclude that ACh-induced signaling involves both nicotinic and muscarinic receptors responsible for a fast and a more delayed component, respectively. Substance P-induced signaling requires functional intracellular Ca2+ stores, and the 5-HT3 receptor mediates the serotonin-induced Ca2+ signaling in cultured myenteric neurons.

Calcium in the control of renin release

1978 ◽  
Vol 235 (1) ◽  
pp. F22-F25 ◽  
Author(s):  
C. S. Park ◽  
R. L. Malvin
Keyword(s):  
Incubation Medium ◽  
Inhibitory Action ◽  
Inhibitory Effect ◽  
Significant Inhibition ◽  
Renin Release ◽  
Juxtaglomerular Cells ◽  
High K ◽  
Intracellular Ca ◽  
K Concentration ◽  
Cortical Slices

The effect of Ca concentrations in the incubation medium and of estimated intracellular Ca concentrations on renin release was examined with use of pig renal cortical slices. In addition, the Ca requirement for the epinephrine stimulatory effect and for the ouabain inhibitory action on renin release was also tested. In mediums containing 5.9 mM K, variations in Ca concentration had no effect on renin release. In contrast, when the K concentration was 59 mM, a significant inhibition of renin release was attained with all concentrations of calcium. The inhibition of renin release in high K mediums by Ca was attributed to an increase in the intracellular Ca concentration. In addition, both the stimulatory effect of epinephrine and the inhibitory effect of ouabain on renin release required Ca in the medium. These results support the hypothesis that the control of renin secretion is mediated, in part, by changes in the intracellular concentration of Ca, most likely in the juxtaglomerular cells.

scholarly journals Electrical stimulation of the mucosa evokes slow EPSPs mediated by NK1 tachykinin receptors and by P2Y1 purinoceptors in different myenteric neurons

2009 ◽  
Vol 297 (1) ◽  
pp. G179-G186 ◽  
Author(s):  
Rachel M. Gwynne ◽  
Joel C. Bornstein
Keyword(s):  
Electrical Stimulation ◽  
Pyridoxal Phosphate ◽  
Enteric Neurons ◽  
Disulfonic Acid ◽  
Myenteric Neurons ◽  
Mrs 2179 ◽  
Neurokinin 1 ◽  
Oxide Synthase ◽  
Stimulation Of

Slow excitatory postsynaptic potentials (EPSPs) in enteric neurons arise from diverse sources, but which neurotransmitters mediate specific types of slow EPSPs is unclear. We investigated transmitters and receptors mediating slow EPSPs in myenteric neurons evoked by electrical stimulation of the mucosa in guinea pig small intestine. Segments of ileum or jejunum were dissected to allow access to the myenteric plexus adjacent to intact mucosa, in vitro. AH and S neurons were impaled with conventional intracellular electrodes. Trains of stimuli delivered to the mucosa evoked slow EPSPs in AH neurons that were blocked or depressed by the neurokinin-1 (NK1) tachykinin antagonist SR140333 (100 nM) in 10 of 11 neurons; the NK3 tachykinin receptor antagonist SR142801 (100 nM) had no effect on slow EPSPs in seven of nine AH neurons. Single pulses to the mucosa evoked fast EPSPs and slow depolarizations in S neurons. The depolarizations were divided into intermediate (durations 300–900 ms) or slow (durations 1.3–9 s) EPSPs. The slow EPSPs were blocked by pyridoxal phosphate-6-axophenyl-2–4-disulfonic acid (30 μM, N = 3) or the specific P2Y1 antagonist MRS 2179 (10 μM, N = 6) and were predominantly in anally projecting S neurons that were immunoreactive for nitric oxide synthase (NOS). In contrast, intermediate EPSPs were predominantly evoked in NOS-negative neurons; these were abolished by MRS 2179 ( N = 8). Thus activation of pathways running from the mucosa excites three different types of slow EPSP in myenteric neurons, which are mediated by either a tachykinin (NK1, AH neurons) or a purine nucleotide (P2Y1, S neurons).

