Tachykinins mediate slow excitatory postsynaptic transmission in guinea pig sphincter of Oddi ganglia

2001 ◽  
Vol 281 (2) ◽  
pp. G357-G364 ◽  
Author(s):  
Brian P. Manning ◽  
Gary M. Mawe
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Receptor Antagonist ◽  
Synaptic Input ◽  
Intracellular Recording ◽  
Small Diameter ◽  
Sphincter Of Oddi ◽  
Receptor Desensitization ◽  
Afferent Fibers ◽  
Excitatory Synaptic Input

Intracellular recording techniques were used to test whether tachykinins could be mediators of slow excitatory postsynaptic potentials (EPSPs) in guinea pig sphincter of Oddi (SO) ganglia. Application of the tachykinin substance P (SP) onto SO neurons caused a prolonged membrane depolarization that was reminiscent of the slow EPSP in these cells. Pressure ejection of the neurokinin 3 (NK3) receptor-specific agonist senktide caused a similar depolarization; however, no responses were detected on application of NK1 or NK2 receptor agonists. The NK3 receptor antagonist SR-142801 (100 nM) significantly inhibited both SP-induced depolarization and the stimulation-evoked slow EPSP, as did NK3 receptor desensitization with senktide. Capsaicin, which causes the release of SP from small-diameter afferent fibers, induced a depolarization that was similar to the evoked slow EPSP in both amplitude and duration. The capsaicin-induced depolarization was significantly attenuated in the presence of SR-142801. These data indicate that tachykinins, released from extrinsic afferent fibers, act via NK3 receptors to provide slow excitatory synaptic input to SO neurons.

Inhibition of Glutamatergic Synaptic Input to Spinal Lamina IIo Neurons by Presynaptic α2-Adrenergic Receptors

2002 ◽  
Vol 87 (4) ◽  
pp. 1938-1947 ◽  
Author(s):  
Yu-Zhen Pan ◽  
De-Pei Li ◽  
Hui-Lin Pan
Keyword(s):  
Receptor Antagonist ◽  
Synaptic Input ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Dorsal Root ◽  
Primary Afferents ◽  
Noradrenergic System ◽  
Analgesic Action ◽  
Adrenergic Agonists ◽  
Excitatory Synaptic Input

Activation of spinal α2-adrenergic receptors by the descending noradrenergic system and α2-adrenergic agonists produces analgesia. However, the sites and mechanisms of the analgesic action of spinally administered α2-adrenergic receptor agonists such as clonidine are not fully known. The dorsal horn neurons in the outer zone of lamina II (lamina IIo) are important for processing nociceptive information from C-fiber primary afferents. In the present study, we tested a hypothesis that activation of presynaptic α2-adrenergic receptors by clonidine inhibits the excitatory synaptic input to lamina IIo neurons. Whole cell voltage-clamp recordings were performed on visualized lamina IIo neurons in the spinal cord slice of rats. The miniature excitatory postsynaptic currents (mEPSCs) were recorded in the presence of tetrodotoxin, bicuculline, and strychnine. The evoked EPSCs were obtained by electrical stimulation of the dorsal root entry zone or the attached dorsal root. Both mEPSCs and evoked EPSCs were abolished by application of 6-cyano-7-nitroquinoxaline-2,3-dione. Clonidine (10 μM) significantly decreased the frequency of mEPSCs from 5.8 ± 0.9 to 2.7 ± 0.6 Hz (means ± SE) without altering the amplitude and the decay time constant of mEPSCs in 25 of 27 lamina IIo neurons. Yohimbine (2 μM, an α2-adrenergic receptor antagonist), but not prazosin (2 μM, an α1-adrenergic receptor antagonist), blocked the inhibitory effect of clonidine on the mEPSCs. Clonidine (1–20 μM, n = 8) also significantly attenuated the peak amplitude of evoked EPSCs in a concentration-dependent manner. The effect of clonidine on evoked EPSCs was abolished in the presence of yohimbine ( n = 5). These data suggest that clonidine inhibits the excitatory synaptic input to lamina IIo neurons through activation of α2-adrenergic receptors located on the glutamatergic afferent terminals. Presynaptic inhibition of glutamate release from primary afferents onto lamina IIoneurons likely plays an important role in the analgesic action produced by activation of the descending noradrenergic system and α2-adrenergic agonists.

