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).

Electrophysiological identification of vagally innervated enteric neurons in guinea pig stomach

1992 ◽  
Vol 263 (5) ◽  
pp. G709-G718 ◽  
Author(s):  
M. Schemann ◽  
D. Grundy
Keyword(s):  
Nicotinic Receptors ◽  
Vagal Stimulation ◽  
Enteric Neurons ◽  
Command Neurons ◽  
Myenteric Neurons ◽  
Release Of Acetylcholine ◽  
Vagal Innervation ◽  
Guinea Pig Stomach ◽  
Stimulation Of

Myenteric "command neurons" are thought to be the interface between extrinsic and intrinsic controls of gut functions and are thought to be responsible for transmission of vagal impulses to enteric microcircuits. To identify, electrophysiologically, myenteric neurons responding to electrical stimulation of the vagus, we developed an in vitro preparation of the gastric myenteric plexus in which the vagal innervation was preserved. The majority of myenteric neurons [102 of 155 (66%)] received fast excitatory postsynaptic potentials (fEPSPs) after stimulation of the vagus. The proportion of neurons receiving vagal input was highest at the lesser curve (98%) and decreased gradually when recordings were made from neurons located toward the greater curve. Only a small proportion of neurons (4 of 85 cells) showed a slow EPSP after a burst of vagal stimulation. No postsynaptic inhibitory potentials were observed. There was no preferential vagal input to either gastric I, gastric II, or gastric III neurons. The fEPSPs were due to the release of acetylcholine acting postsynaptically on nicotinic receptors. The behavior of the fEPSPs suggests multiple vagal inputs to a majority of myenteric neurons. Our observations call into question the concept of enteric command neurons in favor of a divergent vagal input with widespread modulatory influences over gastric enteric neurotransmission.

Extrinsic afferent nerve sensitivity and enteric neurotransmission in murine jejunum in vitro

2009 ◽  
Vol 297 (4) ◽  
pp. G655-G662 ◽  
Author(s):  
Mario H. Mueller ◽  
Bing Xue ◽  
Joerg Glatzle ◽  
Jutta Hahn ◽  
David Grundy ◽  
...  
Keyword(s):  
Pyridoxal Phosphate ◽  
Signal Transmission ◽  
Afferent Nerve ◽  
Enteric Neurons ◽  
Intraluminal Pressure ◽  
Disulfonic Acid ◽  
Experimental Conditions ◽  
Calcium Dependent ◽  
In Series

Enteric and extrinsic sensory neurons respond to similar stimuli. Thus they may be activated in series or in parallel. Because signal transmission via synapses or mediator release would depend on calcium, we investigated its role for extrinsic afferent sensitivity to chemical and mechanical stimulation. Extracellular multiunit afferent recordings were made in vitro from paravascular nerve bundles supplying the mouse jejunum. Intraluminal pressure and afferent nerve responses were recorded under control conditions and under four conditions designed to interfere with enteric neurotransmission. We found that phasic intestinal contractions ceased after switching perfusion to Ca2+-free buffer with or without a purinergic P2 receptor antagonist, pyridoxal phosphate-6-azo(benzene-2,4-disulfonic acid) (PPADS) or cadmium (blocking all Ca2+-channels) but not following ω-conotoxin GVIA (N-type Ca2+-channel blocker). Luminal HCl (pH 2) and 5-HT (500 μM) evoked peak firing of 17 ± 4 impulses per second (imp/s) ( n = 10) and 21 ± 4 imp/s ( n = 13) under control conditions. These responses were reduced to 4 ± 2 imp/s and 5 ± 2 imp/s by cadmium ( n = 7, P < 0.05), to 7 ± 2 imp/s and 6 ± 1 imp/s by Ca2+-free perfusion ( n = 6, P < 0.05), and to 3 ± 1 imp/s and 4 ± 1 imp/s by Ca2+-free perfusion with PPADS ( n = 6, P < 0.05). Responses were unchanged by ω-conotoxin GVIA. Mechanical ramp distension of the intestinal segment to 60 cmH2O was not altered by any of the experimental conditions. We concluded that HCl and 5-HT activate extrinsic afferents via a calcium-dependent mechanism, which is unlikely to involve enteric neurons carrying N-type calcium channels. Extrinsic mechanosensitivity is independent of enteric neurotransmission. It appears that cross talk from the enteric to the extrinsic nervous system does not mediate extrinsic afferent sensitivity.

scholarly journals Establishment of a New Device for Electrical Stimulation of Non-Degenerative Cartilage Cells In Vitro

2021 ◽  
Vol 22 (1) ◽  
pp. 394
Author(s):  
Simone Krueger ◽  
Alexander Riess ◽  
Anika Jonitz-Heincke ◽  
Alina Weizel ◽  
Anika Seyfarth ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Electric Fields ◽  
Cartilage Tissue ◽  
Type I ◽  
Dependent Manner ◽  
New Device ◽  
Alternating Electric Fields ◽  
Cartilage Cells ◽  
Stimulation Of