Mechanism of cGMP contribution to the vasodilator response to NO in rat middle cerebral arteries

2002 ◽  
Vol 282 (5) ◽  
pp. H1724-H1731 ◽  
Author(s):  
Ming Yu ◽  
Cheng-Wen Sun ◽  
Kristopher G. Maier ◽  
David R. Harder ◽  
Richard J. Roman
Keyword(s):  
Nitric Oxide ◽  
Contractile Response ◽  
Cerebral Arteries ◽  
Inhibitory Effect ◽  
No Donor ◽  
Vasodilator Response ◽  
Vasoconstrictor Response ◽  
High K ◽  
Middle Cerebral Arteries ◽  
Intracellular Ca

This study examined the mechanism by which cGMP contributes to the vasodilator response to nitric oxide (NO) in rat middle cerebral arteries (MCA). Administration of a NO donor, diethylaminodiazen-1-ium-1,2-dioate (DEA-NONOate), or 8-bromo-cGMP (8-BrcGMP) increased the diameter of serotonin-preconstricted MCA by 79 ± 3%. The response to DEA-NONOate, but not 8-BrcGMP, was attenuated by iberiotoxin (10−7 M) or a 80 mM high-K+ media, suggesting that activation of K+channels contributes to the vasodilator response to NO but not 8-BrcGMP. The effects of NO and cGMP on the vasoconstrictor response to Ca2+ were also studied in MCA that were permeabilized with α-toxin and ionomycin. Elevations in bath Ca2+ from 10−8 to 10−5 M decreased the diameter of permeabilized MCA by 76 ± 5%. DEA-NONOate (10−6 M) and 8-BrcGMP (10−4 M) blunted this response by 60%. Inhibition of guanylyl cyclase with 1 H-[1,2,4]oxadiazole[4,3-a] quinoxalin-1-one (10−5 M) blocked the inhibitory effect of the NO donor, but not 8-BrcGMP, on Ca2+-induced vasoconstriction. 8-BrcGMP (10−4 M) had no effect on intracellular Ca2+ concentration ([Ca2+]i) in control, serotonin-stimulated, or α-toxin- and ionomycin-permeabilized vascular smooth muscle cells isolated from the MCA. These results indicate that the vasodilator response to NO in rat MCA is mediated by activation of Ca2+-activated K+ channels via a cGMP-independent pathway and that cGMP also contributes to the vasodilator response to NO by decreasing the contractile response to elevations in [Ca2+]i.

Stimulation of voltage-dependent Ca2+ channels by NO at rat myenteric neurons

2007 ◽  
Vol 293 (4) ◽  
pp. G886-G893 ◽  
Author(s):  
Mabruka Sitmo ◽  
Matthias Rehn ◽  
Martin Diener
Keyword(s):  
Enteric Neurons ◽  
Channel Blockers ◽  
No Donor ◽  
Inward Current ◽  
Myenteric Neurons ◽  
Whole Cell Patch Clamp ◽  
Target Organs ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Ca2 Channels

The aim of the present study was to characterize the action of the neurotransmitter NO on rat myenteric neurons. A NO donor such as GEA 3162 (10−4 mol/l) induced an increase in the intracellular Ca2+ concentration as indicated by an increase in the fura 2 ratio in ganglia loaded with this Ca2+-sensitive fluorescent dye. The effect of GEA 3162 was strongly reduced in the absence of extracellular Ca2+, suggesting an influx of Ca2+ from the extracellular space evoked by NO. A similar nearly complete inhibition was observed in the presence of Ca2+ channel blockers such as Ni2+ (5 × 10−4 mol/l) or nifedipine (10−6 mol/l). Whole cell patch-clamp recordings confirmed the activation of voltage-dependent Ca2+ channels, measured as inward current carried by Ba2+, by the NO donor. The peak Ba2+-carried inward current increased from −100 ± 19 to −185 ± 34 pA in the presence of sodium nitroprusside (10−4 mol/l). The consequence was a hyperpolarization of the membrane, which was blocked by intracellular Cs+ and thus most probably reflects the activation of Ca2+-dependent K+ channels. Furthermore, at least two subtypes of NO synthases, NOS-1 (neuronal form) and NOS-3 (endothelial form), were found as transcripts in mRNA isolated from the rat myenteric ganglia. The expression of these NO synthases was confirmed immunohistochemically. These observations suggest that NO, released from nitrergic neurons within the enteric nervous system, not only affects target organs such as smooth muscle cells in the gut but has in addition profound effects on the enteric neurons themselves, the key players in the regulation of many gastrointestinal functions.