Gastrin-releasing peptide directly releases pepsinogen from guinea pig chief cells

1990 ◽  
Vol 259 (5) ◽  
pp. G760-G766 ◽  
Author(s):  
S. Fiorucci ◽  
K. E. McArthur
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Receptor Antagonist ◽  
Fold Increase ◽  
Chief Cells ◽  
Gastrin Releasing Peptide ◽  
Basal Release ◽  
Substance P Receptor ◽  
Bombesin Receptor ◽  
Muscarinic Agents

Gastrin-releasing peptide (GRP) and bombesin can stimulate pepsinogen release by both gastrin-dependent and -independent mechanisms. Using isolated guinea pig gastric chief cells, we determined that GRP can act directly on the guinea pig chief cell to cause pepsinogen release. GRP and bombesin stimulated a 2.5- to 3-fold increase in pepsinogen release above basal release. Substance P also stimulated a small but significant increase in pepsinogen release. No gastrin immunoreactivity was detected in the supernatants of cells stimulated with up to 1 microM GRP or bombesin or 1 mM carbachol. GRP-stimulated pepsinogen release was completely inhibited by GRP/bombesin receptor agonists as well as substance P receptor antagonist but not by antagonists to receptors for gastrin, the octapeptide of cholecystokinin (CCK-8), secretin, vasoactive intestinal peptide (VIP), or muscarinic agents. Substance P-stimulated pepsinogen release was completely inhibited by substance P receptor antagonist but not by GRP/bombesin receptor antagonists. An additive effect on pepsinogen release was seen when GRP was combined with maximally effective concentrations of adenosine 3',5'-cyclic monophosphate (cAMP)-mediated agents (VIP, secretin, 8-BrcAMP) but not with calcium-mediated agents (carbachol, CCK-8, gastrin). These results indicate that GRP can directly stimulate pepsinogen release from guinea pig chief cells by a specific GRP receptor that mobilizes intracellular calcium.

Guinea pig pancreatic neurons: morphology, neurochemistry, electrical properties, and response to 5-HT

1997 ◽  
Vol 273 (6) ◽  
pp. G1273-G1289 ◽  
Author(s):  
Min-Tsai Liu ◽  
Annette L. Kirchgessner
Keyword(s):  
Nitric Oxide ◽  
Electrical Properties ◽  
Nitric Oxide Synthase ◽  
Guinea Pig ◽  
Choline Acetyltransferase ◽  
Synaptic Input ◽  
Action Potentials ◽  
Receptor Desensitization ◽  
5 Ht Uptake ◽  
Oxide Synthase

The morphology, neurochemistry, and electrical properties of guinea pig pancreatic neurons were determined. The majority of neurons expressed choline acetyltransferase (ChAT) immunoreactivity; however, ChAT-negative neurons were also found. Both cholinergic and noncholinergic neurons expressed nitric oxide synthase (NOS) immunoreactivity. Three types of pancreatic neurons were distinguished. Phasic neurons fired action potentials (APs) at the onset of depolarizing current pulse, tonic neurons spiked throughout the duration of a suprathreshold depolarizing pulse, and APs could not be generated in nonspiking neurons, even though they did receive synaptic input. APs were tetrodotoxin sensitive, and all types of neurons received fast and slow excitatory postsynaptic potentials (EPSPs). Fast EPSPs had cholinergic and noncholinergic components. The majority of pancreatic neurons appeared to innervate the acini. NOS- and/or neuropeptide Y-immunoreactive phasic and tonic neurons were found. Microejection of 5-hydroxytryptamine (5-HT) caused a slow depolarization that was inhibited by the 5-HT1P antagonist N-acetyl-5-hydroxytryptophyl-5-hydroxytryptophan amide and mimicked by the 5-HT1Pagonist 6-hydroxyindalpine. A pancreatic 5-HT transporter was located, and inhibition of 5-HT uptake by fluoxetine blocked slow EPSPs in 5-HT-responsive neurons by receptor desensitization.

Participation of substance P present in small-diameter afferent fibers in microcirculatory hemodynamics of rat hindpaw skin

1991 ◽  
Vol 16 ◽  
pp. 37
Author(s):  
Norifumi Yonehara ◽  
Ji-Qiang Chen ◽  
Yasuo Imai ◽  
Sou Takiuchi ◽  
Reizo Inoki
Keyword(s):  
Substance P ◽  
Small Diameter ◽  
Afferent Fibers

Allergic inflammation-induced neuropeptide production in rapidly adapting afferent nerves in guinea pig airways

2002 ◽  
Vol 282 (4) ◽  
pp. L775-L781 ◽  
Author(s):  
Allen C. Myers ◽  
Radhika Kajekar ◽  
Bradley J. Undem
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Sensory Neurons ◽  
Large Diameter ◽  
Sensory System ◽  
Small Diameter ◽  
Allergic Inflammation ◽  
Primary Afferent ◽  
Chemical Coding ◽  
Low Threshold