In cell-based therapies for cartilage lesions, the main problem is still the formation of fibrous cartilage, caused by underlying de-differentiation processes ex vivo. Biophysical stimulation is a promising approach to optimize cell-based procedures and to adapt them more closely to physiological conditions. The occurrence of mechano-electrical transduction phenomena within cartilage tissue is physiological and based on streaming and diffusion potentials. The application of exogenous electric fields can be used to mimic endogenous fields and, thus, support the differentiation of chondrocytes in vitro. For this purpose, we have developed a new device for electrical stimulation of chondrocytes, which operates on the basis of capacitive coupling of alternating electric fields. The reusable and sterilizable stimulation device allows the simultaneous use of 12 cavities with independently applicable fields using only one main supply. The first parameter settings for the stimulation of human non-degenerative chondrocytes, seeded on collagen type I elastin-based scaffolds, were derived from numerical electric field simulations. Our first results suggest that applied alternating electric fields induce chondrogenic re-differentiation at the gene and especially at the protein level of human de-differentiated chondrocytes in a frequency-dependent manner. In future studies, further parameter optimizations will be performed to improve the differentiation capacity of human cartilage cells.

Direct-Current Electrical Stimulation of Tendon Healing in Vitro

1987 ◽  
Vol &NA; (217) ◽  
pp. 303???312 ◽  
Author(s):  
JOSEPH P. NESSLER ◽  
DANIEL P. MASS
Keyword(s):  
Electrical Stimulation ◽  
Direct Current ◽  
Tendon Healing ◽  
Stimulation Of

scholarly journals Properties and Interconnections of Trigeminal Interneurons of the Lateral Pontine Reticular Formation in the Rat

2001 ◽  
Vol 86 (5) ◽  
pp. 2583-2596 ◽  
Author(s):  
M.-J. Bourque ◽  
A. Kolta
Keyword(s):  
Electrical Stimulation ◽  
Reticular Formation ◽  
Motor Pattern ◽  
High Frequency Stimulation ◽  
Motor Nucleus ◽  
Trigeminal Motor Nucleus ◽  
Postsynaptic Potentials ◽  
Frequency Stimulation ◽  
Stimulation Of

Numerous evidence suggests that interneurons located in the lateral tegmentum at the level of the trigeminal motor nucleus contribute importantly to the circuitry involved in mastication. However, the question of whether these neurons participate actively to genesis of the rhythmic motor pattern or simply relay it to trigeminal motoneurons remains open. To answer this question, intracellular recordings were performed in an in vitro slice preparation comprising interneurons of the peritrigeminal area (PeriV) surrounding the trigeminal motor nucleus (NVmt) and the parvocellular reticular formation ventral and caudal to it (PCRt). Intracellular and extracellular injections of anterograde tracers were also used to examine the local connections established by these neurons. In 97% of recordings, electrical stimulation of adjacent areas evoked a postsynaptic potential (PSP). These PSPs were primarily excitatory, but inhibitory and biphasic responses were also induced. Most occurred at latencies longer than those required for monosynaptic transmission and were considered to involve oligosynaptic pathways. Both the anatomical and physiological findings show that all divisions of PeriV and PCRt are extensively interconnected. Most responses followed high-frequency stimulation (50 Hz) and showed little variability in latency indicating that the network reliably distributes inputs across all areas. In all neurons but one, excitatory postsynaptic potentials (EPSPs) or inhibitory postsynaptic potentials (IPSPs) were also elicited by stimulation of NVmt, suggesting the existence of excitatory and inhibitory interneurons within the motor nucleus. In a number of cases, these PSPs were reproduced by local injection of glutamate in lieu of the electrical stimulation. All EPSPs induced by stimulation of PeriV, PCRt, or NVmt were sensitive to ionotropic glutamate receptor antagonists 6-cyano-7-dinitroquinoxaline and d,l-2-amino-5-phosphonovaleric acid, while IPSPs were blocked by bicuculline and strychnine, antagonists of GABAA and glycine receptors. Examination of PeriV and PCRt intrinsic properties indicate that they form a fairly uniform network. Three types of neurons were identified on the basis of their firing adaptation properties. These types were not associated with particular regions. Only 5% of all neurons showed bursting behavior. Our results do not support the hypothesis that neurons of PeriV and PCRt participate actively to rhythm generation, but suggest instead that they are driven by rhythmical synaptic inputs. The organization of the network allows for rapid distribution of this rhythmic input across premotoneuron groups.