scholarly journals Functional Electrical Stimulation for Upper Limbs Flexion-Extension and Prehension Movements in Rehabilitation

2020 ◽  
Author(s):  
Lullo Francesco ◽  
Coccia Armando ◽  
Saltalamacchia Anna Maria ◽  
Cesarelli Mario ◽  
Lanzillo Bernardo ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Functional Electrical Stimulation ◽  
Upper Limbs ◽  
Clinical Environment ◽  
Flexion Extension ◽  
Before And After ◽  
Electrical Pulses ◽  
Prehension Movements ◽  
The Central Nervous System ◽  
Complex Movement

Functional Electrical Stimulation (FES), is a tecnique that uses low-energy electrical pulses to artificially generate muscle contractions, in individuals with damages regarding the central nervous system. The application of FES in clinical environment involves both patients care and rehabilitation. Aim of this work is to introduce a clinical FES protocol for upper limbs rehabilitation, in order to assist and train the execution of complex movement, such as flexion- extension of wrist and fingers and palmar prehension. The new FES protocol has been tested on a cohort of five subjects with different upper limb neuromotor deficits, during their rehabilitation. The benefits deriving from the application of the new FES protocol have been evaluated by comparing specific quantitative electromyographic parameters assessed before and after the treatment. Results show effective improvements in performances of 4 patients out of 5.

scholarly journals Pathophysiological Roles of Neuro-Immune Interactions between Enteric Neurons and Mucosal Mast Cells in the Gut of Food Allergy Mice

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1586
Author(s):  
Tomoe Yashiro ◽  
Hanako Ogata ◽  
Syed Faisal Zaidi ◽  
Jaemin Lee ◽  
Shusaku Hayashi ◽  
...  
Keyword(s):  
Food Allergy ◽  
Mast Cells ◽  
Imaging System ◽  
Receptor Gene ◽  
Nerve Fibers ◽  
Enteric Neurons ◽  
Food Allergies ◽  
Adenosine A3 Receptor ◽  
Myenteric Neurons ◽  
Mucosal Mast Cells

Recently, the involvement of the nervous system in the pathology of allergic diseases has attracted increasing interest. However, the precise pathophysiological role of enteric neurons in food allergies has not been elucidated. We report the presence of functional high-affinity IgE receptors (FcεRIs) in enteric neurons. FcεRI immunoreactivities were observed in approximately 70% of cholinergic myenteric neurons from choline acetyltransferase-eGFP mice. Furthermore, stimulation by IgE-antigen elevated intracellular Ca2+ concentration in isolated myenteric neurons from normal mice, suggesting that FcεRIs are capable of activating myenteric neurons. Additionally, the morphological investigation revealed that the majority of mucosal mast cells were in close proximity to enteric nerve fibers in the colonic mucosa of food allergy mice. Next, using a newly developed coculture system of isolated myenteric neurons and mucosal-type bone-marrow-derived mast cells (mBMMCs) with a calcium imaging system, we demonstrated that the stimulation of isolated myenteric neurons by veratridine caused the activation of mBMMCs, which was suppressed by the adenosine A3 receptor antagonist MRE 3008F20. Moreover, the expression of the adenosine A3 receptor gene was detected in mBMMCs. Therefore, in conclusion, it is suggested that, through interaction with mucosal mast cells, IgE-antigen-activated myenteric neurons play a pathological role in further exacerbating the pathology of food allergy.

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