In the vagal-sensory system, neuropeptides such as substance P and calcitonin gene-related peptide (CGRP) are synthesized nearly exclusively in small-diameter nociceptive type C-fiber neurons. By definition, these neurons are designed to respond to noxious or tissue-damaging stimuli. A common feature of visceral inflammation is the elevation in production of sensory neuropeptides. Little is known, however, about the physiological characteristics of vagal sensory neurons induced by inflammation to produce substance P. In the present study, we show that allergic inflammation of guinea pig airways leads to the induction of substance P and CGRP production in large-diameter vagal sensory neurons. Electrophysiological and anatomical evidence reveals that the peripheral terminals of these neurons are low-threshold Aδ mechanosensors that are insensitive to nociceptive stimuli such as capsaicin and bradykinin. Thus inflammation causes a qualitative change in chemical coding of vagal primary afferent neurons. The results support the hypothesis that during an inflammatory reaction, sensory neuropeptide release from primary afferent nerve endings in the periphery and central nervous system does not require noxious or nociceptive stimuli but may also occur simply as a result of stimulation of low-threshold mechanosensors. This may contribute to the heightened reflex physiology and pain that often accompany inflammatory diseases.

A Role for Histamine and Substance P in Immediate Allergic Responses in Guinea Pig Airways: Characterization of MDL 108,207DA, a Dual H1 / NK-1 Receptor Antagonist

1998 ◽  
Vol 115 (2) ◽  
pp. 169-178 ◽  
Author(s):  
Elizabeth Kudlacz ◽  
Scott Shatzer ◽  
Deborah Logan ◽  
Karl Olsen ◽  
Robert Knippenberg ◽  
...  
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Receptor Antagonist

Involvement of substance P present in small-diameter afferent fibers in microcirculatory hemodynamics of the rat hind instep

1992 ◽  
Vol 37 ◽  
pp. S181
Author(s):  
N. Yonehara ◽  
Y. Imai ◽  
S. Takiuchi ◽  
F-D. Tang ◽  
R. Inoki
Keyword(s):  
Substance P ◽  
Small Diameter ◽  
Afferent Fibers

Volume-sensitive synaptic input to neurons in guinea pig inferior mesenteric ganglion

1990 ◽  
Vol 259 (3) ◽  
pp. G490-G497 ◽  
Author(s):  
T. L. Anthony ◽  
D. L. Kreulen
Keyword(s):  
Guinea Pig ◽  
Synaptic Input ◽  
Intraluminal Pressure ◽  
Postsynaptic Potentials ◽  
Inferior Mesenteric Ganglion ◽  
Synaptic Potentials ◽  
Mesenteric Ganglion ◽  
Excitatory Synaptic Input ◽  
The Relationship

The relationship between changes in intracolonic volume related to propulsive contractions and synaptic potentials recorded intracellularly in neurons in the inferior mesenteric ganglion (IMG) was investigated in vitro. Distension of the colon induced propulsive contractions (frequency, 2-5/min), which reduced intracolonic volume by 88%. Each propulsive contraction was sustained for 10-12 s, after which time the colon refilled. The sustained propulsive contractions were associated with a decrease in the amplitude and frequency of fast cholinergic excitatory postsynaptic potentials (EPSPs) and partial repolarization of the slow EPSP. The pressure-volume relationships of the colonic segments had two limbs: at distension pressures less than 15 cmH2O ("volume limb") the intracolonic volume was proportional to the distension pressure; greater than 15 cmH2O ("pressure limb") the intracolonic volume did not increase further. The changes in synaptic input were related to these pressure-volume relationships. In the volume limb, the frequency and amplitude of fast EPSPs were proportional to intracolonic volume and maximized with volume. In the pressure limb, there was a slow depolarization of the membrane that increased with greater distension pressures. Under isovolumic conditions, the changes in intraluminal pressure associated with colonic contractions were not associated with changes in excitatory synaptic input to IMG neurons. These experiments demonstrate that colonic mechanoreceptors to IMG neurons are sensitive to both intracolonic volume and pressure.

Involvement of substance P present in small-diameter afferent fibers in microcirculatory hemodynamics of the rat hind instep

1993 ◽  
Vol 46 (1-2) ◽  
pp. 220-222 ◽  
Author(s):  
Norifumi Yonehara ◽  
Sou Takiuchi ◽  
Yasuo Imai ◽  
Fa-Di Tang ◽  
Reizo Inoki
Keyword(s):  
Substance P ◽  
Small Diameter ◽  
Afferent Fibers
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