Properties of synaptic inputs from myenteric neurons innervating submucosal S neurons in guinea pig ileum

2000 ◽  
Vol 278 (2) ◽  
pp. G273-G280 ◽  
Author(s):  
B. A. Moore ◽  
S. Vanner
Keyword(s):  
Guinea Pig ◽  
Myenteric Plexus ◽  
Intracellular Recordings ◽  
Guinea Pig Ileum ◽  
Myenteric Neurons ◽  
Synaptic Inputs ◽  
Stimulus Train ◽  
Stimulation Of ◽  
Double Chamber

This study examined synaptic inputs from myenteric neurons innervating submucosal neurons. Intracellular recordings were obtained from submucosal S neurons in guinea pig ileal preparations in vitro, and synaptic inputs were recorded in response to electrical stimulation of exposed myenteric plexus. Most S neurons received synaptic inputs [>80% fast (f) excitatory postsynaptic potentials (EPSP), >30% slow (s) EPSPs] from the myenteric plexus. Synaptic potentials were recorded significant distances aboral (fEPSPs, 25 mm; sEPSPs, 10 mm) but not oral to the stimulating site. When preparations were studied in a double-chamber bath that chemically isolated the stimulating “myenteric chamber” from the recording side “submucosal chamber,” all fEPSPs were blocked by hexamethonium in the submucosal chamber, but not by a combination of nicotinic, purinergic, and 5-hydroxytryptamine-3 receptor antagonists in the myenteric chamber. In 15% of cells, a stimulus train elicited prolonged bursts of fEPSPs (>30 s duration) that were blocked by hexamethonium. These findings suggest that most submucosal S neurons receive synaptic inputs from predominantly anally projecting myenteric neurons. These inputs are poised to coordinate intestinal motility and secretion.

Micturition reflexes in the in vitro neonatal rat brain stem-spinal cord-bladder preparation

1994 ◽  
Vol 266 (3) ◽  
pp. R658-R667 ◽  
Author(s):  
K. Sugaya ◽  
W. C. De Groat
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Brain Stem ◽  
Rat Brain ◽  
Bladder Wall ◽  
Spinal Reflex ◽  
Neonatal Rat ◽  
Evoked Contractions ◽  
Stimulation Of

An in vitro neonatal (1-7 day) rat brain stem-spinal cord-bladder (BSB) preparation was used to examine the central control of micturition. Isovolumetric bladder contractions occurred spontaneously or were induced by electrical stimulation of the ventrolateral brain stem, spinal cord, bladder wall (ES-BW), or by perineal tactile stimulation (PS). Transection of the spinal cord at the L1 segment increased the amplitude of ES-BW- and PS-evoked contractions, and subsequent removal of the spinal cord further increased spontaneous and ES-BW-evoked contractions but abolished PS-evoked contractions. Hexamethonium (1 mM), a ganglionic blocking agent, mimicked the effect of cord extirpation. Tetrodotoxin (1 microM) blocked ES-BW- and PS-evoked contractions but enhanced spontaneous contractions. Bicuculline methiodide (10-50 microM), a gamma-aminobutyric acid A receptor antagonist, increased the amplitude of spontaneous, ES-BW- and PS-evoked contractions. These results indicate that PS-evoked contractions are mediated by spinal reflex pathways, whereas spontaneous and ES-BW-evoked contractions that are elicited by peripheral mechanisms are subject to a tonic inhibition dependent on an efferent outflow from the spinal cord. PS-evoked micturition is also subject to inhibitory modulation arising from sites rostral to the lumbosacral spinal cord. Although electrical stimulation of bulbospinal excitatory pathways can initiate bladder contractions in the neonatal rat, these pathways do not appear to have an important role in controlling micturition during the first postnatal week.

Experimental Migraine Models and Their Relevance in Migraine Therapy

Cephalalgia ◽  
2006 ◽  
Vol 26 (6) ◽  
pp. 642-659 ◽  
Author(s):  
U Arulmani ◽  
S Gupta ◽  
A Maassen VanDenBrink ◽  
D Centurión ◽  
CM Villalón ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Trigeminal Ganglion ◽  
In Vitro Models ◽  
In Vivo Model ◽  
Trigeminal System ◽  
Sagittal Sinus ◽  
Migraine Pathophysiology ◽  
Stimulation Of

Although the understanding of migraine pathophysiology is incomplete, it is now well accepted that this neurovascular syndrome is mainly due to a cranial vasodilation with activation of the trigeminal system. Several experimental migraine models, based on vascular and neuronal involvement, have been developed. Obviously, the migraine models do not entail all facets of this clinically heterogeneous disorder, but their contribution at several levels (molecular, in vitro, in vivo) has been crucial in the development of novel antimigraine drugs and in the understanding of migraine pathophysiology. One important vascular in vivo model, based on an assumption that migraine headache involves cranial vasodilation, determines porcine arteriovenous anastomotic blood flow. Other models utilize electrical stimulation of the trigeminal ganglion/nerve to study neurogenic dural inflammation, while the superior sagittal sinus stimulation model takes into account the transmission of trigeminal nociceptive input in the brainstem. More recently, the introduction of integrated models, namely electrical stimulation of the trigeminal ganglion or systemic administration of capsaicin, allows studying the activation of the trigeminal system and its effect on the cranial vasculature. Studies using in vitro models have contributed enormously during the preclinical stage to characterizing the receptors in cranial blood vessels and to studying the effects of several putative antimigraine agents. The aforementioned migraine models have advantages as well as some limitations. The present review is devoted to discussing various migraine models and their relevance to antimigraine therapy.

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